ECRR

Uranium and Health

The Health Effects of Exposure to Uranium
and Uranium Weapons Fallout
Chris Busby
Documents of the ECRR 2010 No 2
Brussels, 2010

European Committee on Radiation Risk
Comité Européen sur le Risque de l’Irradiation
Secretary: Grattan Healy
Scientific Secretary: C.C.Busby
Website: www.euradcom.org
Uranium, and Health: The Health Effects of Exposure to Uranium andUranium Weapons Fallout.
Documents of the ECRR 2010 No 2
Chris Busby

Copyright 2010: The European Committee on Radiation Risk
The European Committee on Radiation Risk encourages the publication oftranslations of this report. Permission for such translations and their
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The ECRR acknowledges support from:The International Foundation for Research on Radiation Risk,
Stockholm, Sweden (www.ifrrr.org)
Explosion plume, Khiam, Lebanon, 25 July 2006
Photo: Lotfallah Daher,

2Uranium, and Uranium Weapons
For there is nothing hid that shall not be manifested;neither was anything kept secret, but that it should come abroad
Mark 4,22

1 Introduction
The element Uranium is the basis of and parent of almost all releases ofradioactivity to the environment, yet curiously, until it began to be employed
as a weapon, it had been quite neglected as a hazardous component. It is notmeasured routinely near nuclear power stations or reprocessing sites. It istreated as if it were natural which of course it is, but its concentration in theseplaces, and the form it is released in is not.
The intense and increasing interest in the health of the troops who
participated in the first Persian Gulf War in Iraq, and later those who served in
the Balkans, where Uranium weapons were also used, and of course thecivilian populations of those areas have resulted in evidence that the
genotoxicity of Uranium is far greater than the military who used it, and thestates which sanctioned this, believed. Despite the increasing evidence of its
anomalous propensity for harm, from epidemiology and from laboratory andtheory, the ICRP risk model, here as in everywhere else in radiation
protection, is used to deny the evidence and to sanction its continued use as aweapon of war. As with the fallout from bomb tests, Chernobyl and the childleukemias near power stations, clear evidence of harm from exposure to
Uranium is denied on the basis of deductive logic, that the absorbed doses are
too low to cause any measurable effect. By 2006, when massive populationbased evidence that the exposures to so-called Depleted Uranium, DU werecausing harm, and evidence from laboratory studies and theoretical research
had also emerged, UNSCEAR, in their 2006 report allowed 11 lines on one
page in their 400 page report to the consideration of DU effects. UNSCEAR
based its dismissal of any problem with Uranium exposures on three citations,desktop reviews, the RAND corporation 1999 report (Harley et al 1999), the
US Institute of Medicine 2001 report and that of the Royal Society in 2001.
None of these reports were peer-reviewed, and the RAND corporation isbelieved to be closely associated with the US Pentagon. All were selective intheir references. And all were out of date. None of these could deal with theparticulate nanoparticle inhaled Uranium from weapons fallout, since no-one
had studied it. Yet all three (and also countless reports from agencies likeWHO) employed the ICRP model to show that the doses were too low.
Despite the many studies which will be reviewed below and which wereaccessible to UNSCEAR, its 2006 report (which appeared in 2008) states(p53):
There appear to be several possible reasons why Uranium is not. . .
considered a human carcinogen (by the Institute of Health): Uranium is notvery radioactive ( having such a long half life of billions of years, 238U

