WHO Conference paper

WHO Conference paper
Increases in leukemia in infants in Wales and Scotland following Chernobyl: Evidence for errors in statutory risk estimates and dose- response assumptions.
Chris Busby, PhD and Molly Scott Cato, MA, MSc, PhD
[Occasional Paper 2001/7.
Address for correspondence: Green Audit, 38 Queen Street, Aberystwyth, SY23 1PU Wales, UK. email: christo@greenaudit.org]
presented at the 3rd International Conference
Organised by Physicians of Chernobyl/ World Health Organisation
Kiev, Ukraine June 4-8


After the Chernobyl reactor accident in April 1986, rainfall precipitation caused measurable radioactive contamination of Wales and Scotland. Using risk models developed by themselves and by the International Commission on Radiological Protection, the UK National Radiological Protection Board advised that no measurable increase in leukemia was predicted at exposures which they estimated from measurements of contamination. However, cancer registry data from both the Wales and Scotland registries show a sharp increase in cases of infant leukemia age 0-1 in the eighteen month period January 1st 1987 to June 30th 1988. This period is that in which the birth cohort who were in utero in the exposure period following the fallout would be in the age group 0-1.

Compared with an 'unexposed group' consisting of the period 1975-86 the Wales exposed group had a relative risk (RR) of 4.4 (p = 0.004), the Scotland group a RR of 3.7 (p = .001) and the combined Wales and Scotland group an RR of 3.87 (p = .0001). A second unexposed group, those aged 0-1 in 1989-91 had no significant increased risk although after 1991 rates increased slightly. This finding supports earlier reports of infant leukemia effects in Greece, Germany and the U.S. following Chernobyl. The existence of good quality leukemia and exposure data makes it possible to calculate an error in the presently accepted risk factors for radiation induced leukemia following this kind of exposure of about 100-fold or more. In addition, the dose response relationship shown by infant leukemia following Chernobyl in the five countries where it was reported supports a biphasic dose response pattern. These findings, taken with those from the other countries where similar infant leukemia increases occurred, define an event which was unequivocally associated with low level anthropogenic radiation exposure and the very high compound statistical significance procvides strong evidence of the existence of a significant error in contemporary low level radiation risk modelling.

1. How can we resolve arguments about low-level radiation risk?

Energy policy involving decisions about nuclear power is influenced by accurate information about the health effects of exposure to anthropogenic sources. The health effects of low doses of ionizing radiation of anthropogenic origin continue to remain the subject of controversy (1,2,3). The dispute hinges on whether it is scientifically permissible to extend the arguments based on the use of energy averaging units (rems, Sieverts) and external radiation epidemiology (Hiroshima lifespan study) to an analysis of the kinds of internal doses received by populations contaminated by novel man- made radioisotopes (Sellafield leukemia cluster). Such exposures can be highly anisotropic in space and time with very large doses to some cells (100mSv-10Sv) and none to others.

These two world views are now head to head and mutually exclusive. How can we resolve the matter? Extrapolations from external radiation studies are deductive and therefore insecure. Epidemiological studies (nuclear site clusters, downwinders) are inductive and therefore scientifically superior (40). The situation is described in Fig 1.

study group Type of exposure Analytical approach Resulting model
A-bomb survivors High dose
Linear No Threshold
(Low risk)
Nuclear site leukaemia clusters (e.g. Sellafield)
Irish Sea coast effect
Chernobyl infants
Minisatellite mutations
Weapons fallout cancers
DU Gulf veterans
Iraqi children
Biphasic cell response
(High risk)

Fig. 1. Mutually Exclusive Radiation Risk Models

However, the epidemiological difficulty is that both accurate doses to exposed, well described populations and good quality cancer registration data for these populations are rarely both available. Added to this problem is that of specificity: there are usually confounding causes in the case of the cancer or leukemia as end-points since there is an appreciable delay between exposure date and clinical expression of the disease. For this reason, the advocates of the external risk models have large reserves of theories to explain away the findings (e.g.population mixing).

We overcome these problems by focusing on a very restricted group, those infants in Wales and Scotland who were in utero over the period of peak fallout from the Chernobyl accident. The Chernobyl accident in April 1986 dispersed radioisotopes in a global pattern that has been well described. Between 3rd and 5th May, the radioactive cloud caused deposition in parts of Wales, Scotland, Cumbria and the Yorkshire moors.

The UK National Radiological Protection Board (NRPB) advised that the levels of exposure were too low to have any measurable effect on health, and government advice was that food was safe to eat and water and milk safe to drink.

