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In August 1996, Eddie Goncalves of CND wrote a report, Broken Arrow (Golcalves, 1996) which drew attention to a nuclear accident in 1957 in which a USAF bomber had jettisoned its fuel tanks at Greenham Common airbase and caused a fire in which a nuclear warhead had burned, releasing radioactivity to the environment. The evidence was contained in a 1961 letter and other correspondence relating to measurements of Uranium-235 made around Newbury by scientists from AWRE Aldermaston. These showed that levels of the isotope in laurel leaves pointed to a source in some event centred on Greenham: it was stated that about 10gms of U-235 and 20 gms of Plutonium might have been involved, but no measurements of Plutonium were recorded. There was considerable media interest in the story and questions were asked in Parliament. Concern was expressed about the possible consequences of the radiation release to people living near the base and in and around the nearest town, Newbury.

This had several results. Local people began to collect lists of leukaemia cases, COMARE (the Committee on Medical Aspects of Radiation in the Environment) were asked to reopen their enquiry (COMARE, 1989) into increases in cancer in West Berkshire, Newbury Council commissioned a study by Southampton University to measure radioactivity in the area and the National Radiological Protection Board were asked to investigate and comment on possible hazard. Green Audit was already looking at increases in cancer and leukaemia in the areas near Harwell, Aldermaston and Burghfield as part of its on-going study of cancer near nuclear installations on behalf of the Low Level Radiation Campaign. It contacted the relevant cancer registry, the Oxford Cancer Intelligence Unit in September. In a letter, dated 16th October, the director, Dr Monica Roche, refused to release cancer incidence aggregated small area incidence data. She stated that the registry was ‘reviewing the completeness of the data and would probably be undertaking additional work to ensure completeness of case ascertainment.’ It was therefore not possible to establish the incidence of childhood leukaemia near Newbury or within its wards.

To bypass this block, Green Audit contacted the Office of National Statistics and obtained information on leukaemia mortality for the period 1982-1995. This interim report outlines the results of an analysis of this data for children aged 0-14 and also discusses radioactive exposure in the area from Greenham, and more importantly from the triangle AWE Aldermaston, ROF Burghfield, and AERE Harwell. All three of these establishments have been releasing large quantities of radioactive pollution to the 800sq km area defined by the Thames and Kennet valleys since 1952.

Figure 1 shows a schematic map of the area defined by the three nuclear establishments. Figure 2 and Figure 3 shows trends in liquid radioactive isotope releases to the various outfalls into the Kennet and Thames and the water table drained by these two rivers and their tributaries. Total discharges to the area over the period to 1985 are compared with Sellafield discharges to the Irish Sea in Table 1.

It is clear that the density of deposition over the period is comparatively large. Interestingly, there have been few measurements of radioactivity in the area, and in particular measurements of Plutonium isotopes have been very scarce and levels shown have been very variable. In general, except for one value of 15Bq/ kg soil at Greenham recorded in a fact sheet handed out by NRPB in 1996 (claiming to represent the concentration found by Cripps and Stimson in 1961) levels have been in the range of normal global fallout deposition. 15 Bq per kg represents about 3000 Bq.square metre which is much higher than can be accounted for by weapons testing fallout (Cawse et al., 1988). Other sample results, made by the MoD, Harwell or NRPB show no anomalous increases in measured levels of man-made radioactive pollution. This is curious in view of the large quantities of these materials released by the three nuclear sites over the thirty-year period 1950–80.

Table 1. Total releases to the environment defined by the 800km2 area of the Thames and Kennet valleys above Reading 1948–1986, compared with emissions from Sellafield (Mbq)

a For the Sellafield emissions, these figures are included under total alphas.