3

decays very slowly) and its chemical properties are often such that any
inhaled or ingested Uranium is excreted rather quickly from the body.
By 2004, the way that official agency reports ignored the increasing peer
reviewed evidence that Uranium was much more genotoxic than its
radioactivity suggested became so embarrassing that the senior radiation
health advisor to the WHO, Keith Baverstock wrote a paper with Carmel
Mothershill on the issue to the Director General. He was sacked but the paper
was later published (Baverstock 2005).
The scientific investigation of DU gives a curious condensed echo of theearlier investigations into the nuclear site child leukemias. This is not
surprising given the political consequences of having to concede that the low
doses of DU, conventionally assessed, were capable of causing such graphic
and appalling genetic effects on populations exposed to the dust. For if this
could happen with Uranium, it means that all of the basic equations andassumptions of the risk model are wrong. The matter has been painstakingly
researched and reviewed recently by an American academic, Paul
Zimmerman whose conclusions, independently gained by an academic,
closely agree with the ECRR thesis developed in 2003 and in the present 2010
report (Zimmerman 2008).
It is an interesting fact that the military and the nuclear industry internallytake Uranium exposure very seriously as far as handling the material isconcerned. Spills, even small ones have to be dealt with, with all the rigours
associated with contamination by radioactive material. The same is true forthe military, who publish internal documents warning of the health effects.
However, as soon as the Uranium is shot from the gun and has contaminatedthe theatre of war, it suddenly becomes benign, in all the reports of the issue,
and in the denials of the military and its risk agencies and those of thegovernments involved.
The effects of exposure to Uranium are not, of course, restricted to DU
and passive weapons fallout. Uranium is increasingly contaminating theenvironment, near nuclear sites, near isotope separation plants, near fuelmanufactories, near Uranium mines and in atomic and thermonuclear
weapons fission fallout, near and remote from the test sites. Uranium isincreasingly found in food and drinking water as it is a significant componentof agricultural fertilizer. It is therefore also found near fertilizer factories andphosphate mines and in the transportation of phosphate ore and its agricultural
products (Eisenbud and Gesell 2000, Busby and Schnug 2008). The mining of
Uranium began at the beginning of the last century. Also beginning at thesame time was a new disease: childhood leukemia, which is believed to result
from a mutation in utero. The temporal correlation between the incidence of
this disease and the production of Uranium (modeled as Radium) is startling,
and is shown in Fig 1 below. Despite this, Uranium seems to have beenforgotten in investigations into contamination near nuclear sites, diseases
associated with weapons fallout, Chernobyl effects. It is the invisible
substance. Measurements made new nuclear sites will show concentrations of
exotic isotopes, vanishing concentrations of Plutonium in fish, but few
4measurements are made of the Uranium emerging from the nuclear sites. In
the COMARE analysis into the Sellafield child leukemias, it was concluded
that although the doses from Plutonium to the tracheobronchial lymph nodesof the children were high, the doses from natural radionuclides were higher,
and so the nuclear site could not be responsible, even if these were the sourceof the disease. After Chernobyl, large amounts of Uranium were released asfuel particles, but no measurement of Uranium is to be found in any of thereports on Chernobyl fallout.
ECRR set up a sub-Committee to examine the issue of Uranium weapons.
This report presents a brief account of the findings, reviews the evidence for
DU and Uranium effects and makes recommendations.
Fig 1 Trend in child leukemia mortality (line) and world Radium production(g) (Source: Busby 2002 acknowledging Bramhall R)

2 Depleted Uranium: Uranium weapons.
Depleted Uranium is a by-product of the nuclear industry where the fissile
isotope U-235 in natural Uranium ore is concentrated to produce reactor fuelconsisting of ‘enriched Uranium’. The isotope discarded by this process is
Uranium 238 which is generally classed by the risk agencies as a low
radiation hazard material owing to its long half life (4.5 x 109 y) and its weak
gamma emission of 48keV. However, it is an alpha emitter and thus poses aningestion risk owing to the high ionization density of alpha tracks and theirhigh biological effectiveness in inducing mutation. In addition, there is a risk
from the beta-emitting daughter isotopes Thorium 234 (β 0.26MeV, half life
24 days) and Protoactinium-234m (β; 0.23MeV, half life 6.75 hours) which
decay through one another to Uranium-234, also an alpha emitter with a halflife of 2.47 x 105 years. The overall activity of Uranium 238 therefore
increases as soon as it is produced due to ingrowth of the beta daughters andby 30 weeks these are in total secular equilibrium. The activities per kilogram
are given in Table 1 below. Uranium-238 has a low specific activity,
12MBqkg-1 which means that, unlike most radionuclides which are considered5

