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On Internal Irradiation and the Health Consequences of the Chernobyl Accident

Chris Busby PhD
Presented at the Sixth Conference of the British and Irish Charity organisations on Mitigating the Consequences in Belarus of the Chernobyl Catastrophe, London April 6th 2001.

Occasional Paper 2001/5 Aberystwyth: Green Audit April 2001


1.Confusion More than 15 years after the event, the health outcome of the Chernobyl catastrophe has been extremely difficult to evaluate. How is this possible? Members of the public, in the West, are simultaneously being asked (by the charities) to give aid to countries like Belarus, and shown pictures of children with cancer or birth defects, and also being told (by the atomic scientists in the IAEA and elsewhere) that the levels of radiation exposure are comparable with a holiday in Cornwall, (natural background radiation) or a flight to Majorca (cosmic rays) and that any problems are due to ‘radiophobia’. What are we to believe? I hope to be able to reduce some of this confusion today, by distinguishing between internal and external radiation exposure, and showing that the models which were used by the scientists to predict cancer in people exposed to Chernobyl fallout were not appropriate. I will argue that the radiation has caused, and will cause, terrible illness in those living in the contaminated territories, and that the human race has an opportunity to learn from this event, that the demons constrained within the atom, are released at a fearful price. I will show this unequivocally. 2. The Chernobyl Infants I was trained as a chemist. As a chemist, I could stand before you and mix a clear solution of the indicator, phenolphthalein and a clear solution of the base, sodium hydroxide to produce a startling red colour. I cannot hold up a child and mix it with low level radiation to produce leukemia. A very close experiment to this has, however, been recently described and you should be aware of this. It shows, without any doubt, that the concerns of those who argued, either emotionally, or illogically, or with good scientific arguments, that low-level radiation was killing people near nuclear sites, were correct. These consequences of slight leakages and minor licenses discharges were a taste of what was to come, when a nuclear plant exploded and discharged most of its inventory to the biosphere. Following the Chernobyl accident in 1986, in five different countries, the cohort of children who were exposed in their mother’s womb to radioisotopes from the releases suffered an excess risk of developing leukemia in their first year of life. This ‘infant leukemia’ cohort effect was first reported in Scotland [Gibson et al, 1988], and then in Greece [Petridou et al, 1996], in the United States [Mangano, 1997] and in Germany [Michaelis, et al. 1997]. We first reported increases in childhood leukemia in Wales and Scotland following the Chernobyl accident in 1996 [ Bramhall, 1996] but more recently examined the specific infant leukemia cohort in Wales and Scotland [Busby and Scott Cato 2000]. Unlike the earlier researchers, who merely showed the existence of a significant rise in infant leukemia, we decided to examine the relationship between the observed numbers of cases and those predicted by the present radiation risk model. This was an invaluable opportunity since the specificity of the cohort enabled us to argue that the effect could only be a consequence of the exposure to the Chernobyl fallout. There could be no alternative explanation, like the ‘population mixing hypothesis’ advanced to explain away the Sellafield childhood leukemia cluster. However implausible such theories may be, they have acquired popularity, and their proponents status, as a consequence of their utility to the nuclear lobby. However, population mixing may not occur at Sellafield but it cannot occur in the womb. Because the National Radiological Protection Board had measured and assessed the doses to the populations of Wales and Scotland and because they themselves had also published risk factors for radiogenic leukemia based on ICRP models it was a simple matter


