Unpublished personal note by Ernest Sternglass for Radiation Public Health Project (RPHP) 8nov03
Part of the reason why Strontium-90 is so damaging is that radioactive Yttrium-90, which has different chemical properties than Strontium-90, concentrates in the hormone producing soft-tissue glandular organs such as the pituitary gland, the pancreas, the thyroid and the male and female reproductive organs. Thus, key hormones such as estrogen and testosterone can be affected both during early development and later in life, when they play a major role in breast and prostate cancer, as well as in reduced fertility, premature births, sexual development and sexual orientation. Thus, Strontium-90/Yttrium-90 is a powerful hormone disrupter, often acting synergistically with other nonradioactive chemicals in the environment such as pesticides, smoke and diesel exhaust.
Another reason why low dose exposures to fission products such as Strontium-90 is so serious is that protracted exposures over periods of days, months or years were discovered by Petkau to be much more damaging biologically than the same dose received in short diagnostic medical exposures or flashes from a nuclear bomb explosion by factors of hundreds to thousands of times. This is due to the greater efficiency of free-radical oxygen molecules in puncturing cell-membranes when they are produced one-by one and do not become deactivated by colliding with each other in the dense cluster produced during short X-ray or gamma ray exposures. Thus, chronic exposures to Strontium-90 produces cancer, immune system and respiratory damage such as asthma at very low doses.
Moreover, it has been found in laboratory studies that Yttrium-90 also concentrates in the lung, so that the ingestion of Strontium-90 can cause lung cancer, explaining recent rises in lung cancer mortality in counties downwind from the Diablo Canyon nuclear plant in San Louis Obispo that started in 1984, while lung cancer mortality declined in California as a whole as well as in the San Francisco-Sacramento area, where the nearby Rancho Seco nuclear plant was shut down in 1989.
Aside from the dose due to Strontium-90, it is an indicator of other radiation doses received from the many shorter-lived fission products that are produced together with Strontium-90 and released from nuclear reactors both in liquid and airborne effluents that do not rise high into the atmosphere.
Elements such as Iodine-131, with an 8 day half-life and others with even shorter half-lives, can produce many times the radiation dose of Strontium-90, just as occurred during the early period of A-bomb testing in Nevada when the fallout came down in a matter of hours. The recently published study in Suffolk County, Long Island, surrounded by nuclear plants, shows that a single picoCurie per gram calcium in recent baby teeth is associated with nearly a doubled risk of childhood cancer, about three times as serious as the Strontium-90 in baby teeth measured in the early 1960s in St. Louis that originated from high altitude H-bomb tests when fallout came down from the upper stratosphere over a period of years. The reason for the increased risk per picoCurie of Sr-90 near nuclear plants as compared with high altitude H-bomb tests is that many short-lived radioactive isotopes such as Strontium-89 with a half-life of 50 days, Barium-140 with a half-life 12.8 days along with Iodine-133 with a half-life of only 21 hours can be inhaled following repeated routine batch-releases or steady leak-ages from corroding steam generators, pipes and valves since winds carry the airborne emissions to nearby towns and large cities in a matter of only a few hours.
The greatly increased risk of low doses produced by nuclear fission products as compared with the risk estimated from high doses produced by short external medical or A-bomb exposures has recently been summarized in a report issued by the European Committee on Radiation Risk [ECRR] prepared at the request of members of the European Parliament issued in January 2003 edited by Busby et al. As indicated in the Executive Summary, [below] available at the web-site http://www.euradcom.org, the biological damage from internal radiation at low dose is some 100 to 1000 times greater than estimated by the government sponsored International Committee of Radiation Protection (ICRP) [http://www.icrp.org]largely based on extrapolation of the results of the study of A-bomb survivors in Hiroshima and Nagasaki exposed to short, high doses of gamma rays and neutrons.