in risk analyses, at environmental concentrations which represent a
radiological exposure, the chemical concentration is significant. 1Bq is 83µg
and 1Bqg-1 in tissue represents a concentration of 3.5 x 10-4 M which is asignificant physiological concentration.
Over centuries, the specific activity of U-234 should be the same as theparent U-238, and thus the environmental concentrations of these isotopes are
generally the same if the source is natural. The specific total activity is thus
about 37MBq/Kg. It should be pointed out that DU material recently found inbattlefields in Europe contains small quantities of isotopes of Plutonium,
Neptunium and other fission products: thus the source of this DU isrefinement of nuclear reactor waste. However, the quantities are very small
and are not considered by the Committee to be of serious radiologicalsignificance. More curious are reports of weapons which have isotopic
signatures showing enriched Uranium, first reported in Lebanon, then Gaza,and most recently in analysis of biological materials from a veteran of theBosnia theatre in 1996 (Busby and Williams 2006, 2008, Ballardie et al2008). Indeed, tables of isotope ratios in environmental post conflict samples
published by the United Nations Environment program UNEP show clear
evidence of enriched Uranium usage in Bosnia (UNEP Bosnia report 2002).
(UNEP have consistently denied finding enriched Uranium, and this mistake
was quickly covered up when pointed out: the table has been taken off the
UNEP website). For this reason, the ECRR prefers the term Weapons Derived
Uranium (WDU) to describe the issue.
Table 1 Specific Activity (MBq/kg) in decay of U-238 in Depleted Uranium
to U-234 and ingrowth of daughters
Weeks
0
5
10
20
30

U-238 (α,γ)
12.43
12.43
12.43
12.43
12.43

Th-234 (β)
0
7.89
10.77
12.21
12.4

Pa-234 (β)
0
7.84
10.75
12.21
12.4

U-234 (α,γ)
0
0.001
0.004
0.01
0.017

Owing to the high density of Uranium, (19 g.cm-3 metal and 10.96 g. cm-3 forthe dioxide) and the fact that the metal is pyrophoric (burns in air) the
substance is used in the manufacture of armour piercing shells, missile nose
cones and penetrators. It is also employed in certain ballast materials in someaircraft (e.g. helicopter rotors, commercial aircraft counterweights). As aweapon, on impact, the DU burns to a fine aerosol of ceramic Uranium oxide
particles of mean diameters from about 1000nm (1µ) down to below 100nm
depending on different study results and distances from targets. These
particles are long lived in the environment (and in tissue), and can travel
significant distances from the point of impact up to thousands of miles (Busbyand Morgan 2005). They become resuspended in air, are found in air filters in6

