Additional Evidence A1
to the paper:
Science on Trial
On the Biological Effects and Health Risks following Exposure to Aerosols produced by the use of Depleted Uranium Weapons
Chris Busby PhD.
First Presentation to the Royal Society London, March 13th 2001
Occasional Paper 2001/2 Aberystwyth: Green Audit March 12th, 2001

Introduction

This short paper is intended to be read in conjunction with the presentation Science on Trial and contains further evidence and consideration of some of the points made in the latter.

1. The Chernobyl Infants and Scientific Method

Previously, an account was given of how the analysis of infant leukemia in the ‘in utero’ cohort exposed to the Chernobyl fallout in five separate countries showed that the risk models presently used to assess cancer yield were in error of about 100-fold for internal exposure. In addition, it was argued that scientific method has, in this area, been wrongly employed and that the largely deductive approach, based on the acute external exposures of the Hiroshima Lifespan Study cohorts is not scientific. In particular, I drew attention to the way in which incorrect theories may be defended by circularity and, after Michael Polanyi FRS, compared scientists in this area with Azande witchdoctors who defend one unsupportable notion by reference to another. A good example of such a process has come about following the formal response from the National Radiological Protection Board to the implications of the Chernobyl Infants analysis. NRPB’s response was written by Dr Colin Muirhead, their chief epidemiologist, and the person who is the main defender of the present risk model in this area of epidemiology. In his haste to dismiss the implications of the leukemia increases he has stepped off the cliff. To demonstrate this I quote from a letter I wrote to Dr Roger Clarke, Director of NRPB:

Dear Dr Clarke
I have recently been sent a copy of a ‘note’ written by Dr Colin Muirhead and sent to a number of people who have been asking for a response from NRPB to the publications of several different groups highlighting statistically significant increases in infant leukemia in various countries in the cohort who were exposed ‘in utero’ or whose parents were exposed just before conception to internal radiation from Chernobyl fallout. One of these papers [1] compared the observed excess numbers of cases with those predicted by NRPB and deduced an error of about 100-fold in the present model for such exposures.

Dr Muirhead’s note, entitled ‘Leukemia after Chernobyl’ was written to address this evidence of error. In his first paragraph, numbered (1) he begins with a clear statement:

"If exposures vary within geographical areas, as was the case within Wales and Scotland, it is not possible to tell, using correlation studies, whether the persons who developed the disease in question received higher exposures than the population as a whole".

This seems to be an admission by Muirhead that the risk models themselves are useless. Such models are themselves based on correlation studies and exactly the same technique is used in reverse by the model to make linear predictions of the number of cases of cancer expected following any given dose. Indeed, all that we did in our paper was to examine the predictions of such a risk model. We would be the first to agree with Dr Muirhead’s novel realization that in a geographical area some people might get high doses and therefore suffer greater risk. However, it is my understanding of the concept of a ‘linear relationship’ and the model that you use, that if some get a higher dose this necessarily means that other people get a lower dose and therefore the overall risk in the population of the geographical area is the same and the total number of cases of leukemia is the same. Otherwise what is the point of the model?

Muirhead was wrong about what we did: our study was not primarily an epidemiological study but primarily a test of the NRPBs predictions, one which it failed.

There are two ways of looking at this. First, Muirhead is correct, and the few people in an exposed population who get the high dose are the ones who get the leukemia, forcing a total number of cases higher than that predicted by the linear no-threshold model (by 100-fold) in which case the model is useless, for this could always happen in any situation of risk assessment (e.g.Sellafield). Otherwise Muirhead is wrong, and it follows that our correlation study was valid and showed that the predictions of the model were too low by a factor of 100 (which also explains the Sellafield child leukemias).

I recently instructed the solicitors of The Low Level Radiation Campaign, Humphreys and Parsons of Machynlleth to put the Environment Agency under notice that recent studies of the infant leukemia rates after Chernobyl in five separate countries made it clear that the risk models used by NRPB and ICRP to underpin statutory dose limits for exposure to man-made radioactivity were insecure and that from the date of receiving this information they could no longer rely on a plea of lack of knowledge in any subsequent litigation. In this context, I should be grateful if you could let me have a reply to this letter explaining whether NRPB agrees with Dr Muirhead’s evident belief that it is not possible to examine the predictions of the LNT model in a geographical area because "the persons who developed the disease in question received higher exposures than the population as a whole".

Ref
[1] Busby C and Cato M (2000) ‘Increases in Leukemia in Infants in Wales and Scotland following Chernobyl: Evidence for Errors in Statutory Risk Estimate’ Energy and Environment 11(2) 127-139

I have not had a reply to this letter although it is hard to imagine how there could be any defense. My reason for highlighting the Muirhead argument is that it is a perfect example of the epicyclical defense which I outlined I my original contribution. I feel that it shows the bankruptcy of NRPB’s advice base and that of the present risk assessment modelling in general.

