TL: Plutonium in the environment SO: David Sumner, Greenpeace International (GP) DT: June 1992 Keywords: plutonium nuclear weapons facts plants gp greenpeace risks safety transporation reference / by David Sumner June, 1992 Plutonium being transported is in one of the following forms: (1) plutonium dioxide (PuO2) as a powder, whose particle size distribution depends on the method of preparation. (2) plutonium dioxide mixed with uranium dioxide and formed into sintered pellets to be used as fuel in fast and thermal reactors. (3) plutonium metal. According to evidence submitted by the EDRP Inquiry, 90% of past exports of plutonium have been in the form of the dioxide [1]. Plutonium derived from civil power reactors consists mainly of plutonium-239, although there will also be plutonium-238, 240, 241, and 242 present. [3]. The chemistry of plutonium is complex. In the environment it exists in four different valency states. The total quantities of plutonium presently in the environment have been estimated at about 300 kCi 239Pu (1.1 x 10 16 Bq) and 20 kCi (7.4 x 10 14 Bq)238 Pu, with most coming from weapons fallout and the burn up of the SNAP-9A satellite power generator in April 1964. Accidents at Thule, Greenland and Palomares, Spain have contributed an additional few curies of plutonium into relatively localised areas. An accidental release of plutonium on land would create an immediate inhalation hazard to anyone caught in or entering the affected area, until all the particles have settled to the ground. The size of this hazard will depend on the concentration of plutonium and its particle size distribution, the individual's breathing rate, and the length of time (s)he is exposed. The hazard is not over when the particles have settled to the ground, as they can subsequently resuspended (see below). Plutonium in soils Some information on the distribution and movement of plutonium in soils has been obtained from the study of plutonium deposited from weapons fallout in Nevada and New Mexico, discharged into the sea at Sellafield and Dounreay, and deposited following the Chernobyl accident. Healey [15] emphasizes that plutonium can be present in soils under a variety of conditions: (1) a fresh deposit of plutonium exposed on the surface of the ground with a rather uniform particle, readily available for resuspension; (2) a weathered deposit that has become distributed throughout the soil and is only partly available; and (3) a transition period between the first and second condition, in which the plutonium spreads over a large area by surface creep and is partially redeposited on vegetation. Livens and Baxter [12], in a study of soils in Cumbria, have found that plutonium is mostly associated with the organic fraction of the soil. Cook et al [13], in a study of soils near Dounreay, have found that about 65% of plutonium is associated with the organic matter fraction, 28% is bound to mixed oxides, and the remainder tightly held in mineral lattices. As a result they claim that it will be relatively immobile, although there are inevitably uncertainties in the long-term, especially if the soil is subject to environmental stress (e.g. waterlogging, acid rain). Romney et al [16] have observed downward migration of plutonium in undisturbed desert soil to depths varying from 6 to 9 cm during the decade after fallout was deposited. Movement from the surface down into the soil reduces the surface contamination and therefore the probability of resuspension, but on the other hand it gradually brings the plutonium more closely in contact with plant roots. Analysis of soils downwind of the Trinity test in New Mexico showed relatively uniform plutonium concentrations throughout the upper 7.5 cm of several 30-cm-depth soil cores obtained in the desert soils out to a distance of 24 km from Ground Zero; however, beyond that point the plutonium was found to be increasingly concentrated in the upper 2.5 cm. The distribution of plutonium was found to be related to water percolation rates; light, porous soils with nearly uniform plutonium throughout the 30 cm depth had water intake rates of 192 mm/hr, compared to 92 mm/hr in clay soils in which 90% of the plutonium was concentrated in the upper 2.5 cm [4]- These results illustrate the importance of soil properties - such as soil layers with various particle size distributions, surface crusts, and soil structure - in determining rates of plutonium migration through soils. It is possible that, with the passage of time, plutonium becomes more biologically available as a result of weathering processes. Microbial activity may also have an influence (see below). Plutonium in plants Plants may become contaminated by plutonium in one or more of three ways: (1) direct interception and retention of atmospheric deposition, (2) resuspension of plutonium-bearing soil particles to plant surfaces, and (3) root uptake. Following atmospheric deposition of plutonium, the highest plutonium concentrations are in grasses and the lowest