cars at some distance from the attacks, and are respirable. Because theirdiameters are so small, below 1000nm, they are able to pass through the lung
into the lymphatic system and in principle can lodge anywhere in the body.
Here they may remain for several years in the same place. The biological halflife of such particulate Uranium is unknown but is very long. According toresearch with animals it can be greater than 13 years (Royal Society 2001).
A single Abrams 120mm tank shell contains about 3kg of DU (111MBq
of radioactivity) and there is 275g in a 30mm GAU3A A-10 Thunderbolt
Gatling Gun round. These munitions were used in Gulf War 1. More recently
evidence has emerged that hard target warheads have been deployed on cruise
missiles and bunker busting bombs, each containing up to one tonne of
Uranium. Estimates of the quantity of Uranium used in Gulf War 2 in 2003
are as high as 1700 tonnes (Al Ani and Baker 2009).
Military penetrators explode on impact with hard targets with about 80%
conversion to micron diameter Uranium Oxide particles of a ‘ceramic’ nature.
These particles are highly mobile and extremely long lived in theenvironment, owing to the very high degree of insolubility of Uranium Oxides
UO2 and U3O8. They can be inhaled and the sub-micron diameter particles
are translocated from the lung to the lymphatic system, building up in the
tracheobronchial lymph nodes and potentially able to circulate everywhere in
the body since they incapacitate macrophages (Kalinich et al. 2002). They canpass through the skin and through most gas-mask filters. Alpha and beta
disintegrations from these particles cause very high and repetitive doses tocells local to the range of the disintegration i.e. about 30 microns for the alphaand 450 microns for the beta tracks. The instantaneous (t = 0) dispersion(spectrum) of particle size from DU impacts was obtained using special
cascade impactor collectors at the US Aberdeen proving grounds by
Glissmeyer et al. (1979). The mean geometric diameter for particles collectedbehind the target was found to be 0.8µ. Μore recently, the EU SHER (2010)
report states that 31% of the particles have mean diameters below 0.18µ.
Particles of this size are effectively gaseous and can pass through the skin andpenetrate to any part of the body. They are therefore not comparable tohistoric studies of Uranium exposures since such concentrated forms havenever existed and have never been studied: they are completely new
exposures that have to be assessed de novo.
The reason that DU is employed is that the weapons are astoundingly
successful and have revolutionised warfare, rendering the tank and its armour
useless. In addition, its use represents a route for the nuclear industry to rid
itself of a waste product which would otherwise be expensive to dispose of.
But the downside is that the material clearly represents a radiation hazard
which is indiscriminate: battlefields are going to be contaminated and civilian
populations are going to be exposed.
Apart from the evidence that Uranium is far more genotoxic than ismodeled, which will be reviewed below, there is an immediate argument fromquantity of radioactivity. The average Natural Uranium content of soil isabout 10-20 Becquerels per kilogram, including all the Uranium isotopes. The
average excretion of Uranium in urine is less than 10nBq l-1 (in the UK) as a7result of absorption of natural Uranium in food and water. Pure Depleted
Uranium contains about 12.4MBq of U-238 per kilogram and in Kosovo,
some soil samples analysed by the United Nations Environment Program(UNEP) contained 250,000Bq/kg (UNEP 2001, Annex). The 350 tonnes of
DU used in the first Gulf War represent 4.3 TBq (4.3 x 1012 Bq) of Uraniumalpha activity (13.0 x 1012 if the radioactive beta emitting daughter isotopes
are included). The 1700 tonnes that were used in the 2003 war, represents 63
TBq of activity dispersed mainly into a populated area of perhaps 100km2.
This gives a mean density of deposition of radioactivity of 630,000Bq/m 2.
These sums are instructive and are collected together in Table 2.
It is possible to find a comparison to illustrate the overall radiologicalsituation. As an alpha emitter and long-lived environmental particle Uranium
can be compared with Plutonium-239 a radionuclide released by Sellafield
and a major contaminant of the Irish Sea. Plutonium in the environment isalso in the form of sub-micron sized oxide particles. The comparison is madein Table 3. Like DU, these Plutonium Oxide particles are long lived andmobile. Plutonium from Sellafield has been measured in autopsy specimens
across the UK, in sheep droppings on the east coast of England 100 km from
Sellafield at the same latitude and even in the teeth of children up to 200 km
from the site in south east England. U-238 has a very long half life, 4500
million years, so owing to its much shorter half life of 24,100 years, thespecific activity of Pu-239 is far greater. It is 2.3TBq/kg. But this means that
350 tons of DU (or 4.30TBq of U-238) is equivalent in activity (quantity ofradiation) to about 2 kg of Plutonium-239. The ethical dimensions of theintentional scattering of 2kg of Plutonium-239 over a populated area are easy
to imagine.

8

Table 2 Mean density of deposition of radioactivity from DU in the two Gulf
Wars and Kosovo including decays from U-238 and beta daughters Pa-234m
and Th-234 compared with other radioactive contamination.
Event

Activity released or
estimated deposited

10 tons of DU in Kosovo
350 tons of DU in Iraq 1
1700 tons of DU in Iraq 2
Global weapons fallout
Strontium-90 (Sr-90)
Northern Hemisphere lat. 5060deg (UNSCEAR, 2000)
Chernobyl 30km Exclusion
Zone measured Sr-90 (IAEA)
UK North Wales Radioactive
Sheep restrictions measured
Caesium-137 (Cs-137)
UNSCEAR definition ofcontaminated area. (Cs-137)
Irish Sea cumulative
Plutonium from Sellafield
1952-1996 [Busby, 1995]

0.37TBq
13 TBq
63TBq
73.9PBq

Mean activity density
Bq per square metre(area)
3700
130,000 ( into 100 km2)
630,000 ( into 100 km2)
460

