Compendium of evidence

3)studies which are said to demonstrate that there is no unappreciated risk but which have demonstrable flaws or which do, in fact, show an excess risk.

Muirhead 1998 review of studies of childhood cancer near nuclear plant (but also including selected studies of radiation workers)











As is expected from NRPB, unsubtle misdirection, confusion, and general reassurance.
Dr. Muirhead concludes that nothing can really be learnt from these studies and hopes that the UK Childhood Cancer Study will reveal the cause of the disease. LLRC has however established that the CCS "has made no attempt whatever to ascertain exposure to .. discharges from nuclear plant." (Cartwright 1998)
Muirhead says some of the cited studies of clusters outside UK are inconclusive because they lack statistical power, but there was no need to keep to aggregated and large area studies, such as the cited Michaelis 1994, while ignoring e.g. a 5-fold cluster around Krummel shown by Ziggel (Ziggel 1998).
Muirhead's reservations about the Jablon 1991 study are a distant echo of Sternglass's criticisms ((Sternglass 1996), ( Gould et al. 1995)
Muirhead stresses the difficulties of getting statistical power from studies of radiation workers, but studiously ignores all findings that internally contaminated workers suffer the highest risks or pass high risks on to their children. (There are several such studies, with abundant statistical power)
He accepts the reality of clusters near nuclear sites, but repeats (over and over) COMARE's opinion that doses from radioactive emissions are too low to account for the disease rates, emphasises population mixing as an alternative explanation, and repeats Cook-Mozzaffari's observation that while Sellafield's emissions are orders of magnitude greater than any other nuclear plant, the ratio between excess leukaemia risk near Sellafield and excess risk near other plant is "relatively small" - i.e. "only" six to one. Bizarrely, this is held to justify the claim that there is no evidence that the massive pollution at Sellafield has anything to do with the higher disease rates. Of course, it assumes that NRPB's straight line dose:reponse curve is correct.
It also begs the question: Has there been a six-fold excess of population mixing at Sellafield?

Prof. Bryn Bridges, Chair of COMARE: "...I don't think there's any question [but] that there is a real enhanced risk in ... Sellafield and Dounreay ...[but they] are both in isolated rural areas, they're both subject to this other phenomenon of population mixing the real extent of which we really don't know."

BBC reporter: "Surely the population mixing, for example, has been going on for fifty years. Should it still be showing itself in a higher incidence of these diseases?

Bridges: Our view is that it's surprising if it does. Yes, I think we would agree that the population mixing idea can certainly very largely in all probability account for the small limited cluster around Dounreay. It seems very strange that it should go on for thirty perhaps almost forty years in somewhere like Seascale. So that alone doesn't convince us that that is the explanation.

BBC: So not even the Government's scientific advisers can continue to sustain the argument that the mixing of populations could ... be the only cause. (Bridges 1998)

Cook-Mozzaffari 1989b This followed up Cook-Mozzaffari 1989a - which found increased leukaemia near nuclear sites. The second study found increased leukaemia in an aggregated population living in places considered but rejected for siting nuclear reactors. Concluded that "areas near existing and potential (nuclear) sites might share unrecognised risk factors other than environmental radiation pollution." This conclusion ignored the possibility that radiation from nuclear weapons tests - falling with the high rainfall of the aggregated areas, and now known to be associated with elevated levels of cancer and leukaemia - was a confounding factor.





Draper and Vincent 1997 High leukaemia death rate probably due to chance.


Problematic attack on Busby and Scott-Cato 1997 (unexpectedly high leukaemia mortality near Aldermaston, Harwell etc.). Draper and Vincent unreasonably compared incidence to mortality and used inconsistent datasets - see Busby and Scott-Cato's reply on same page of BMJ.
Watson and Sumner 1996 case control study of fission-product body burden of leukaemia and cancer patients.