concentrations in shrubs or trees. The explanation for this may be that grass presents more surface area for trapping air-borne particles moving near the ground surface; or that the physical structure of the roots and/or their position within the soil profile are more favourable for the uptake of plutonium [3]. Once in the soil, the availability of plutonium to plants probably depends on soil structure, organic matter content, soil pH, and the amount and kind of clay mineral present. The transfer of radionuclides to plants is generally characterised by transfer factors, which are the ratio of plant activity to soil activity. Although transfer factors (soil to plant) for plutonium are generally very low, they are also very variable: concentration ratios for plutonium vary from 10-9 to 10-3 for the same plant. This may be partly also because plutonium is much more difficult to measure than radiocaesium, but probably also because plutonium tends to shift valency states in different environmental situations [Ref 8 p 1269]. The usefulness of available information on transfer factors from soil to plant and from plant to animals is therefore limited by the great variability in the reported data. According to Eisenbud: 'a fundamental weakness in the risk assessment models now in use to predict the effects of the actinide elements is the inadequacy of reliable information on transfer factors, particularly under field conditions'. [Ref 9, p 102] The study of root uptake of plutonium by plants in nature is also complicated by the possibility of both internal and external contamination of the vegetation. Concentration factors for native plants growing in plutonium contaminated soils may be as much as 10,000 greater than the concentration ratios observed in laboratory studies. The higher ratios observed under field conditions are usually attributed to external contamination of plant surfaces and not to a greater uptake of the plutonium. Micro-organisms can contribute significantly to bio-availability and transport of plutonium in the environment; for example, plutonium enters the spores of the bread mould (Aspergillus niger) and can be transported to other soil fractions or the biomass by this route. [Ref 8, p 1213]. Pavlotskaya, studying the relative behaviour of plutonium in soils after Kyshtym and Chernobyl accidents, has claimed that over the 30 years following Kyshtym more than 90% of plutonium has remained in the soil with migration up to 20 to 40 cm, particularly in brown soils (because of their carbonate content) and in peat soils be complexing with organic compounds. She claims that plutonium appears to migrate to considerable depths in colloidal solution when complexed with organic entities, although this is controversial [10]. Resuspension Because of the low uptake of plutonium by plants, surface contamination of plant foliage from resuspended deposits in soil is an important pathway for transfer to humans. [Ref 7, p 6] Erosion of soil by wind action causes particles on the surface to become resuspended. This is particularly important for alpha -emitters such as plutonium because of the increased likelihood of inhalation of the particles. [Ref 9, p95]. Where there are ongoing releases into the atmosphere, atmospheric deposition will probably be the principal contamination mechanism. Where plutonium releases and deposition have occurred in the past, resuspension is likely to be the predominant mechanism in moving plutonium to grain crops. The greater relative importance of resuspension versus root uptake is likely to be the case for most sites of plutonium contamination except possibly for some trees where foliage can be at considerable heights above the ground surface [1]. The resuspension factor is defined as the ratio of the plutonium concentration in the air above the contaminated surface to the surface contamination level. According to Hanson, it is '...extremely difficult to derive the resuspension ratio because of the staggering number of interrelated variables that involve several phenomena that are within themselves highly variable in time and place'. [4] The major mechanism for contamination of soy-beans and wheat grown in soil that is superficially contaminated with plutonium is resuspension due to mechanical harvesting. Plutonium in animals Uptake of plutonium from soil into animals has been studied in animals grazing on land contaminated with fallout from nuclear weapons testing in Nevada. Studies of grazing animals carried out by EPA at its Las Vegas Laboratory showed measurable plutonium activities in bone, liver, gonads, lungs and lymph nodes; although the amounts are very small, 'it must be remembered that these figures were from only a few years of grazing, and long-term accumulation or lack of it over many years of grazing in a contaminated area has not yet been ascertained...many questions remain unanswered, especially when really long-term behaviour is to be considered'. [Ref 8, p 1251- 1216] The main source of plutonium ingested by wild animals is that deposited on the surface of the vegetation they eat, or that picked up directly from the soil while eating and from the fur while grooming. Resuspension may be an important source of exposure to plutonium for animals. 