37,000 to
more than 111,000
15,000 to 30,000> 37,000
1350TBq

20,000

Table 3 Comparing Plutonium-239 and Uranium-238 in the environment
Environmental form
Density of material g.cm-3
Solubility
Environmental Longevity
Main radioactive emissions
Alpha particle energy
Half life
Specific activity
Main present contamination
sourceMass for equal activity

Uranium-238
0.2-2µ oxide particles(UO 2 ) 10.9;(U3O8) 8.3
Insoluble
Long lived
Alpha + beta + beta
4.19MeV
4.51 billion y
37.2MBq/kg (α + β)DU
175 tons

9

Plutonium-239
0.2-2µ oxide particles(PuO2) 11.46
Insoluble
Long lived
Alpha
5.15MeV
24400y2.3TBq/kg (α)
Fuel reprocessing e.g.
Sellafield
1kg

3 The evidence of harm from Uranium exposures
Uranium oxide nanoparticle exposure from weapons does not represent thesame kind of hazard as Uranium exposures in people living in highbackground Uranium areas, nor those who work as Uranium miners andmachinists. The exposures are quite different in quality and type.
Comparisons of miners exposed to Uranium ore dusts will compare those who
inhale particles which have very low concentrations of Uranium and which
are fairly large. In Gulf war veterans and civilian populations the Uranium isalmost pure. The local doses to and concentrations in tissue will be thousandsof times greater in the case of the weapons exposures and the much smaller
particle sizes will ensure the rapid internalisation of the uranium, throughcompletely evolutionarily novel routes, though the lungs or directly throughthe nose to the mid brain or even through the skin. The nanoparticles will
penetrate individual cells. Thus the highest concentrations will begin in thecells, where the DNA is, and concentration will fall towards the blood supply
reservoir, the opposite of what happens with those who ingest uranium
contaminated solutions of food. Comparing Uranium urine excretions or
blood concentrations to get an idea of similar levels of exposure and making
calculation on the basis of average dose conversion coefficients will also be
invalid for this reason. It is an averaging problem, like all the others
associated with comparing external and internal irradiation. Nevertheless,because there are overlaps, the effects of exposure to Weapons Derived
Uranium will be discussed in parallel with other Uranium exposures. We
should expect many of the effects found but at much lower apparent doses in
the case of WDU. The above caveat should be borne in mind.
3.1 Health effects: epidemiology
Uranium is primarily genotoxic. Exposure to Uranium causes genetic andgenomic changes and therefore impacts most organs in mammals. Particularly
targeted are the kidney, the brain and the reproductive system. A list ofreported conditions associated with Uranium exposure is given in Abu Quareand Abou-Donia 2002 and Craft et al 2004. Bertell 2005 has reviewed thearea and drawn attention to significant gaps in knowledge and recently anumber of authors have discussed the problem in a UN report (UNIDIR
2008).
The teratogenicity of exposure to Uranium weapons aerosols is reviewed
by Hindin et al (2005). Many reports of congenital defects in children born in
Iraq following the first and 2nd Gulf wars (e.g. Hamburg 2003) have not been
followed up by any studies by WHO or any responsible authorities. The main
reported illnesses and conditions associated with exposure to Uranium arelisted in Table 4
It will be apparent that Uranium exposure will have a profound effect on
the health of any population, and that the range of effects covers the entire
spectrum of disease.