Leukemia is widely accepted as an outcome of exposure to ionizing radiation. The numbers of infants registered with leukemia is small but the statistical significance of any step change can be investigated by assuming that childhood leukemia follows a Poisson distribution. Furthermore, the restricted time period involved makes any significant observation of excess less likely to have a confounding cause. A sudden peak in infant leukemia for the in utero cohort is very likely attributable to the exposure. Wales and Scotland have excellent cancer registration and population data and the many measurements made in those countries by the NRPB enable doses to the infants to be accurately established. Thus everything is in existence to examine the correctness of the contemporary radiation risk model.

2. Method

Annual incidence data for all leukemias in the age group 0-1 were obtained from the Wales Cancer Intelligence Unit or the Information and Statistics Division of the Scottish Health Services. Population data were obtained from the Welsh Office or Scottish Office.

For comparison purposes the unexposed controls were defined as two groups, first those aged 0-1 years between 1975 and 1985 and second those aged 0-1 between 1989 and 1991. The exposed birth cohort was taken to be those aged 0-1 in the 18 months between January 1st 1987 and June 30th 1988. Conception in these infants occurred between April 1st 1985 and September 31st 1987 and most of them will have been exposed in utero to radioactive isotopes from Chernobyl. We extend the period to eighteen months because whole body measurements of radio-Caesium in humans in the UK (4) showed that the body content peaked in July 1987 (See Figure 2) and therefore an in utero effect from this exposure might be manifest up to April 1988 or later. The risk factors used for calculating expected leukemia yields are those adopted by the National Radiological Protection Board in their various publications, most particularly those used to assess the risk of childhood leukemia near the Sellafield plant in West Cumbria, namely, .0065 per Sievert for children age 0-10, 0.0125 for in utero exposure and 0.004 for heritable genetic damage. (5) These risk factors are broadly similar to those published by the International Commission on Radiological Protection (6) and the BEIR V committee (7).

graph: whole body monitoring of Caesium after Chernobyl, points and trend. (21Kb)

Figure 1 Whole body content of Caesium-137 + Caesium-134 measured in the two years following Chernobyl. (source: Etherington and Dorrian [5])

3. Exposure Dose Equivalents and Expected Leukemia Increases following Chernobyl

The NRPB calculated the 1986 exposure dose equivalent to high rainfall areas of the UK at 88 mSv (8). The World Health Organization has given the one-year exposure in high- rainfall areas of the UK at 110 mSv. (9) The predicted leukemia yield in the population of infants age 0-1 in Wales is given in Table 1 below.

Table 1
Predicted increase in Leukaemia in exposed age group 0 - 1 in Wales and Scotland using NRPB risk estimates and exposures. (source NRPB)
Risk Factor (/Sv) 1 year exposure (µSv) Predicted Leukemia yield (cases)b Scotland (pop. 66,100) Predicted Leukemia yield (cases)b Wales (pop. 38,300)
0.0125 (in utero) 88
0.0065(age 0 - 10) 88
0.004 (heritable damage) 10a 0.0026 0.0015

a = estimate of dose to fathers' testes over pre-conception period
b = over lifetime of person exposed

4. Observed increases in infant leukemia in Wales and Scotland, 1975 - 1992

The numbers of recorded cases of infant leukemia in Wales and Scotland over the period 1975 to 1994 are given in Table 2. The number of cases in Wales and Scotland increased sharply to 14 in the combined years 1987 and 1988 over the average level of 4.2 per two- year period as defined by the ten earlier years 1976-85. Infants who were in utero over the period of the fallout would be age 0-1 over both of these years and a better period for defining them would be the 18-month period from 1st Jan 1987 to 30th June 1988, in which there were 3 cases in Wales and 9 in Scotland, a statistically significant excess over previous averages.

In Table 3 we collect together the numbers of cases, calculated relative risks and Poisson Distribution cumulative probability values based on the Group 1, 1975-85 ten- year, pre-Chernobyl unexposed populations as controls. The expected values used in Table 3 were obtained by assuming the average rate for the control period applied to the exposure period.