LLRC has consistently called for such a study. Citing this paper even before its publication, NRPB's Frances Fry sought to answer LLRC, saying that no correlation had been found. Problems: The study was funded by BNFL. Study group consisted of four children with leukaemia - the others had died. Statistically, the four cases make an impossibly small study group. The study group was bulked out by measuring contamination in other members of their families. This invalidates the study; The leukaemia victims had significantly higher counts of Americium-241 than the healthy siblings. The method used was incapable of detecting inhaled hot particles of plutonium which is the contamination route of most interest because of: (1)Dounreay's history of plutonium leaks (2) the propensity of tracheobronchial lymph nodes to concentrate plutonium - measured at 100 to 10,000 times higher than all other body tissues (McKinroy 1991) West central Scotland is a poor control for Caithness since plutonium levels there are high, because of higher rainfall and pollution from Sellafield. All these criticisms remain, even after publication of correspondence (LLRC 1997).
Bithell 1994 and Steward 1994 Using the method of Stone; Bithell found no significant excess of leukaemia 1966 - 1987 within 25 km of 23 nuclear sites; Steward found no relationship between cancer and the two nuclear power stations in north Wales. Problems: The method of Stone is predicated on the assumption that emissions are evenly distributed round the source. There are, in fact, strongly prevailing directionalities of wind and water flows; high dose and low dose effects are therefore averaged out. Steward compounded this error by applying the method of Stone to two separate sites, and ignored the the Irish Sea - yet another confounding source of contamination.
NOTE: Dr Steward has told Dr Busby that he was the author of this paper. In July 1999 he told LLRC (in a telephone conversation) that he did not. LLRC is writing to the Chief Medical Officer for Wales to ask who did write the paper (and, since peer review seems to be such a big deal, who reviewed it)





Darby 1992 Claimed to find no relationship between childhood leukaemia in nordic nations and weapons test fallout. Four pages of detailed analysis of shortcomings in Busby 1995 pp124 - 128. Lectures at London School of Hygeine and Tropical Medicine have taken this paper as a case study of badly designed epidemiology, invalidated by the change of study population mid-way through the study period.
Nevertheless the data do show an increase in the disease, contrary to the claim in the abstract (and contrary to Dr. Valentin's claim in Radiological Protection Bulletin No. 208)
Doll now (2001) says that this is "one of the few papers providing any evidence of a possible leukaemogenic effect of radioactive fallout." (ref.)
Parkin 1996 Pan European 5-year follow-up of leukaemia after Chernobyl. Said by NRPB (Green Audit 1987 page 35) to show that Chernobyl caused no changes in this disease. Outrageous epidemiology, a boundary looseners' jamboree, full of flaws:- The entire population of Europe was allocated to only three dose bands, despite intense local variability of deposition (e.g. up to 30-fold variations in Baden-Wurttemburg (Hohenemser 1986)) internal dose not known, as dose bands were constructed from Caesium gamma monitoring; confounders ignored - wide variation in genetic, dietary, lifestyle and environmental factors, rural/ urban split; selection of inappropriate time periods.
Parkin did, nevertheless, find an effect on the border of statistical significance, as well as an overall 10% increase in childhood leukaemia 1981 - 1991.
Archer 1987 increased leukaemia in USA states which had high Strontium-90 levels. This was fitted into the establishment paradigm by assuming high doses, in particular Archer reconstructed the dose to 5 - 9 and 5 - 19 yr olds as a 50 years dose! For detailed critique see Busby 1995 pp130 - 1.



Holm 1988
This study of internal contamination by injection of 35,000 patients with 131-I underpins conventional estimate of risk from Iodine 131.
Flaws are: inappropriate control population,
and disregarding all thyroid cancers occurring in first five years after injection.
For detailed critique see Busby 1995 pp138 - 9.