to compare their predictions with the observations and test the contemporary risk model. The method simply assumed that infants born in the periods 1980-85 and 1990-92 were unexposed, and defined the Poisson expectation of numbers of infant leukemia cases in the children who were in utero over the 18 month period following the Chernobyl fallout. This 18 month period was chosen because it was shown that the in utero dose was due to radioactive isotopes which were ingested or inhaled by the mothers and that whole-body monitoring had shown that this material remained in the bodies of the mothers until Spring 1987 because silage cut in the Summer of 1986 had been stored and fed to the cattle in the following winter. The result was startling. First, there was a statistically significant 3.8-fold excess of infant leukemia in the combined Wales and Scotland cohort (p = 0.0002). Second, the leukemia yield in the exposed ‘in utero’ cohort was about 100 times the yield predicted by the model. Table 1 compares the effect in the three main studies. In passing it should be noted that this number, 100, is very close to the error required to explain the Sellafield childhood leukemia cluster. At this stage we must close another denial exit. It should be noted that the possibility of the effect being due to chance may be obtained by multiplying the p-values for the null hypothesis that the effect was due to chance in each of the separate countries and studies to give an overall p-value less than 0.0000000001. Thus it was not a chance occurrence: it was a consequence of the exposure to low-level radiation from Chernobyl. I am sorry to have to keep banging the gong but I want you to be quite clear about this point. And since the World Health Organization has given approximate exposure levels in Greece, Germany and the United States, it was also possible to examine the leukemia yield in the infant ‘exposed cohort’ reported by the several other studies and establish a dose response relationship. This is shown in Fig 1. It is a curious shape and goes up, down and up again, and this shape should be noted. It means that the highest doses give the least effect. Indeed, there was a weak effect in Belarus (Ivavov et al, 1998). I will return to this point below. Before moving on, I will summarise this important result: Exposure to internal isotopes from the Chernobyl fallout caused increases in infant leukemia in five different countries with a yield that showed an error of upwards of 100-fold in the ICRP risk models for low dose. The dose response curve was biphasic. 3. Mechanism of low dose exposure I will briefly account for how the risk models of the International Commission on Radiological Protection and its satellites managed to be in error by such a large amount. The method used to calculate dose models absorbed dose as energy per unit volume. Humans are imagined to be bags of water into which energy is transferred. Fig 2, taken from an ICRP publication, shows the phantom used for this approach. In assessing the health consequences of radiation exposure, the Japanese inhabitants of Hiroshima, who were exposed to the Abomb in 1945, were studied. Doses were calculated, using the bag-of-water model and the cancer yield over the lifetime of the exposed individuals, was matched up to the doses, for people standing at various distances from the hypocentre of the explosion. This therefore was a study of a single, very large, acute flash exposure. All the cells in the bodies of the exposed had the same dose, the same number of tracks of charged particles, and the same damage. If this damage was higher than about 1 to 5 Joules per kilogram (1 to 5 Gray), enough of the cells died to cause the death of the individual. The relationship between dose and subsequent cancer in this Japanese population, together with a few other studies of external acute radiation, has formed the basis for the risk model. However, it is easy to see that such a risk model should not be applied to internal