10

Table 4 Illnesses and conditions reported in the literature to be associatedwith exposure to Uranium.
Mutagen: Reproduction: teratogenic and genotoxic; causes lower fertility,
miscarriages, heritable defects in children, stillbirths, childhood cancer andleukemia. Oestrogenic mimic with responses in humans and animals.
Mutagen: Cancer and leukemia increases in those exposed and their offspring inhumans and animals.
Kidney disease generally, problems below 100ng/g contamination, glomerular
and tubular lesions, tumorigenic changes, creatinine levels alter with dose,
glomerular structures altered, IgE and IgG nephropathy, persistent structural andfunctional and functional damage.
Blood; cytotoxic and leukemogenic; reduction in red blood cells.
Brain; targets the brain and causes wide range of effects associated with damage
to deep brain and brainstem fuction, effects shown by objective tests. Basis of the
Gulf War syndrome. Weapons Uranium particles enter the mid brain directlyfrom the nose.
Concentration: circulates as uranyl ion which has the same affinity as Calcium,
therefore binds to and targets DNA, nervous tissue, bone, sperm. For this reason
most organs will be affected (mitochondrial DNA affecting energy conversions
in cells).
Chromosome aberrations found in those exposed to Uranium; the effect is out of
proportion to the ICRP calculated dose for external radiation.
Mutagen: retinoblastoma rates highest in Navajo tribes living on Uranium
tailings; rates also high in offspring of Sellafield workers and near Rocketdynesite near Los Angeles contaminated with Uranium.
Mutagen: Sex ratio effects in offspring of male Uranium miners
Inflammation: associated with oxidative stress at site of Uranium
Carcinogen: cancer increases in BNFL Uranium fuel-element workers

Despite this, there have been virtually no epidemiological studies carried outof populations exposed to weapons Uranium. The one exception is a study
carried out at the request of the Italian military into cancer in the Balkans
peacekeepers. The first report showed a significant excess of lymphoma(equivalent to 8-fold) in peacekeepers stationed in Bosnia and Kosovo (Italianreport 2001). More recent investigation of the data shows that the cancers
were mainly from those who served in Bosnia, making the relative risk more
like 14-fold. A recent update on the situation seems to have been kept
confidential; reports are that levels of cancer in this cohort are startlingly highand checks are being carried out. No credible study of cancer or birth defects
in UK or US veterans has been published although parliamentary questions
have elicited data which show an increase in lymphoma in UK veterans of the
1st Gulf War. Recently, a coroner’s jury in the UK found that a British Gulf
war veteran, Stuart Dyson, died of colon cancer because of exposure to
Depleted Uranium in Iraq (Dyson 2009) and the Minister was informed under
Section 43 of the UK Coroners Act. Evidence was taken from ECRR andfrom scientists from the UK Ministry of Defence but clearly the jury believedthat the cancer was caused by the exposure.

11Cancer data from Sarajevo in Bosnia has been reported, and show
remarkable increases (up to 20-fold) in the incidence at many sites (Hamburg
2003). A cohort study of cervical cancer in Greece concluded that exposure to
Uranium aerosols was the cause of a statistically significant increase in the
disease those exposed as shown by cervical smear screening results(Papathanasiuo et al 2005). There have also been many reports of high levelsof cancer in Iraq following the bombing both in 1991 and later in 2003, but nosystematic study has been published. An early study by McDiarmid et al(2002) found no evidence of increased risk of cancer in US veterans of thefirst Gulf war, though ill health from many conditions (generally, Gulf War
syndrome) was reported.
Gulf war syndrome itself was examined in a sophisticated Factor Analysis
by Haley et al (2000) in the USA, funded by Ross Perot. The syndrome
encompasses many conditions, problems which the military and their advisors
in the UK blamed on stress, but which Haley identified as having in common
that they resulted from damage to the brainstem and lower brain housekeeping
functions. Haley went on to show that this was the case by carrying out amagnetic resonance imaging case control study of US veterans. The P32 andH1 studies identified significant loss of viability in cells in the brain
associated with the housekeeping functions of the brain which weremanifesting themselves as Gulf War syndrome. Haley was not aware of thetargeting of the brain and lower brain by Uranium and blamed the effects hefound on exposures to organophosphates. However, research which was
carried out some years after Haley’s work showed the profound targeting of
this area of the brain by Uranium, and the fact that inhaled Uranium has adirect access to these parts of the brain through the olfactory lobe (see below).
The situation in Iraq has become serious: genotoxicity of Uranium
exposures has resulted in a catastrophic increase in cancer and congenital
disease. This was reported at the September 1998 General Conference of the
IAEA and has been comprehensively reviewed by Al Ani and Baker (2009).
In the same volume, these authors review other evidence of increases ingenetic and genomic based disease in those parts of Iraq contaminated with
Uranium and cite the many studies that report the levels of contamination andalso the health indicators. However, none of these reports has been consideredby the risk agencies and in addition no western based study has been carriedout on the populations of Iraq in order to investigate the concerns. The
Committee is currently engaged in a study of cancer and congenital birthdefects in Iraq.
Statistically significant Uranium effects have been reported at the
Springfields fuel fabrication plant in the UK (McGeoghegan and Binks 2000).
A strong association, related to Uranium exposure, was reported for
Hodgkin’s lymphoma and Non Hodgkin lymphoma, though the authors did
not believe the relation was a causal one since the absorbed doses were too
low.