Table 2
Infant leukaemia (ages 0 - 1) in Scotland and Wales and both countries combined (Source: Wales Cancer Intelligence and Surveillance Unit; Scottish Health Services)

Year Scotland Wales Both 2-year groups
1975 1 0 1  
1976 3 0 3 4
1977 1 2 3  
1978 2 0 2 5
1979 0 0 0  
1980 2 0 2 2
1981 4 0 4  
1982 0 1 1 5
1983 1 0 1  
1984 3 0 3 4
1985 1 1 2  
1986 0 1 1 3
1987 6 0 6  
1988 4 4 8 14
1989 2 1 3  
1990 2 1 3 6
1991 0 1 1  
1992 3 2 5 6
1993 3 1 4  
1994 1 0 1 5

Note: In the period 1st Jan. 1987 to 30th Oct. 1988 there were three cases in Wales and nine in Scotland.

5. Discussion

Following Chernobyl there have been a number of attempts to examine whether the incidence of leukemia in children has increased in countries affected by the fallout. Published studies of trends in leukemia rates in the age group 0-14 in Belarus, Finland and Sweden--countries badly affected by the pollution-- reported no significant increases after April 1986 (10,11,12) On the other hand, increases in childhood leukemia have been reported for parts of Belarus by Savchenko (13) and others (14). A very large study by Parkin et al. on behalf of the World Health Organization examined the whole of Europe and pooled data from over 20 cancer registries. The latest report of this group found no significant step-change in childhood leukemia after Chernobyl either in the 0-4 or the 0-14 age groups. However, their final adjusted model yielded a positive parameter for the absolute risk per unit dose despite the very crude exposure assessment and strong indication for differential underascertainment of cases in the countries of the former Soviet Union. Despite this, Parkin et al. concluded that the risk factors presently used to predict the effects of low levels of ionizing radiation were broadly correct.

A further criticism of the Parkin et al. study is that it involved a very large number of different countries each with different populations with different susceptibilities to leukemia and with a very wide range of exposures to individuals. If the response to radiation were functions of dose and population genetic makeup (7) and if the dose/response were non-linear, as we find below, it would be predicted that there might only be a general average increase throughout the period, and no clear correlation with dose, effects which the group found.

Two earlier studies of Scotland and Wales found modest but significant increases in leukemia in the 0-4 age group. Gibson et al. 1988 (17) drew attention to a sharp increase in leukemia in the 0-1 age group in Scotland in 1987 and Busby, 1996 (18) compared the pre- and post-Chernobyl cases to show a significant but modest increase in Wales in Lymphoid leukemia in the 0-4 age group.

In 1996, Petridou et al. (19 ) reported a significant ( P = 0.003) 2.6-fold increase in infant leukemia in Greece, a country where the average Chernobyl exposure dose was about 2000mSv. Petridou et al. compared an exposed group born between July 1986 and January 1988 with an unexposed group born between 1980 and 1986. The total number of infant leukemias in their exposed group was 12 compared with 22 in their control. These numbers are similar to those we have found in Wales and Scotland with a smaller population base. Although they argued that their results showed an exclusive in utero cause, it is not at all clear how they came to this conclusion since their exposed period covered eighteen months. Moreover, almost half of their birth cohort would have received no radiation from Chernobyl in the first trimester, a period known to be sensitive to radiation damage.

Further evidence for an increase in infant leukemia following the Chernobyl exposure was provided by the German Childhood Cancer Registry (Michaelis et al. (35)). They examined the same birth cohorts as Petridou et al. and showed that, in Germany, the exposed cohort, born between 1st July 1986 and 31st Dec 1987 exhibited increased relative risk of 1.48 (35 cases) compared with the same combined unexposed birth cohorts. It is not possible to exactly replicate the analysis of Petridou et al. and Michaelis et al. using the data from Wales and Scotland since we have not been able to obtain birth data of the cases from the cancer registries. Each year of data for cases age 0-1 represents the centre of a birth cohort with a span of two years centred around January 1st of the data year being considered. It is possible, however, because we have data by six-month period between 1986 and 1988 to provide a good approximation to the periods defined by these workers. Their 'exposed' cohort 'B' were those born between 1st July 1986 and 31st December 1987. For our data set of children aged 0-1 this period approximates most of those in 'year 87' plus the first half of 'year 1988'. Their unexposed period 'A' was for births between Jan 1st 1980 and 31st Dec 1985. For this we used children aged 0-1 in years 1981 to 1985. For their unexposed cohort 'C', born between Jan 1st 1988 and Dec 31st 1990 we used children aged 0-1 in years 1989, 1990 and 1991. This comparison is given in Table 4.