Table 2. Comparison of density of cumulated alpha and beta radioactive pollution, excluding Tritium and noble gases to Thames and Kennet valleys (1948-86) with that from Sellafield to the Irish Sea (1952-95), and weapons testing fallout

Sources:

Previous Studies

Following interest in childhood leukaemia near nuclear sites generated by the reports of a ten-fold excess in Seascale near BNFL Sellafield in 1984 (Gardner and Winter, 1984), studies were made of populations near Dounreay (Heasman et al., 1986) and also Aldermaston and Burghfield (Roman et al., 1987). Initial investigations of childhood leukaemia incidence in West Berkshire and North Hampshire regions by Roman and colleagues found a small but significant excess of childhood leukaemia in the age group 0-14 (RR = 1.3 p<.05) and in the 0-4 age group (RR= 1.6, p<.01) relative to national averages. (RR = risk relative to the national average.) Looking inside areas 10 km from the nuclear sites the same authors found relative risks of 1.4 (p<.001) and 2.0 (p<.05) for the same age groups. Following from this, an investigation by COMARE (1989) confirmed the increases but found that the cause of the excess could not be radiation from any plant as the exposure levels were too low to account for them on the basis of risk factors based on the survivors of the Hiroshima bomb. This is essentially the same argument used by COMARE in exonerating BNFL Sellafield in the Seascale cluster, an argument first used in that case by the Black committee in 1984 (Independent Advisory Group, 1984).

Mortality Results

Leukaemia mortality in the age group 0-14 in the Newbury District Council area, (which extends from Hungerford in the East to Pangbourne in the West) is given in Table 3 together with the approximate populations. The population at risk aged 0-14 is approximately 27,000 in 1981 and 25,600 in 1991 (census figures). Census populations were also used in conjunction with mortality data for England and Wales from OPCS to generate an average annual national rate for the comparison periods 1981-90 and 1986-95 and 1991-95.

Table 3. Mortality from leukaemia ICD 204-208, all persons aged 0-14: average annual rates per 100,000

Notes: Population figures are approximated from available census figures.

Table 4. Statistical analysis of data blocks: Newbury CD versus England and Wales

Note: Calculations were performed using Epi-Info V6.

There are now reports of increased risk from childhood leukaemia and other cancers near many of the main sources of man-made radioactive pollution in the world. In Europe, the focus of interest has been on Sellafield, Dounreay and La Hague, in Normandy. The increased incidence in Sellafield is about ten times the national average for childhood leukaemia. In Dounreay it is eight and near La Hague about fifteen times the respective national averages. The Newbury triangle, as we can see from Tables 1 and 2, has received large quantities of radioisotopic pollution of generally the same type as that released by Sellafield and over a similar period.

While the latter has been releasing its pollution to the sea, where it is dispersed more easily, the nuclear sites at Harwell, Aldermaston and Burghfield, have been releasing their radioactive isotopes to a highly populated area inland defined by the drainage basins of two rivers, the Thames and Kennet. Drinking water for the local populations is abstracted from both these rivers, which are also part of the source for water supplies as far away as London and the Medway towns in Kent. The water table has also been polluted by significant quantities of chlorinated solvents, originating in various processes at Harwell and Aldermaston. Discharges of radioactive gases have been made to the air, and liquid wastes have been routinely discharged to both the Thames at Sutton Courtenay (Harwell) , the Thames at Pangbourne (Aldermaston) and Silchester Sewage Works, Foundry Brook and Kennet (Aldermaston). In addition, the pipeline from Aldermaston to the Thames discharge point at Pangbourne has leaked and contaminated land (COMARE, 1989).

The trend in radioactive pollution shown in Figures 1 and 2 indicate maximum exposures occurring during 1955 to 1965 from Harwell. For Aldermaston alphas peaked in 1955–65 and beta emitters peaked in 1964–68. From 1965 onwards large quantities of Tritium were released from both sites. The pollution from ROF Burghfield was generally much lower and was discharged through normal drains to the local sewage works.