Stokke, T., Oftedal R, and Pappas A. Effects of Small Doses of Strontium-90 on the Rat Bone Marrow. Acta Radiologica 7: 321, 1968. The authors found that extremely small radiation doses by Strontium-90 in laboratory animals comparable to that from a month or two from natural background sources produced significant declines in the number of bone-marrow cells. This weakens the immune system and thus allows cancer cells anywhere in the body to proliferate more rapidly, and also causes infectious diseases to take a greater toll.
Petkau, A. Effect of Na-22 on a Phospholipid Membrane, Health Physics. 22: 239,1972, Protection of Acholeplasma laidlawii B by superoxide dismutase, Int. J. Radiation Biology, 26: 421-426, 1974; Protection and Repair of Irradiated Membranes, in Free Radicals, Aging, and Degenerative Diseases, 481-508 (Alan R. Liss. Inc., 1986). These articles describe the discovery that protracted radiation exposures such as occur from inhaled or ingested fission products accumulating in bone or other organs are hundreds to thousands of times as damaging as the same dose given in a short burst, such as diagnostic X-rays or the flash from a nuclear bomb. This is due to the action of free-radicals such as negatively charged oxygen molecules, whose efficiency in puncturing cell membranes and thus killing cells increases greatly as the radiation dose per unit of time decreases. This is unlike the case of direct damage to the DNA in very short diagnostic or therapeutic X-ray exposures and the flash of a nuclear detonation, where repair mechanisms are able to reduce the DNA damage to healthy tissue and the free radicals produced in high concentrations deactivate each other before most of them can reach cell membranes.
Gould, J M et al. Strontium-90 in Deciduous teeth as a Factor Early Childhood Cancer. International Journal of Health Services, 30: 515-539, 2000. This article describes findings of a high correlation between rising and declining Sr-90 concentrations in children and the number of newly reported leukemia and cancer rates in Suffolk County, Long Island, and higher cancer rates downwind from nuclear reactors than in distant areas, similar to what was found at the time of large-scale nuclear weapons testing in the atmosphere in the 1950s and early 1960s.
Busby, C., Berets, R., Schmitz-Feuerhake, I., Cato, M. and Vablokov, A. 2003 Recommendations of the ECRR. The Health Effects of Ionising Radiation Exposure to Low Doses for Radiation Protection Purposes. Green Audit Press, Castle Cottage, Aberystwyth, 5V 23 IDZ UK. A 186 page report by a non-government group of independent scientists that documents the recent evidence that low dose internal exposures by radioactive chemicals released be nuclear detonations and nuclear reactors have been a major factor in the recent cancer epidemic and the rise of other types of ill health due to the nuclear fuel cycle, and that nuclear power is a costly way of producing energy when human health deficits are included in the overall assessment. [below]
source: Sent by Dr. Sternglass 8nov03
ECRR 2003 Recommendations of the European Committee on
Radiation Risk The Health Effects of Ionising Radiation Exposure at
Low Doses for Radiation Protection Purposes. Regulators’ Edition.
This report outlines the committee’s findings regarding the effects on human health of exposure to ionising radiation and presents a new model for assessing these risks. It is intended for decision-makers and others who are interested in this area and aims to provide a concise description of the model developed by the committee and the evidence on which it depends. The development of the model begins with an analysis of the present risk model of the International Commission on Radiological Protection (ICRP) which is the basis of and dominates all present radiation risk legislation. The committee regards this ICRP model as essentially flawed as regards its application to exposure to internal radioisotopes but for pragmatic reasons to do with the existence of historical exposure data has agreed to adjust for the errors in the ICRP model by defining isotope and exposure specific weighting factors for internal exposures so that the calculation of effective dose (in Sieverts) remains. Thus, with the new system, the overall risk factors for fatal cancer published by ICRP and other risk agencies may be used largely unchanged and legislation based upon these may also be used unchanged. It is the calculation of the dose which is altered by the committee’s model.
- The European Committee on Radiation Risk arose out of criticisms of the risk models of the ICRP which were explicitly identified at the European Parliament STOA workshop in February 1998; subsequently it was agreed that an alternative view should be sought regarding the health effects of low level radiation. The committee consists of scientists and risk specialists from within Europe but takes evidence and advice from scientists and experts based in other countries.