Michaelis et al. were also able to split their data into high, medium and low exposure categories, based on Caesium deposition in regions of the Federal German Republic. They were able to show that the dose-response relationship was not linear. For low, medium and high Caesium-137 deposition, Relative Risk was in the order 1.87, 0.25, 1.29. Thus the highest Relative Risk (1.84) occurred for the region of lowest Caesium deposition. On the assumption that there should be a continuously increasing response to dose, they concluded that the leukemia was not caused by the radiation exposure. Petridou et al. responded by arguing that this finding was probably due to artefacts in the data.(36)
Although this is possible, given the small numbers and other factors discussed by Petridou et al., we believe that the data presented by Michaelis et al. represents further evidence of a biphasic response to low-level exposure to ionizing radiation. Such a response has been found in a meta-analysis of studies of leukemia and ionizing radiation exposure by Burlakova (37) and its origin is discussed further in Section 6 below. In addition, such a biphasic response is to be clearly seen in the results of the very large base studies of cancer and leukemia in the children of nuclear industry employees in the UK (41,42).

In 1997, Mangano examined the United States for infant leukemia following the Chernobyl accident (20) and demonstrated that even at the low doses involved at this remote distance from Chernobyl , probably less than 10mSv, there was a modest increase in infant leukemia of 30% (RR =1.3 P < 0.09). Mangano also compared the birth cohort 1986-87, which he considered exposed, to an unexposed cohort which was an aggregate of 1980-85 and 1988-90.

Figures for England, which received much less contamination than Wales of Scotland show a slight increase similar to that found by Mangano in the US, though the numbers are too small for statistical significance in this case. There was a general increase in infant leukemia over the whole period with a non-statistically significant peak (averaging 24 cases per year) over the years 1988, 1989 and 1990 compared with an average of 17.7 per year for the ten years from 1976 to 85 (RR = 1.36; p = 0.1).

At the high end of the dose range, results from Belarus showed a small increase in infant leukemia (43).

6. Implications for risk factor models

The results from Wales and Scotland reported here by us show a clear effect with high relative risk values in the range 3 to 4.4 and a high degree of statistical significance. This finding supports the earlier observations of increases in infant leukemia in five other countries and show that the effect of the Chernobyl fallout in Wales and Scotland were part of a real effect. The probability of the effect being a chance coincidence in all seven countries may be shown to be less than 10 10.

The utility of the UK data is that good estimates of the average exposure were available based on many measurements of fallout isotopes in the air, on the ground, in food, milk and water. It is therefore possible to examine the accuracy of the presently accepted risk factors for radiogenic leukemia. The application of these risk factors to the populations of Wales and Scotland predict no measurable effect. From Table 1 where we see that the fallout exposure to the combined Welsh and Scottish population of 88 to 110mSv predicts between 0.11 and 0.136 leukemia cases compared with 12 observed. This shows an error in these risk factors of between 109-fold and 88-fold respectively. Use of the in utero risk factor of 0.0125 reduces the error to between 55 and 44-fold but the real number may be much higher since we only have the 1 year fraction of the total 70 year prediction. If the cause were pre-conception exposure to the fathers then the risk-factors for heritable damage of 0.004 may be used to calculate an error of upwards of 2000-fold. Although such errors seem extraordinary, there are two points worth making. First, errors in the use of the external risk models to assess internal effects of between 250 and 1000- fold are exactly correct to explain the nuclear site and downwinders observations. Second, advances in technology have enabled the measurements of mutation rates in the minisatellite DNA of children born after the Chernobyl accident. In the very latest study which elegantly uses an internal comparison of siblings born before and after the exposure, a seven-fold increase in mutation rates is seen in the offspring of the Chernobyl liquidators. Such a discovery highlights a 700,000-fold error in the genetic damage models developed from studies of the Hiroshima offspring where no mutations were reported at doses which were far greater, but acute and external (44)

The NRPB risk factors and those of the other international risk agencies like the International Commission on Radiation Protection (ICRP), the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) and the Biological Effects of Ionizing Radiation (BEIR) sub-committee of the US National Academy of Science all publish broadly similar analyses of leukemia and cancer risk from radiation.

These risk models are almost exclusively based on external acute radiation exposure and have based their risk factors on the study of the cancer and leukemia yield in the survivors of the Hiroshima bomb. This model cannot address risk from internal exposure to ingested and incorporated radionuclides since both the study group and the controls were similarly contaminated. Furthermore, the largely physics-based radiation exposure models were originally devised before the biology of the cell and its complex responses to radiation damage, particularly the repair and replication cycle, were discovered. Indeed, many of the linear averaging models still used to predict radiation action on cells were devised before the discovery of DNA structure and function.