'Redistribution of residual plutonium onto vegetation ingested by animals appears to be an important continuing process in the desert environment, and probably in other kinds of terrestrial environments...small mammals, sampled periodically in fallout areas during a 10-year period, continued to have relatively high levels of plutonium passing through their gastrointestinal tracts....periodic resurveys of study plots in fallout areas indicate that the initially deposited fallout debris gradually is moved from bare ground areas by wind and water erosion and redeposited under nearby shrub clumps.' [2] Romney et al, 1970 [16] have studied the contamination of jackrabbits and kangaroo rats exposed to plutonium contamination at the Nevada Test Site. The accumulation of plutonium into tissue was highest for the bone with lesser amounts in lung. The concentrations of plutonium in bone and lung tissue from samples obtained during an eight year observation period continually increased, raising the question of whether or not residual plutonium becomes more biologically available with time. In fact several studies suggest that plutonium into a more biologically available form [3]. Plutonium in marine organisms Plutonium concentration factors in marine ecosystems appear to be substantially greater than for plants. Concentration factors for weapons fallout plutonium in marine organisms range from 100 in filter feeders, such as mussels and clams, to 1000 in zoo plankton, and 10,000 in seaweed. [4] One marine plant has been found which can concentrate plutonium by a factor of 100,000. [3] The Thule accident In January 1968 a United States Air Force nuclear-armed B-52 bomber crashed into North Star Bay, about seven miles Thule Air Base, Greenland. About 25 Ci of insoluble plutonium oxide with a median particle size of 2 um was released into the marine environment. Strong tidal currents at the bottom stirred up sediments, causing horizontal and vertical dispersal of plutonium. In addition, worms and other bottom animals may displace plutonium to greater depths in the sediments through their biological activities. It has been estimated that molluscs contain the major part of the plutonium in the biota; the transfer coefficient to the molluscs is an order of magnitude greater than the transfer coefficient to brittlestars and shrimps. Concentrations in components of the ecosystems were increased as follows [4]: Seawater twice pre-accident Sediment 10-100 times pre-accident Bivalves 10-1000 times pre-accident Crustacea, Polychaeta Echinodermata 1000 times pre-accident Bottom fish: 10-100 times pre-accident Zooplankton, sea plants, birds seals, walruses 10-100 times pre-accident In 1968 increased plutonium concentrations were measured as far as 15km from the point of impact; in 1970, contamination had moved as far as 30 km from the point of impact. The integrated plutonium level of the biomass of bottom animals had decreased by a factor of about four; higher animals such as fish and seals did not show significantly higher levels that in 1968 [5]. Future accidents The possible health consequences of an atmospheric release of plutonium powder following an air crash on land have been estimated by the Advisory Committee on the Safe Transport of Radioactive Materials (ACTRAM). It is assumed that the plutonium powder produced by BNFL has a 'respirable fraction' of 0.05%. The requirements of the IAEA Regulations are that in a very severe accident the release of plutonium is not greater than a few mg/week. According to ACTRAM 'the radiological consequences of a release of 5 mg, in one hour, of plutonium in a suburban location have been calculated for a range of UK weather conditions. Such a release would result in a mean value of 0.000003 fatal cancers in the next 50 years.' The dose is estimated using a computer program me called CRACUK in which 'account is taken of dry and wet deposition processes, radioactive decay and any variation with time in the meteorological conditions prevailing after the release'. Although is doesn't say so explicitly, the calculation presumably only includes effects of the acute inhalation, and does not take into account long-term resuspension, weathering, and movement through the soil (presumably the 'time' referred to in the 'variation with time in the meteorological conditions prevailing after the release' is rather shorter than the tens of thousands of years for which plutonium will be radioactive). Conclusion The behaviour of plutonium in the environment is complex and still a long way from being fully understood. ACTRAM's estimate of the possible risk arising from a plutonium accident appears to concentrate on the short term inhalation hazard. But, as is clear from the studies referred to above, this is only