- The report begins by identifying the existence of a dissonance between the risk models of the ICRP and epidemiological evidence of increased risk of illness, particularly cancer and leukaemia, in populations exposed to internal radioactive isotopes from anthropogenic sources. The committee addresses the basis in scientific philosophy of the ICRP risk model as applied to such risks and concludes that ICRP models have not arisen out of accepted scientific method. Specifically, ICRP has applied the results of external acute radiation exposure to internal chronic exposures from point sources and has relied mainly on physical models for radiation action to support this. However, these are averaging models and cannot apply to the probabilistic exposures which occur at the cell level. A cell is either hit or not hit; minimum impact is that of a hit and impact increases in multiples of this minimum impact, spread over time. Thus the committee concludes that the epidemiological evidence of internal exposures must take precedence over mechanistic theory-based models in assessing radiation risk from internal sources.
- The committee examines the ethical basis of principles implicit in the ICRP models and hence in legislation based on them. The committee concludes that the ICRP justifications are based on outmoded philosophical reasoning, specifically the averaging cost-benefit calculations of utilitarianism. Utilitarianism has long been discarded as a foundation for ethical justification of practice owing to its inability to distinguish between just and unjust societies and conditions. It may, for example, be used to underpin a slave society, since it is only the overall benefit which is calculated, and not individual benefit. The committee suggests that rights-based philosophies such as Rawls Theory of Justice or considerations based on the UN Declaration of Human Rights should be applied to the question of avoidable radiation exposures to members of the public resulting from practice. The committee concludes that releases of radioactivity without consent can not be justified ethically since the smallest dose has a finite, if small, probability of fatal harm. In the event that such exposures are permitted, the committee emphasises that the calculation of ‘collective dose’ should be employed for all practices and time scales of interest so that overall harm may be integrated over the populations.
- The committee believes that it is not possible accurately to determine ‘radiation dose to populations’ owing to the problems of averaging over exposure types, cells and individuals and that each exposure should be addressed in terms of its effects at the cell or molecular level. However, in practice, this is not possible and so the committee has developed a model which extends that of the ICRP by the inclusion of two new weighting factors in the calculation of effective dose. These are biological and biophysical weighting factors and they address the problem of ionisation density or fractionation in time and space at the cell level arising from internal point sources. In effect, they are extensions of the ICRP’s use of radiation weighting factors employed to adjust for differences in ionisation density resulting from different quality radiations (e.g. alpha-, beta and gamma).
- The committee reviews sources of radiation exposure and recommends caution in attempting to gauge the effects of novel exposures by comparison with exposures to natural radiation. Novel exposures include internal exposures to artificial isotopes like Strontium-90 and Plutonium-239 but also include micrometer range aggregates of isotopes (hot particles) which may consist of entirely man-made isotopes (e.g. plutonium) or altered forms of natural isotopes (e.g. depleted uranium). Such comparisons are presently made on the basis of the ICRP concept of ‘absorbed dose’ which does not accurately assess the consequence for harm at the cell level. Comparisons between external and internal radiation exposures may also result in underestimates of risk since the effects at the cell level may be quantitatively very different.
- The committee argues that recent discoveries in biology, genetics and cancer research suggest that the ICRP target model of cellular DNA is not a good basis for the analysis of risk and that such physical models of radiation action cannot take precedence over epidemiological studies of exposed populations. Recent results suggest that very little is known about the mechanisms leading from cell impact to clinical disease. The committee reviews the basis of epidemiological studies of exposure and points out that many examples of clear evidence of harm following exposure have been discounted by ICRP on the basis of invalid physical models of radiation action. The committee re-instates such studies as a basis for its estimates of radiation risk. Thus the 100-fold discrepancy between the ICRP model’s predictions and the observed cases in the Sellafield childhood leukemia cluster becomes an estimator of risk for childhood leukemia following such exposure. The factor is thus incorporated by the committee into the calculation of harm from internal exposure of specific types through its inclusion in the weighting factors used to calculate the ‘effective dose’ to the children in Sieverts.