In the last twenty years, and increasingly since the Chernobyl accident, a significant number of epidemiological and theoretical studies have called into question the accuracy of applying these external radiation based models to the effects of internal irradiation. Internal irradiation involves exposure to substances like Plutonium-239 or Strontium-90 which never existed on earth over the period of evolution and which mimic natural elements. Furthermore the decay scheme of many of these novel radioisotopes involve sequential disintegrations which have a finite probability of causing sub-lethal cell damage and setting up a repair replication cycle. Cells in such a repair replication cycle are hundreds of times more susceptible to radiation killing and mutagenesis (21,22). This is the basis of cancer radiotherapy, where rapidly dividing cells are selectively killed. Recent calculations suggest that there is a finite risk enhancement associated with the 'Second Event' double sequential dose pathway, where a first sub-lethal 'hit' causes the cell to set up the repair-replication sequence and a second, subsequent 'hit' intercepts this critical 'window'. The magnitude of the effect for different isotopes or aggregate particle sizes is the subject of some dispute (31,32). Fractionated and split-dose radiation exposure to local tissue also results from 'hot particles' of the type known to have been released by the Chernobyl accident. Such exposures are also common near nuclear reprocessing plants and sea or river discharge areas. Inhaled particles in the micron size range may become resuspended, inhaled and translocated to the lymphatic system where tissue volumes and cells local to the particles will receive doses and temporal fractions which are qualitatively and quantitatively different from those resulting from external irradiation.

The Second Event approach nevertheless draws attention to the existence of the small sub-populations of cells which are routinely in repair-replication phase and which, therefore would be very much more susceptible to damage than the majority of cells which are not replicating. This immediately suggests that in the low-dose range, there should be a biphasic response to increasing dose. As exposure increases from zero, there should be a sharp rise in effect due to exposure of the sensitive sub-population of normally dividing cells. This would be followed by a reduction in effect as these cells are killed and then the effect would rise again as the normal cells are affected. Burlakova et al. has pointed out that such dose-response curves are common in studies of radiation and leukemia and the effect is also seen in other radiation cancer studies and in animal studies also (21, 37). Her explanation involves the interaction between induced repair response curves and transformation curves. Whether this or the sensitive sub-group of cells is the explanation the result of Michaelis et al. is perhaps an example of this type of process, where we see that the highest dose does not carry the highest risk. And examination of the dose response relationship shown by combining the results from Wales and Scotland with those from Greece and Germany, UK and the US provides a similar example. This is shown in Fig 3. Relative risk was highest in Wales and Scotland where the dose was lower, although at the very lowest doses in England and the US, the effect was modest. As the dose increases, the results from Germany and Greece show that the leukemia risk falls, and is again low at the high dose found in Belarus. Such responses may seem curious to a physicist, but biological systems are not so amenable to such stress vs strain analyses (3).

figure 1. dose-response relationship post-Chernobyl infant leukaemia  (17 KB)

Fig. 3. Dose response relationship for infant leukemia following Chernobyl in Wales, Scotland, Germany, Greece, England and US. Relative Risk vs. average dose given in Savchenko, 1995, Ref 14. (Data points from low to high dose: US, England, Scotland, Wales, All Germany, Greece)
Horizontal axis = dose (mSv): vertical axis = leukaemia risk
Data points from left:- United States, England, Scotland, Wales, Germany, Greece

Table 3 Relative risk of leukemia in infants born in 1987 and 1988 in Wales and Scotland and exposed to Chernobyl fallout compared with group born in the 11 year period 1975-86. Also shown is the risk in the unexposed group born between 1989 and 1991.
I Wales

Group Observed Cases Expected Cases aO/E (Relative Risk: RR) bCumulative Poisson P
Unexposed (I) 1975 - 86 5 - 1.0 -
Exposed Jan. 1987 to Jun. 1988 3 0.675 4.4** 0.004
1988 alone 4 0.45 8.9** 0.002
1987 and 88 4 0.9 4.5** 0.0135
Unexposed (II)
1989 - 91
3 1.36 2.2 0.143

II Scotland
Group Observed Cases Expected Cases aO/E (Relative Risk: RR) bCumulative Poisson P
Unexposed (I) 1975 - 86 18 - 1.0 -
Exposed Jan. 1987 to Jun. 1988 9 2.46 3.7*** 0.001
1987 and 88 10 3.28 3.05** 0.002
Unexposed (II)
1989 - 91
4 4.9 0.8 0.566