the first part of what may well be a very long story. Plutonium not actually removed from the environment of the accident will be available for resuspension and uptake into plants and animals. Bearing in mind also our uncertain knowledge of the risks of plutonium exposure in humans (not to mention other species), estimates such '0.000003 fatal cancers in the next 50 years' should be treated with a great deal of scepticism; they are obtained from a combination of many parameters, nearly all with associated large uncertainties and many without experimental validation. David Sumner June 1992 Commissioned by Greenpeace International References 1. Pinder J E et al Atmospheric deposition, resuspension, and root uptake of Pu in corn and other grain-producing agroecosystems near a nuclear facility. Health Physics, 59, 853-867 (1990) 2. Romney EM and Davis J J Ecological Aspects of plutonium dissemination in environments. Health Physics, 22, 551-557 (1972) Quoting from: W H Langham, P S Harris and T L Shipman, USAEC Document, LA-1981 (Revised) (1966) 3. T E Hakonson Environmental pathways of plutonium into terrestrial plants and animals. Health Physics, 29, 583-588 (1975) 4. Wayne C Hanson Ecological considerations of the behaviour of plutonium in the environment. Health Physics, 28, 529-537 (1975) 5. A AArkrog Environmental behaviour of plutonium accidentally released at Thule, Greenland. Health Physics, 32, 271-284 (1977) 6. The Transport of Civil Plutonium by Air Advisory Committee on the Safe Transport of Radioactive Materials London: HMSO 1988 7. Ecological Aspects of Radionuclide Release Coughtrey P J, Ed. Blackwell Scientific Publications, Oxford, 1983 8. Radioactivity and Health: A History J Newell Stannard Office of Scientific and Technical Information Battelle Memorial Institute, 1988 9. Environmental Radioactivity (Third Edition) M Eisenbud Academic Press, 1987 10. All-Union Conference on Geochemical Pathways of Artificial Radionuclide Migration in the Biosphere, Gomel 15-19 October, 1990 Printed in SCOPE-RADPATH, the Newletter of the Scientific Committee on the Problems of the Environment, No 11, Feb 1991. 11. Hardy et al., Nature, 241, 444-445 (1973) 12. Livens F R and Baxter M S (1988) Chemical Associations of Artificial Radionuclides in Cumbria Soils. J. Environ. Radioactivity, 7, 75-86 13. Cook G T, Baxter M S, Duncan H J and Malcolmson R (1984) Geochemical associations of plutonium and gamma-emitting radionuclides in Caithness Soils and marine particulates. J. Environ. Radioactivity, 1, 119-131 14. McCarthy W and Nicholls T M (1990) Mass-spectrometric analysis of plutonium in soils near Sellafield J. Environ. Radioactivity, 12, 1-12 15. Healey J W (1971) Some thoughts on plutonium in soils In: Proc. of Environmental Plutonium Symposium USAEC Report LA-4756 University of California, Los Alamos Scientific Laboratory 16. Romney E M, Mork H M and Larson K H (1970) Health Physics, 19, 487 Health Effects of Plutonium Plutonium being transported is in one of the following forms: (1) plutonium dioxide (PuO2) as a powder whose particle size distribution depends on the method of preparation. (2) plutonium dioxide mixed with uranium dioxide and formed into sintered pellets to be used as fuel in fast and thermal reactors. (3) plutonium metal According to evidence submitted to the EDRP Inquiry 90% of past exports of plutonium have been in the form of the dioxide [1]. Plutonium derived from civil power reactors consists mainly of plutonium 239, although there will also be plutonium 238, 240,241 and 242 present [3]. The biological behaviour of plutonium is influenced considerably by the physical and chemical form in which it enters the body. From the point of view of industrial and accidental exposure, the oxides form probably the most important class of compounds. Because plutonium-239 is an alpha particle emitter, it is potentially more toxic than a radioactive material which only emits beta particles or gamma rays, this is because the alpha particles have a range of only about 50 micro metres, and deposit their energy in a very small volume, perhaps a single cell. Because the range of the alpha particles is so small, plutonium presents a danger only when it gets into the body. Plutonium can enter the body in three main ways: by being breathed in (inhalation), eaten (ingestion) or through a wound. In addition animal studies have been done in which plutonium is injected intravenously. Inhalation and ingestion are considered in more detail below. Inhalation If insoluble plutonium particles are inhaled, they are first deposited in the lung: the amount deposited in different regions of the lung depends on the size of the particles. The plutonium then slowly migrates via the lymphatic system to the tracheobronchial lymph nodes. Plutonium entering the lungs and lymph nodes will eventually reach the bloodstream, but the time it takes to do so varies between days and many months depending on the size and chemical composition of the particles. Plutonium dioxide