radiation in the low dose region. Internal radiation exposure results from point sources within the body. These are either radioactive atoms like Strontium-90 or Plutonium-239, or Caesium-137, or they are small particles of radioactive material, ‘hot particles’ of radioisotopes. In many cases they will give high doses to local tissue from short range decays of beta or alpha particles. In the case of the hot particles and sequentially decaying isotopes like Strontium-90 or Tellurium-132, they have the ability to decay twice or several times. This can result in a second event hazard because an initial hit to a cell can force it into repair and replication sequences during which a second hit will result in an invisible mutation, because the cell will not be able to do a second repair before it replicates. [Busby 1997, Cox and Edwards, 2000, Busby, 2000] All of these considerations result from inhomogeneities of energy deposition. We could compare the two approaches, in terms of sitting in front of a fire and warming oneself (ICRP model) or eating a hot coal (internal radioisotopes). To Summarise: The external average dose risk model applied by the ICRP is incorrect when applied to internal radioisotope contamination because internal hot particles and isotopes may give very high doses to some cells but no doses to others. Since it is cell genetic damage which results in cancer, it is cell dose which is the causal parameter. 4. Dose response curve: the Burlakova response. It has been known from almost the beginning of the radiation age that rapidly replicating cells are more sensitive to radiation damage [Bergonie and Tribondeau, 1906]. Indeed, this is the basis of radiotherapy for cancer where it is the rapidly proliferating cancer cells that are preferentially destroyed. Most cells in a living organism are in a non-replication mode, sometimes labelled G0. These cells are contributing to the organism as part of the normal living process and do not need to replicate unless there is some signal requiring this, perhaps because of tissue growth, damage or senescence. Throughout the growth and lifespan of individual organisms, there is a constant need for cellular replication, and therefore there are always some small proportion of cells which will be replicating: the magnitude will naturally depend upon the type of cell. When cells receive the signal to move out of stasis or G0, they undertake a fixed sequence of DNA repair and replication, labelled G0-G1-S-G2-M, with various identifiable check points through the sequence which ends in replication M or Mitosis. The period of the repair replication sequence is about 10 to 15 hours and the sensitivity of replicating cells to damage including fixed mutation is extremely high at some points during this sequence. This has been known for some time: Fig 3 shows the results of early experiments on Chinese hamster cells indicating up to 600-fold variation in the cell radiation sensitivity over the whole cycle. [ Morton and Sinclair, 1966] If we display this response variation on a scale that shows the normal cell lifespan in the organism, rather than just over the cell cycle in vitro, the window of opportunity for cell mutation at high sensitivity becomes apparent Fig 4. So the picture of isotropic dose to equivalent cells, the ‘bag of water’ phantom model, has to be reviewed. Perhaps 1 percent of these cells are actively dividing and are in repair replication sequences that we will assume, for argument, are 600 times more sensitive to being ‘hit’ by a track. What would we expect the dose-response to look like? Well as the dose was increased from zero, the sensitive cells would begin to be damaged and a proportion of these hits would results in fixing a mutation and increasing the possibility of cancer. As the dose increased further, eventually this rise in response would peak as these sensitive cells were killed. The mutation yield would then begin to fall. However, at some point, the insensitive G0 cells would begin to be damaged and the whole process would begin again, with a rise in cancer. Ultimately there would be a second fall, but this level of exposure


would probably result in the death of the organism (although such considerations have been used to explain an observed fall-off in effect from alpha emitters at high dose). So the dose response would look like that in Fig 5. This type of response was shown to occur in several experiments by Burlakova, although she gave a different explanation for it, involving a combination of increasing damage and induced repair curves. [Burlakova.1996] The results of animal studies on beagle dogs and mice also show these biphasic effects in the low-dose region [Busby, 1995] . Incidentally, it is quite easy to see how such a result might be interpreted as ‘hormesis’, the radiation-is-good-for-you concept advanced by the nuclear lobby and its scientists. All that is necessary is to plot the biphasic response but leave out the first zero point. The deductive conclusions from high-dose experiments could not be squared with the possibility of such variation in this low dose region so either the points were interpreted as scatter or they were forced into a hormesis dip by leaving out the lowest dose responses as outliers. Note that this type of curve is seen in the Chernobyl infant studies collected together in Fig 1. To summarise: The dose response curve in the low dose region, results from effects in two separate sub groups of cells, those which are engaged in repair-replication, and those which are in quiescent phase. This results in a biphasic response with a high sensitivity window for mutation and cancer in the low dose region below 10mSv. Inappropriate conclusions about results in this region have led to the development of the concept of hormesis, which maintains that low doses of radiation cause good health. 5. The Second Event Theory There is large variation in sensitivity over the cell lifespan. Although naturally dividing cells may accidentally receive a ‘hit’, this process can be modelled by averaging over large masses of tissue, even if the dose response curve is not linear, as thought. However, unplanned cell division, preceded by DNA repair can be forced by a sub-lethal damaging radiation track: this is one of the signals which push the cell out of G0 into the repair replication sequence. It follows that two hits, separated by about eight hours, can generate a high sensitivity cell and then hit this same cell a second time in its sensitive phase. This idea, the ‘Second Event Theory’ is described and supporting evidence advanced in Busby 1995 and its mathematical description has been approached slightly differently in Busby 2000. It has been the subject of some dispute by NRPB (Cox and Edwards, 2000, Busby, 2000a) Very recently, developments in micro techniques have enabled some new evidence that supports the two hit idea to emerge. Miller et al., [1999] in a consideration of Radon exposure risks, have been able to show that the measured oncogenicity from exactly one alpha particle hit per cell is significantly lower than for a Poisson distributed mean of one alpha particle hit per cell. The authors argue that this implies that cells traversed by two alpha particles or more contribute most of the risk of mutation, i.e. single hits are not the cause of cancer. There are two types of internal exposure for which there would be expected to be an enhancement of risk from this Second Event source. The first, due to sequentially decaying radioisotopes like Strontium-90 has been discussed in Busby 1995, Cox and Edwards, 2000 and Busby, 2000. Following an initial decay from an Sr-90 atom bound to a chromosome, the second decay from the daughter, Yttrium-90, whose half-life is 64hrs can hit the same cell in the induced replication sequence with a probability that is simple to calculate. The same dose from external radiation has a vanishingly small chance of effecting the same process. The second type of Second Event exposure, referred to in Busby 2000a, is from micron or sub-micron sized ‘hot particles’. If lodged in tissue, these will decay again and again