2. Mechanistic considerations:Beta emitters and the bystander effect.

Since I last spoke with the committee, I have been able to measure radiation levels is areas where DU was used in Iraq and in Kosovo. I will report some of these findings below, but what struck me most was the high levels of radiation from the beta emitting daughter isotopes Thorium-234 and Protoactinium-234. These two isotopes have short half-lives (24 days and a few hours respectively) and are thus in secular equilibrium with the parent U-238. What this means, in effect is that the number of cells which may be considered to be within range of decays from a micron-sized Uranium Oxide particle is orders of magnitude greater as far as the beta tracks are concerned. Thus the original model proposed, one in which a proximal cell volume of radius equual to a few cell diameters now becomes a much large cell volume of radius perhaps 400 cell diameters. Second Event beta decays from a point source have been addressed in the original theory (cited in the previous contribution and references therein). In these arguments it has been accepted that the number of cells likely to receive two tracks which overlap are very small, and defined by the distance a free radical or ionizied moiety can travel once it is produced in the matrix. Thus the main effect is restricted to cells which are close to, or a few cell diameters away from, the micron-sized particle or sequential emitter sources. However, there is a development. It has been recently shown that there exists what is called a bystander effect: this is a response in a cell to radiation tracks traversing cells nearby. [Wright et al., 1998] The range of this effect seems quite large in cellular terms. This finding suggests that it may not be necessary for track overlap, i.e. two sequential hits to occur for a Second Event enhancement of hazard to occur. A track traversing one cell will results in lesions in all the nearby cells, thereby setting them all up as potential Second Event cells which may be then mutated by a second track separated in time by 8 to 12 hours, the repair replication period. This idea would extend the hazard of the Second Event process by orders of magnitude.

3. Mechanistic arguments: Linear Quadratic dose response

The Second Event theory identifies an oversight in the averaging of exposure over time. However, it is possible to demonstrate inconsistency in the present model in its averaging in space also. The full model for radiation response which emerges from the various external studies shows that at higher dose, above the level where a cell receives two or more hits in one acute exposure, there is a quadratic term. Thus the full response equation over the low to medium exposure range is of the form [e.g. BEIR V,1990, p 21]:

Effect = aDose + bDose2

Now it is clear from this that inhomogeneities of dose in large tissue volumes, such as would be the result of local deposition of dose from micron diameter particles emitting alpha or beta disintegrations would, as I showed in my contribution, result in local doses in the quadratic region of the full dose response curve. To make it very simple, imagine the irradiated tissue as a sheet of A4 paper and model the external dose situation as five chess pawns. Since the dose is externally delivered, the dose is uniform over the paper sheet and the pawns are placed equidistantly on the paper, say, in the form that they show on the face of a die. Assume, then that each pawn carries unit risk of cancer. The risk then, in this case, is five units of cancer risk. Now move all the pawns to one corner of the sheet of paper. The dose is five times as high in this corner, but, of course, it is zero for the rest of the sheet, and the linear theory assumes that the total risk is the same, that is, five risk units. But in reality, the cells in the corner are now in the quadratic region, so their risk is twenty five. We can start again and assess the effect of doubling dose. We will place ten chess pawns equidistantly on the sheet. The doubled dose just doubles the risk and the risk is now ten risk units assuming a linear dose response. But move them all to one corner and the risk is one hundred. Thus it is clear that doses from particles which are sufficiently active to give local doses higher that those conventionally placed in the low dose region i.e. under 10mSv, will even in the present theoretical framework, manifestly cause much higher risks that are presently given by the external averaging risk model.

4. Environmental mobility and fate of DU particles

Between 19-22nd Jan 2001, I accompanied a Nippon TV crew to Kosovo to advise on the possible health effects of Depleted Uranium (DU). Using maps and information supplied by NATO, KFOR and the Italian Army I visited areas where DU had been used and employed an alpha- and beta- radiation detecting Scintillation counter to attempt to establish whether there was still significant contamination there after 18months. The machine was an Electra 1A with a Type DP2 dual phosphor 4 inch scintillation probe. We visited over ten sites near the towns of Prishtine, Prizren, Djakove and Peje and the villages of Brodosava, Bresalc, Zur, Cermjan and Decan where I measured radiation and collected soil and dust samples. I also obtained air filters from three vehicles for further analysis.

A preliminary analysis of the beta-activity of a sample of dust taken from a car park near the destroyed VJ barracks in Gjakove showed the presence of 4500Bq/kg of beta- activity almost certainly due to the presence of Uranium. The normal background levels of Uranium in soil are between 15 and 100Bq/kg. This finding provided evidence that Uranium dust remains in the environment for more than 18 months and is available for inhalation. The highest radiation count rate over the dust was 25 counts per second, which may be compared with the general count rate in Kosovo remote from sites where there may have been military activity of 3.0 to 6.5 cps or occasionally more and control regions of 2.7 to 3.1 cps.

The area where the Gjakove dust sample was taken from was one of high population density and several children were playing in the vicinity at the time. On return we made some NaI(Tl) gamma measurements and long count period beta meaturements of the samples. In addition BBC ‘Newsnight’ paid some money to analyse two of the samples and I personally paid for two other samples to be analysed for Uranium isotopes and other isotopes by gamma spectroscopy. Some of the results are given in Table A1 below. It is of some considerable interest that such high levels of the daughter isotopes Th-234 and Pa-234 exist in the environment 18 months after the attack. The half life of this sequence is only 24 days since this is the half life of the parent Th-234. In addition, in one of the Gjakove samples, the beta daughters were present at ten times higher concentration than the parent. The question that this raises is how such quantities of a rapidly decaying isotope is present in the presence of such low concentrations of both U- 235 and U-234. The latter should be in equilibrium with the Th-234 i.e. the number of Bequerels per kilogram should be the same. It suggests that the Uranium has a very different mobility in the environment to the Thorium. However, both isotopes are extremely insoluble as oxides and have similar densities. The question raised for me by this observation is one which may answer my hypothesis that micron sized particles may actively transport and resuspend by electrostatic repulsion from each other and the Earth surface field. The origin of the dust in Gjakove is thus likely to be the recent snows which had just melted when we arrived at the site, and it is the radioactive Uranium dust, suspended in the atmosphere, which had been precipitated by the snow which trapped the Uranium. Subsequently the snow had melted and the alpha emitters were becoming resuspended as aerosols. This is an area where some further research is indicated.