Jablon 1990 Exculpatory study of cancer downwind of 62 reactor sites. skewed by selection of small study populations and contaminated control areas (see Bramhall 1997 page 127 and Gould and Sternglass 1995)
Draper Little et al 1997
1.8-fold increased risk in children of male nuclear industry workers, rising to 2.9-fold risk where fathers were monitored for internal contamination.
The authors' abstract and media coverage concentrated on fact that lowest risk was for children whose fathers had highest external dose (i.e. measured by film badge). Authors speculate that "observed associations may be due to chance findings or result from ... infective or other agents." but the findings were 95% certain of not being due to chance; no infective agent for leukaemia has ever been identified, whereas radiation is known to cause it - only the risk factors for internal radiation fail to account for the observations.
Busby and Cato have pointed in the BMJ out that "Exposure to internal radioisotopes may be responsible" Draper's conclusion that exposure to radiation is not the cause of the leukaemia and that the Gardner hypothesis is refuted is unwarranted because exposure to internal radioisiotopes may be responsible.
Cancer epidemiologist
Freda Alexander believes that radiation cannot be ruled out and that the relative risks are far too high to be explained by population mixing.

Nishiwaki 1972 Fallout and infant Mortality in Japan - a study of internal beta and gamma radiation at less than Natural Background;   Denied a correlation but data shows there was one.



Popplewell 1985 The published version of this paper was used at the Hinkley public inquiry.



What is interesting (or, rather, scandalous) is that it omits figures for Tracheo-bronchial lymph nodes. A crucially different version of the paper was "published" in NRPB's house mag, the Radiological Protection Bulletin Popplewell 1986. This includes figures for TBLNs which are extraordinarily high, showing that hot particles can pass through the lung wall into the lymphatic system. This means that they can in principle migrate almost anywhere in the body. If this had been available to the Hinkley objectors the outcome might have been different. see also the massive Pu levels in TBLNs in McKinroy 1991 (data on this site) and note that Watson and Sumner's 1996 study of (a tiny sample of) leukaemia victims relied on urinary plutonium. Refractory particles of plutonium are only soluble in Hydro fluoric acid, so have no chance of showing up in urine. A further problem with Watson and Sumner's study is that treating Strontium-90 as a surrogate for plutonium is a nonsense. Sr-90 is soluble, and so will be distributed around the body and excreted, rather than remaining as a hot particle.

Latest developments

Carpenter et al. Nuclear workers monitored for internal contamination have a higher risk of cancer. There are no uncontaminated controls, since we all have man-made radionuclides inside us from Sellafield, weapons tests, Chernobyl etc. etc; we do not know that the workers were actually contaminated - only that they were monitored; nor is there any information about the speciation or the concentration of the isotopes in their bodies. The statisticians fiddled their figures to minimise the effect but still the data in this study shows a definite excess. See the latest issue of Radioactive Times for more detail.
Muirhead 1999 A major new analysis of radiation workers which compared cancer rates in nuclear industry workers with the general population to find a strong "Healthy Worker Effect" (HWE). Bizarre logic. The HWE can only be used for comparisons within the industry, and workers start out healthier than the average. In this study, however, cancer rates were compared with the general population. Reanalysis of the data has been used to generate an HWE specific to nuclear workers, and shows a cancer mortality rate 6 times that expected on the basis of official radiation risk factors. See this link for more detail.
Roman et al 1999 Cancer in the children of nuclear industry workers. Authors claim "Overall the incidence of all cancers and of leukaemia was similar to that expected in the general population" Completely inappropriate methodology. When reanalysed with a simpler and more suitable model a risk of 4.4 times the national average appears. See correspondence in New Scientist 29.5.'99 and 12.6.'99 and

Miller 1999
Cells were irradiated with single alpha particles. Follow up of cancer transformation showed that the prodominant effect was associated with two tracks. Single particles had very little effect.
This is to be compared with the Second event theory.

Other categories of evidence:
studies on which radiation protection standards are based, and those which undermine them:
2) epidemiological studies showing a risk not accounted for by NRPB/ ICRP model
4) animal studies
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