increasing the probability of multiple hits to the same cell inside the 10 hour repair replication period. That such hot particles were a feature of the Chernobyl fallout can be seen by the autoradiograph in Fig 7. A hazard enhancement from radiation exposure occurs when the dose is fractionated in such a way as to provide two hits to a cell within the cell repair replication cycle period of 8-12 hours. This process is called a second event, and mutation is introduced because the first hit causes cells to enter a sensitive and irreversible sequence of repair and replication within which a second hit causes damage that cannot be repaired. This process is very unlikely to occur with external radiation at normal background levels but can occur with internal sequential emitters like Strontium-90 and Tellurium-132, or from particles. 6. Independent evidence on low dose internal exposure. The Chernobyl Infants studies show errors in the risk models of upwards of 100-fold. There is insufficient space to review all the other studies that show responses to internal radiation exposure which cannot be explained by the external risk models of the ICRP. For a review up to 1995 see Busby 1995. This includes examination of the clusters of childhood cancer and leukemia at all three main nuclear fuel reprocessing sites in Europe, Sellafield in Cumbria, England, Dounreay in Caithness, Scotland and La Hague, in France. In addition there are many cancer and leukemia clusters near nuclear sites in the UK [Busby, 1995, Beral and Bobrow, 1994] Europe and the United States. A list of studies reporting evidence for errors in the external risk model may be found on the website of the Low Level Radiation Campaign, 7. Health Consequences of Chernobyl exposure in Belarus 7.1 Non cancer effects. There are many consequences of the irradiation of cells. These include cell death, mutation leading to dysfunction and mutation leading to tumour and cancer. In the lifespan of humans, these results will show themselves as a very wide range of conditions. These will begin with infant and perinatal mortality, congenital abnormality and foetal development problems. They will include diseases which follow continuous stresses on vital organs, heart, brain, stomach, kidney and immune system. There will be increases in genetic based diseases like diabetes. All these will feed back on the organism’s ability to survive any of the other illnesses, and the general effect will show itself as an increase in morbidity from all causes, with a lowering of the vital signs of populations such as infant mortality indicators and lifespan. The ICRP and other radiation risk models only address cancer as an indicator of the effects of radiation. However, the responses of populations all over the world to the global weapons fallout, and in particular the increases in infant mortality produced by the internal average radiation doses of about 1mSv from these isotopes, show how sensitive the human organism is to internal radiation. [Sternglass, 1972, Whyte 1990, Busby 1995]. Sharp depression in the birth rate was seen in many countries in Europe exposed to the radiation from Chernobyl, and there were increased in low-birth weight babies reported in many parts of the world. [Busby 1995]. Despite this, no attempt has been made by ICRP or other risk agencies to examine non cancer effects. Important measurements of various indicators of health and biological parameters have been made by Bandashevsky [Bandashevsky, 2000]. He has shown that various serious conditions result from internal exposure to Caesium. For example, there are degenerative heart conditions as shown by heart muscle conduction anomalies amongst children and students from the Gomel region of Belarus. For children under 14 living in the contaminated