We have established that the population of the Newbury leukaemia triangle has received exposure to similar levels of many of the same radioisotopes that populations exhibiting high relative risk for childhood leukaemia have received at Sellafield, Dounreay and La Hague. It is clear that childhood leukaemia mortality, and therefore, presumably, incidence, is increasing. What is the cause? If it is radiation exposure, then the 1957 Greenham bomb fire represents a far lower risk than the emissions under licence over the period 1952 to the present day. But could such emissions, at levels of overall exposure below natural background have caused an increase in leukaemia of 400%, twenty years after they peaked in the sixties, in children who were born later, in the period 1986-95?

The risk factors for radiation-induced cancer, including leukaemia, are published by the radiological protection agencies. In the UK the relevant agency is the National Radiological Protection Board. In the last ten years, particularly since Chernobyl, the underlying assumptions upon which such risk-factors are based has been challenged (Busby, 1995). The main basis for this is the increasing understanding of the molecular basis of radiation mutagenesis at the level of the cell. It is now widely believed that the study used to deduce risk from radiation, the Hiroshima survivors lifetime study of people exposed to a single large acute flash, is unsafe when used to deduce risks for chronic internal contamination by radioactive elements that mimic normal atoms used by living organisms (Bramhall, 1996).

In particular, it is now known that cancer and leukaemia are essentially genetic diseases, and that genetic damage can be passed on to children and grandchildren. For example, a specific man-made radioisotope, the beta emitter Strontium-90, is a most hazardous substance in this regard since it binds to chromosomes and has a sequential decay scheme which can bypass normal cellular repair. Man-made radioisotopes cannot generally be compared with natural background radiation against which living organisms have developed repair systems. Thus reports by COMARE on the increases in leukaemia near Sellafield (1996) and also Aldermaston (1989) are wrong to use risk factors based on the Hiroshima survivors to exonerate radioactive pollution from the plants.

We believe that there is now considerable evidence, which this study supports, that exposure of parents to internal man-made radioisotopes caused genetic damage which, amongst other consequences, may be expressed in their children as leukaemia. This is essentially the Gardner hypothesis (Gardner et al., 1990) but with internal exposure rather than external exposure as the cause.

The alternative hypothesis, advanced by COMARE, and others is that population mixing and a hypothetical virus cause childhood leukaemia (Kinlen et al.,1988,1991). Population mixing levels in the Newbury area and their comparison with national averages indicate that this is unlikely to be a factor in the increases shown here. We intend to report on this shortly.

Finally, we are concerned at the difficulty we have had obtaining cancer incidence data down to ward level. This data is essential if an analysis of the cause of the disease is to be located. An alarming situation exists when information needed to identify a possible environmental threat is kept from the public, and this situation is even more worrying when the establishment is ultimately part of an organisation whose director was also, until recently, also director of the main organisation whose activities constitute the threat.

In this situation are we to believe the results of studies made by COMARE, whose chairman, Professor Bryn Bridges, once worked at Harwell and whose secretariat is now based at Harwell? Or we are to look for advice to the National Radiological Protection Board, also at Harwell? We might expect that problems of health in the area would be addressed by the Regional Health Authority, whose chairman is Dr Peter Iredale. But can we rely on their objectivity when we know that Dr Iredale moved suddenly to this post in 1992 from his job as director of the Harwell laboratory? (Didcot Herald, 12 Mar. 1992). Independent work on the health effects of low level radiation is urgently needed.

Conclusions

Childhood mortality from leukaemia in the Newbury District Council area has been increasing relative to the national average over the period 1981-95. In the five-year period 1991-95 it was 4.4 times the average in England and Wales and over ten times the average for Berkshire. The cause of this increase is unlikely to be the nuclear warhead fire at Greenham in 1957, since the amounts of radiation involved were too small. It is suggested that the cause is radioactive emissions from Aldermaston and Harwell which peaked in the 1960s causing genetic damage to the parents of the affected children. There must be concern at the cancer registry refusal to release small area incidence data which would enable a more comprehensive analysis to be carried out.