III Wales and Scotland combined
Group Observed Cases Expected Cases aO/E (Relative Risk: RR) bCumulative Poisson P
Unexposed (I) 1975 - 86 23 - 1.0 -
Exposed Jan. 1987 to Jun. 1988 12 3.1 3.87*** 0.0001
1987 and 88 14 4.18 3.34*** 0.0001
Unexposed (II)
1989 - 91
7 6.27 1.1 0.47

a Based on the unexposed group (I)
b Probability assuming a Poisson distribution that the number of observed cases or more than that number might occur by chance.
c Significant at the 0.05 level*, the 0.01 level** and the 0.001 level***

Table 4: Comparison between infant leukemia rates after Chernobyl in Wales and Scotland and similar data from Greece and from the former Federal Republic of Germany
Group aWales and Scotland bGreece cGermany
Exposed cohort B      
Cohort size 156,600 163,337 928,649
Number of cases 12 12 35
Rate 7.67 7.34 3.77
Exposed cohort A+C      
Cohort size 835,200 1,112,566 5,630,789
Number of cases 18 31 143
Rate 2.15 2.79 2.54
Risk ratio 3.6 2.6 1.5
Cumulative Poisson probability 0.0002 0.0025 0.015
a See text for A, B and C periods
b Petridou et al. (1996)
c Michaelis et al. (1996)

The main exposures from the Chernobyl pollution in Wales and Scotland were to the short-lived Iodine-131 and Tellurium-132 isotopes, and from longer lived Caesium-134 and 137. Tellurium-132 has a sequentially decaying isotope through its daughter Iodine-132 and is theoretically capable of inducing Second Event damage (18,31,32). However, most of the Te-132 will have delivered its dose in the first few weeks and if we approximate a fifteen week period of spermatogenesis in humans then leukemia in the children would be expected in the birth cohorts from June 1987 to January 1988. This could conceivably fit the finding of the peak in incidence in Wales occurring in the first half of 1988 since we are dealing with the whole 0-1 age group at diagnosis. However, the exposure to Caesium-134 and Caesium-137 would certainly have provided pre-conception irradiation from May 1986 up to mid 1987 (see Fig 1) owing to the use of Caesium-contaminated silage cut in the Summer of 1986 as feed for cattle in the winter of 1987.

In addition the accident caused the release of particulates containing mixtures of radioisotopes, and such particles which reached the UK were in the size range which made inhalation or ingestion possible (45,46). Without more accurate information on birth dates it is not possible to distinguish the origin of the leukemia between in utero exposure or pre conception exposure to parents or a combination of the two effects.

Since leukemia may be a genetic disease, initiated in utero (39), it is of interest that there is some other relevant evidence of general genetic damage to the immediate post Chernobyl in utero cohort irradiated. This comes from data on very low birth weight babies obtained from the Office of Population Census and Surveys and reported as a Chernobyl effect in 1995 (21). There was a significant increase in very low birth weight babies (<1500g) born in Wales just after Chernobyl, peaking between January 1987 and January 1988. Monthly data we have obtained from OPCS shows that the peak months for the birth effect were October November and December 1987 and January 1988. Infant mortality following radiation exposure from weapons fallout in the period 1959-1963 is well documented (33,34) and the effects of internal exposure to radioisotopes on foetal development have been reviewed in Busby 1995 (21)

Increased incidence of childhood leukemia has now been verified near most of the main sources of radioisotopic pollution in Europe. This includes a ten-fold excess near Sellafield (26), 8-fold near Dounreay (27 ), fifteen fold near La Hague in France (28), two fold near Harwell in Oxfordshire and also near the Atomic Weapons Establishment at Aldermaston in Berkshire.(29) A significant childhood leukemia cluster was reported in the 0-5km vicinity of the Kruemmel nuclear reactor in Germany (38). There is further support for the concern that the genetic effects of novel man-made radioisotopes like those in the Chernobyl fallout and the releases from nuclear sites are much higher than presently modelled. These are the reports already referred to of anomalous increases in human minisatellite mutation rates in children living in territories of the ex-Soviet Union which were contaminated by the fallout (30, 44)

Therefore, this present observation of infant leukemia increases associated with a fairly well assessed exposure dose in two countries with good quality cancer ascertainment and supported by similar observations elsewhere calls into question the risk models and factors used to assess the cases of the leukemia clusters near sources of radiosiotopic pollution and places a figure on the error involved in using external Hiroshima-based epidemiology to consider risk from internal exposure from novel radioisotopes. A reassessment of the hazard to health of such exposure should be the subject of urgent research effort since the problem of risk from such pollution carries important human health policy decision implications.


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