region, , with an average body activity of 30Bq/kg between 55 and 98% have cardiac activity disorders. For students aged 18 to 20 years, there were 48.7% who showed pronounced ECG modifications. The average Caesium activity in these young people was 26Bq/kg. The dose response relationship was also significant. Children with different doses of Cs-137 also showed dose dependent increases in arterial blood pressure. About 41% of children from the contaminated region showed symptoms of arterial hypertension. Bandashevsky also shows effects of internal contamination on increases in illness and biological indicators of illness for diseases of the kidney, liver, immune system, eye, brain and nervous system and blood [Bandashevsly, 2000] Other reports of correlations between objective indicators of biological competence and incorporated radiosotopes are given in the book by Burlakova [Burlakova, 1996], Nestorenko [Nestorenko, 1997,1998] and contribution to the alternative Chernobyl Conference in Vienna in 1996 [IPB, 1996] In view of the long time lag between initiation and expression for most cancers, it may be that most people will die of other responses to radiation before they will express cancer.

7.2 Cancer: conventional approach of ICRP and others using external risk model.

The external ICRP risk model requires knowledge of the doses to the population at risk and applies the risk factors for fatal cancer obtained by linear interpolation from the high dose exposures of the Japanese A-bomb populations. The first requirement is to obtain the doses to the populations at risk. This is followed by multiplying each dose by the exposed population numbers and the ICRP fatal cancer risk factor to obtain the fatal cancer yield. I will give the calculations based on four different appreciation’s of the doses to populations in Blears. 7.2.1 Method using overall population and average dose calculated by the IAEA for the strictly controlled zones which surround the 30km exclusion zones. This approach follows Cards et al., 1996 The results of applying an ICRP risk factor of 0.125 per Sv to these people living in the controlled zone is given in Table 1. Table 1. Collective effective dose for persons living in Strict Controlled Zones of contaminated territories of Ukraine and Belarus (Source Mould, 2000) Contamination level (kBq/sq.m) 37-555 >555 Lifetime dose (person Sv) 52500-150000 15000-30000 Population size 6800000 270000 Fatal cancers in 70years 6562 -18750 1875 - 3750

It is possible also to use this approach to calculate the fatal yield in the whole population of Belarus. The result depends upon the value which we choose to use for the exposure. Savchenko has given the first year committed effective dose to the whole population of Belarus as 2mSv. Assuming that half the radiation from the radio-Caesium is given in the first ten years, we can estimate the overall ten year dose at 10mSv. Thus the total collective dose for the 9.9million population is 99,000 person Sieverts. The cancer yield, using the ICRP risk factor of 0.125 is thus 12,375 fatal cancers


7.2.2. Gofman’s calculation Dr John Gofman has used estimates of the inventory of the core and the fraction released to establish the approximate level of contamination of the whole of Belarus. He has then employed the United Nations model which relates contamination to dose to calculate the cancer yield in Belarus, using a risk factor of 0.26 per Sievert. His result is 26,400 fatal cancers.[Gofman, 1990] 6.2.3 Choice of exposure values. The models which have been used to convert ground contamination to collective dose in the above examples seem to give results which are too low. I have not seen external dose rate measurements of the affected territories but can do some calculations based upon the published levels of Caesium contamination. The results suggest exposures doses far higher than those given by the risk agency models. I will not address this problem further here. 7. Calculations based on global weapons fallout cancer increases in Wales The above calculations are based on the risk factors reduced from the external radiation studied of the Hiroshima survivors. There is another approach, which is use the method of scientific induction, and compare like with like. In this case I will use the global weapons fallout from the 1959-63 period and compare the average contamination levels of Belarus with global fallout contamination of Wales and England. In order to do this I will use a value of 10mSv for the average dose to the population of Belarus from Chernobyl and compare this with perhaps 4mSv cumulated dose to the population of Wales from the weapons fallout [Busby, 1995]. I have shown elsewhere [Busby, 1995] that there is a very good correlation between Strontium-90 cumulative dose and cancer incidence in Wales, 20 years later. The relation is seen in Fig.7. The regression equation of Standardised Registration Ratio for all malignancies on cumulative dose (microSieverts) from Sr-90 is : SRR = 0.012 [Sr90] + 104.57 R-squared = 0.96; F-statistic 315 on 1 and 14 degrees of freedom; p<10-11 This means that for the 2mSv Sr-90 dose there was an approximate 25% increase in cancer, twenty years later. If we use this model to predict the cancer increase in Belarus, twenty years after the accident, we get a value of 125%. The real result may be lower, because I have not included the other isotope doses in the Wales calculation, since it was my belief that it was the strontium-90 that was the Second event isotope responsible. In addition, cancer in Wales began to increase five years earlier that cancer in England, because the dose was about half. On this basis I would expect the Belarus cancer increases to begin less than ten years after the event, i.e. in the early 1990’s, and what I have seen of the data supports this. Comparisons between Belarus contaminated by Chernobyl and Wales contaminated by weapons fallout suggest that there will be a 125% increase in cancer in Belarus beginning less than ten years after the exposure, i.e. in the early 1990s. 8. Thyroid Cancer and Leukemia I should say something about the marked increases in Thyroid cancer in the affected areas, and also the apparent low level of leukemia. First, I believe that the surprises about the high