particles, being poorly soluble are cleared fairly slowly: plutonium nitrate and citrate, in contrast, are soluble and are cleared more rapidly. Ingestion Ingested plutonium is usually said to be much less important than inhaled plutonium, because the fraction of ingested plutonium that is absorbed by the body seems to be small - probably less than 0.1%. Nevertheless, there is considerable uncertainty in the size of this fraction. It probably depends on many factors, such as the chemical and physical form of the ingested material, whether or not the person is fasting, other substances present in the gastrointestinal tract, and concomitant disease. One important factor is certainly age - plutonium absorption may be increased by at least a factor of ten in infants. A Nuclear Energy Agency Report published in 198* said that '..for incompletely absorbed metals... such as plutonium...[the fraction absorbed]..may by increased or decreased by factors of from about two or more than tenfold. Both animal and human studies also show that quite large variation from individual to individual may occur, at least for some elements' [4] The Report recommended a value of 0.1% for the absorption of plutonium. Despite this, NRPB have concluded that for plutonium incorporated in Cumbrian winkles the absorption can be assumed to be only 0.002% [5]. This value is based mainly on the results of a study done by MAFF in just eight volunteers, who consumed Cumbrian winkles and then collected their urine to find out how much plutonium they had absorbed. [NRPB criticised this study when it first appeared because 'high individual values of urinary excretion of plutonium and americium were excluded...on the grounds that they indicated contamination; the possibility could not be discounted that some of these values reflected normal variation in gut transfer. Distribution of plutonium in the body Of the plutonium that finds its way into the blood stream, about *05 is eventually excreted and 80% retained mainly in the liver and skeleton. The partition of the 80% retained plutonium between liver and bone varies widely from individual to individual: a very rough average is probably 50% in the skeleton and 30% in the liver. The half-life of retention in the body is probably around 50 years in the skeleton and 20 years in the liver. In the skeleton, plutonium is deposited mainly on the surfaces of mineral bone. There is very little human data on which to base assessment of the health effects of plutonium; it is often claimed that 'we know of no case of death or serious illness resulting from human intake of any transuranium element [2]. This does not of course mean that plutonium is not potentially toxic, indeed there a large number of animal studies showing that plutonium can cause both acute and delayed effects. We will summarise this evidence first, before returning to consider possible health effects in humans. [Note: In what follows, amounts of plutonium are given Bq*300 Bq of plutonium-239 is equivalent to one millionth of a gram]. Animal Studies An important part of our knowledge of the effects of inhaled plutonium comes from long term studies in beagle dogs - over 1000 have been studied for more than 30 years - which continue to this day. Inhalation of large amounts of plutonium results in the destruction of lung cells and therefore 'deterministic effects' O radiation pneumonotis and fibrosis, similar to that observed following external radiotherapy. In dogs, deposits greater than 700 Bq per gram of lung have caused fatal fibrosis. Lung disease is dogs has occurred up to seven years after exposure, and it has been suggested recently that 'people exposed to aerosols of relatively insoluble plutonium resulting in moderately high lung burdens could develop radiation and pneumosis and pulmonary fibrosis at relatively long times after the exposure' [12] Inhalation of smaller amounts of plutonium increases the risk of lung and bone cancer. None of the animal experiments with inhaled particles suggest an enhanced risk when the material is deposited in the form of 'hot particles'. In fact it is probably the other way around - there is an increased risk when the material is dispersed. For example, in the mouse, the highest lung-tumour incidence was seen with the smallest plutonium dioxide particle size, indicating that the most homogeneous distribution of dose is also the most carcinogenic. Another feature of some mice experiments is the presence of a 'reverse dose rate effect': a given activity of plutonium dioxide administered to mice produces more lung cancers when the dose is protracted rather than given in a single exposure [13]. This is the opposite way round to the situation observed for X- rays and beta particles. 2. Liver Liver tumours have been observed in some life-span studies of inhaled radionuclides in dogs and Chinese hamsters, but not in the life-span studies of beagle dogs that have inhaled plutonium compounds. However, cancers of the liver and bile ducts have occurred in beagle dogs given plutonium-239 intravenously. The BEIR Committee have pointed out that this finding does not mean that inhaled plutonium compounds in humans will not cause liver cancer. 