- The committee reviews the models of radiation action at the cell level and concludes that the ‘linear no threshold’ model of the ICRP is unlikely to represent the response of the organism to increasing exposure except for external irradiation and for certain end points in the moderately high dose region. Extrapolations from the Hiroshima lifespan studies can only reflect risk for similar exposures i.e. high dose acute exposures. For low dose exposures the committee concludes, from a review of published work, that health effects relative to the radiation dose are proportionately higher at low doses and that there may be a biphasic dose response from many of these exposures owing to inducible cell repair and the existence of high-sensitivity phase (replicating) cells. Such dose-response relationships may confound the assessment of epidemiological data and the committee points out that the lack of a linear response in the results of epidemiological studies should not be used as an argument against causation.
- In further considering mechanisms of harm, the committee concludes that the ICRP model of radiation risk and its averaging methods exclude effects which result from anisotropy of dose both in space and in time. Thus the ICRP model ignores both high doses to local tissue caused by internal hot particles, and sequential hits to cells causing replication induction and interception (second event), and merely averages all these high risk situations over large tissue mass. For these reasons, the committee concludes that the unadjusted ‘absorbed dose’ used by ICRP as a basis of risk calculations is flawed, and has replaced it with an adjusted ‘absorbed dose’ which used enhancement weightings based on the biophysical and biological aspects of the specific exposure. In addition, the committee draws attention to risks from transmutation from certain elements, notably Carbon-14 and Tritium, and have weighted such exposures accordingly. Weightings are also given to radioactive versions of elements which have a particular biochemical affinity for DNA e.g. Strontium and Barium and to certain Auger emitters.
- The committee reviews the evidence which links radiation exposure to illness on the basis that similar exposures define the risks of such exposures. Thus the committee considers all the reports of associations between exposure and ill health, from the A-bomb studies to weapons fallout exposures, through nuclear site downwinders, nuclear workers, reprocessing plants, natural background studies and nuclear accidents. The committee draws particular attention to two recent sets of exposure studies which show unequivocal evidence of harm from internal irradiation at low dose. These are the studies of infant leukemia following Chernobyl, and the observation of increased minisatellite DNA mutations following Chernobyl. Both of these sets of studies falsify the ICRP risk models by factors of between 100 and 1000. The committee uses evidence of risk from exposures to internal and external radiation to set the weightings for the calculation of dose in a model which may be applied across all exposure types to estimate health outcomes. Unlike the ICRP the committee extends the analysis from fatal cancer to infant mortality and other causes of ill health including non-specific general health detriment.
- The committee concludes that the present cancer epidemic is a consequence of exposures to global atmospheric weapons fallout in the period 1959-63 and that more recent releases of radioisotopes to the environment from the operation of the nuclear fuel cycle will result in significant increases in cancer and other types of ill health.
- Using both the ECRR’s new model and that of the ICRP the committee calculates the total number of deaths resulting from the nuclear project since 1945. The ICRP calculation, based on figures for doses to populations up to 1989 given by the United Nations, results in 1,173,600 deaths from cancer. The ECRR model predicts 61,600,000 deaths from cancer, 1,600,000 infant deaths and 1,900,000 foetal deaths. In addition, the ECRR predict a 10% loss of life quality integrated over all diseases and conditions in those who were exposed over the period of global weapons fallout.
- The committee lists its recommendations. The total maximum permissible dose to members of the public arising from all human practices should not be more than 0.1mSv, with a value of 5mSv for nuclear workers. This would severely curtail the operation of nuclear power stations and reprocessing plants, and this reflects the committee’s belief that nuclear power is a costly way of producing energy when human health deficits are included in the overall assessment. All new practices must be justified in such a way that the rights of all individuals are considered. Radiation exposures must be kept as low as reasonably achievable using best available technology. Finally, the environmental consequences of radioactive discharges must be assessed in relation to the total environment, including both direct and indirect effects on all living systems.
source: http://www.euradcom.org/2003/execsumm.htm 18nov03