levels of thyroid cancer are because the study which informs the models of radiogenic thyroid cancer are flawed. The main study, by Lars Eric Holm, rejected cancer cases that appeared within five years of the irradiation as being due to pre-existing lesions [Gofman, 1990]. In addition, there was very high exposure after Chernobyl to a short lived isotope Tellurium132, which decays to another radioisotope Iodine-132 which is thyroid seeking. These two isotopes represent a perfect second event sequence. I suggested that this was the origin of the high thyroid cancer in 1996 [Bramhall 1996]. As far as the leukemia is concerned, I have seen different accounts of the levels of leukemi in Belarus and the Ukraine, and believe that the data has not been adequately collected. The ECLIS studies in Europe suffer from a number of faults and I have criticised them elsewhere [Busby and Scott Cato, 2000] 9. Dispersion of radionuclide particles. Recent work that our group has done in connection with cancer near the Irish Sea and three different nuclear sites in the UK suggest nuclear waste becomes attached to small dust particles which concentrate in river valleys and tidal estuaries. We have found evidence that exposure to radioactive particles near rivers and the sea carry high risk of cancer. These particles become concentrated and move under the influence of geophysical and electrostatic forces. This suggests a way of removing them from the environment. 10. Conclusions and Recommendations The risk models which have been applied to predict the cancer yield of the Chernobyl accident are insecure because they only apply to external irradiation. Recent studies show that they are in error by more than 100-fold. The main hazards are from particulate inhalation and ingestion and also from internal exposure to second event emitters. The main hazards here are Tellurium-132 and Strontium90 and long lived hot particles. There should be study of the movement of radioactive dust particles and of factors affecting their dispersion and concentration in the environment and their availability for inhalation.

Figures and Tables


Fig 1 Dose response relationship between exposure to the infants who were in utero at the time of the Chernobyl fallout and the subsequent risk of leukemia.

Table 1 Increases in infant leukemia in the children who were in utero and exposed to the radiation from the Chernobyl accident from four countries in Europe. Exposed cohort (B) born between July 1986 and Jan 1988. Unexposed cohort (A) born 1980 to 1985 plus (C) born 1989 to 1991 (Busby and Scott Cato, 2000).


Fig 2 Phantom used by ICRP to calculate dose.

Fig 3. Variation in sensitivity of Chinese Hamster Ovary cells over the cell cycle in vitro (Source: Sinclair and Morton, 1966)


Fig 4. Displaying the 10-hour repair replication cycle high sensitivity window in terms of the normal cell lifespan in the living organism.

Fig 5. Predicted dose response relationship for mutation in an organism made up of two subclasses of cell sensitivities: high sensitivity replicating cells and low sensitivity quiescent cells. Sensitive cells are first mutated and then killed as dose increases.


Fig 6 Hot particles were a feature of the fallout from Chernobyl. The autoradiograph is from th a skirt worn by a traveller who visited Kiev on 29 May 1986. (Source: Dr B.L.Reece, Birmingham University).

Fig 7. Relationship between weapons fallout cumulative dose from Strontium-90 and cancer incidence standardised registration ratio (SRR) in Wales. The dose (full line and triangles) has been lagged by 20 years and plotted together with the SRR (dotted line and circles). References


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