3. Bone High doses of plutonium deposited in bone can result in pathological fractures, most frequently in the ribs. In beagles the maximum incidence of fractures occurs following the injections of between 37,000 and 111,000 Bq of plutonium-239 per kg body weight. Administration of plutonium-239 at levels above 111,000 Bq per kg body weight greatly reduces bone growth [14]. Low doses of plutonium can result in bone cancer. In the studies in beagle dogs referred to previously, inhaled 23PuO2 has not caused bone tumours because of its long retention time in respiratory tract tissues and its consequent low rate of transfer to bone. Inhaled 238PuO2 and 239Pu(NO3)4 (plutonium nitrate, on the other hand, are potent inducers of bone-tumours in dogs. An initial lung burden of 740 Bq plutonium-238/kg body weight is the lowest dose at which fatal bone cancer has occurred (although the study is not yet complete). 4. Lymph Nodes When plutonium is deposited in the lungs, there is a reduction in the number of lymphocytes (a type of white blood cell). This is especially notable in dogs exposed to plutonium dioxide; a reduction in lymphocytes has been detected after lung depositions greater than 25 Bq per gram of lung. Although we rely heavily on animal studies for estimates of the risks of plutonium exposure, there are a number of problems in transferring risks from one species to another. For example: many human lung cancers are in the * , but this is a very unusual tumour site in experimental animals; animal studies take no account of other competing risks to which humans may be exposed, and which may interact with radiation in complicated ways; and, perhaps most important, calculated radiation doses have considerable associated uncertainty because of the very localised way in which alpha particles deposit their energy. Health effects of plutonium of humans Nuclear Industry Workers As noted above, it is often claimed that no cases of illness or death can be attributed to plutonium. Although it may have been (just) possible to argue this ten or even five year ago, recent studies make it a much less tenable position now. It is certainly difficult to do studies of the health effects of ionising radiation, because cancer is a common disease and there are many confounding factors. A negative study does not necessarily mean that there is no effect, it means that one has not been detected; a real effect could have been masked by statistical fluctuations. A recent study by Wilkinson et al at the Rocky Flats plant in the USA [8] claims to be the 'first epidemiologic findings that suggest an association between exposure to plutonium and untoward health effects in humans'. In this study * workers were classified into those with a body content of plutonium greater than 74 Bq, and those with a body content of less than 74 Bq. The death rates form all cases. and some cancers (notably leukaemias and lymphatic cancers) were greater in the exposed group. Similar, although not conclusive, suggestion of plutonium related effects were found by Beral et al in a study of workers at the Atomic Weapons Research Establishment at Aldermaston [9]. In workers monitored for possible internal exposure to plutonium and other radionuclides, mortality from all cancers was not increased but after a ten year lag death rates from pro static and renal cancers were generally more than twice the national average. The excess cancers were in a small group of workers monitored for exposure to multiple radionuclides. Though mortality from lung cancer in workers monitored for exposure to plutonium was below the national average, it was some two third higher than in other radiation workers. 26 white males who worked with plutonium-239 during World War II at Los Alamos have now been followed up for 42 years [7]. Inhalations was the primary mode of exposure. Up to 1986, four men had died. The cause of the four deaths were: lung cancer, myocardial infarction, accidental injury and congestive heart failure/respitory failure due to pneumonia. Since 1987, three more have died, from atherolsclerotic heart disease, lung cancer and bone cancer. This latter case could well be due to plutonium. The latent period (between exposure to the plutonium and development of the cancer) is 43 years. The estimated plutonium deposition in this man at the time of his death was 560 Bq. The average dose to the skeleton is similar to the lowers range of doses for dogs that have developed bone tumours when exposed to plutonium either by injection or inhalation; moreover, the dose is estimated to be below current radiation protection guidelines. It seem likely that a clearer picture of the risks from plutonium exposure will emerge over the next few year as worker studies are enlarged and updated; it is important to have a long follow up period, as the time between exposure to radiation and appearance of cancer may be several decades. In members of the public Sellafield in Cumbria has been discharging radioactive material including plutonium into the Irish Sea since 1953. Estimates of radiation doses to the population of Cumbria, especially so called 'critical groups' who receive higher radiation doses because some aspect of their life-style (e.g. eating a lot of winkles) are made using complex models. On the bases of these estimates official thinking at least was that there would not be any observable health effects in people living near Sellafield, or indeed any other nuclear installation. However, in 1983 Yorkshire television produced a film which claimed that in the village of Seascale, near Sellafield, there was a much higher incidence of childhood leukaemia than would be expected from national incidence rates. The Prime Minister at that time, Margaret Thatcher, was sufficiently concerned to set up a Committee of Enquiry, chaired by Sir Douglas Black. The Black Committee asked NRPB to estimate the probable radiation doses to children in Seascale from the discharges. These calculations showed that using conventional dosimetry and risk factors, the radiation doses likely to have been received from the discharges were much too low to have been responsible for the observed incidence of leukaemia. However, several people pointed out the logical flaw in this argument: the more leukaemias that occurred in Seascale the less likely they were to be caused by Sellafield. Alternative possibilities were that the environmental and/or metabolic models were incorrect or incomplete in some way; perhaps there were other exposure pathways that had not been allowed for, or perhaps the 'target cells' had been incorrectly identified. The finding of the Seascale cluster (as it came to be known) stimulated other studies to investigate whether there were increased incidences of leukaemia and other cancers around the nuclear installations. A number of other clusters were reported, although none as dramatic as the Seascale cluster. Several follow up studies of the Seascale leukaemias have been carried out on the recommendations of the Black Committee. the most important of these was a case control study by Martin Gardner and colleagues, which was published in 1990 [15]. This found an association between childhood leukaemia and radiation dose of the father, the implication being that radiation may have cause changes in the chromosomes of the sperm cell which eventually results in leukaemia in the child. The Gardner findings have tended to move the spotlight away from environmental radioactivity onto worker radiation doses. However, there are problems with the Gardner explanation: the estimated risk factor appears to be much larger than the risk factor for genetic effects that has been inferred from animal experiments; and it is not yet clear why, if the leukaemia is a generic effect of radiation, there has not been an increase in other abnormalities. It remains possible that environmental radioactivity is in some way to blame. If it is, then it is likely to be substances containing plutonium and other transuranic element, because of the greater radioactivity of alpha emitting radionuclides. Recently a study published by the MRC Radiobiology Unit at Didcot has shown just how incomplete is our knowledge of the biological effects of alpha particles [10]. In this study mouse bone marrow cells were exposed to alpha particles from plutonium-238. This was found to cause damage in the cells that was not obvious at first, but resulted in chromosome abnormalities later in the same cell line. The implications of these results have been well summarised by Evans: 'these findings imply that ...alpha-particle exposure may induce damage that is transmitted to daughter cells and...may result in the expression of a genetic instability in late cell generations ... an alpha-emitting speck of plutonium will have a high probability of killing cells in it immediate vicinity. but if it engendered instability in nearby surrounding surviving cells its effect would be very much greater than that predicted on the total body dose received' [11]. Summary The most important route of entry of plutonium into the body is by inhalation. Inhaled plutonium slowly moves out of the lung and eventually reached either the liver or skeleton, where it can be retained for many years. The fraction of ingested plutonium that is absorbed is small, but variable and still uncertain. There is clear evidence from animal experiments that inhaled plutonium can cause lung cancer. Plutonium entering the body by any route can cause bone and liver cancer. Human studies on the effects of plutonium are still somewhat inconclusive, although suggestive of an increased risk of cancer. The role of plutonium in the induction of childhood leukaemia around Sellafield is still unclear. References to be inserted David Sumner June 1992 Commissioned by Greenpeace International