12

3.2 Genetic damage: chromosome aberrations
Chromosome aberration analysis can be used as a flag for earlier exposure toionizing radiation. Indeed, it is possible to reconstruct the doses and makesome assumptions (on the basis of the types of chromosome damage,dicentrics and centric rings) on the type of exposure, whether low or high LET(Hoffman and Schmitz Feuerhake 1999).
Unexpectedly high levels of chromosome aberrations in Uranium miners
in Namibia were reported by Zaire et al 1997. Studies of chromosome
aberrations in a set of Gulf War veterans suffering from Gulf War syndrome
were also examined by Schroeder et al, 1999. Results showed levels ofdamage consistent with earlier exposures of about 150mSv although clearlythese veterans could not have been exposed to more depleted Uranium thanwould account for a committed dose of 100µSv. Both these studies identify anerror in the calculation of dose from the Uranium exposures of approximately
1000-fold. It should be noted that chromosome damage leaves the body with ahalf life of about 2 years, yet these Gulf veterans were showing this damage
some ten years after the exposures, suggesting some depot of Uranium which
was long lived. The Royal Society (2001) cite references to support the viewthat the half life of some types of Uranium in the body is longer than 10 years
and may be considered to be perhaps indefinite. Chromosome aberrations
have been found in a case control study of New Zealand Atomic test veterans(also exposed to Uranium at the test sites) some 40 years after the exposures.
Chromosome aberration analysis in Bosnia has shown significant
Uranium exposure effects in an ecological study by Ibrulj et al (2007). The
study evaluated peripheral lymphocytes from 84 individuals split between
inhabitants of Hadzici where NATO strikes involved Uranium (and UNEP
measurements showed presence of Uranium in 2002) and a control area where
there was little exposure. Results showed a statistically significant increase inchromosome aberration frequencies in the exposed group in 2007, some ten
years after the attacks. Micronuclei were also increased in peripheral
lymphocytes in the same populations exposed to Uranium (Ibrulj et al 2004).
Hadzici in Bosnia was also studied by Krunic et al (2005) to evaluate thegenetic damage to those who were exposed to Uranium weapons. The authors
were able to show excess micronuclei in peripheral lymphocytes comparedwith controls from west Herzegovina.
In cell culture experiments, Miller et al 2002 were able to induce dicentricchromosome changes and neoplastic transformation in human cells exposed todepleted Uranium at 50µM (i.e.200ng/l) for 24hrs. This is a very low
concentration and the presence of alpha emissions per cell is stochasticallyabsent. Using different Uranium isotopes the study showed that there was aspecific activity related effect and the conclusion was that radioactivity canplay a role in the neoplastic transformation frequency. Nevertheless, theexposure was so low that this result supports the argument for secondary
photoelectron enhancement outlined in Chapter 6 and reviewed below.
From these studies it can be concluded that Uranium exposure causes
chromosome damage and micronuclei formation in human populations at13

levels of radiation exposure (conventionally assessed) which are more than
1000 times too low to explain these effects. The recent report by Darolles etal (2010) is of interest. The authors report differences between enriched anddepleted Uranium in cell culture studies at quite low concentration levels.
Reduced to basics, depleted Uranium causes aneuploidy and micronuclei
formation whereas the enriched Uranium causes chromosome aberrations.
This would, of course, be an expectation of the two types of action implicit in
the discussions of mechanism above. Owing to the higher activity of U-235
the main chemical species in solution is uranyl U-238 in both the enriched andthe depleted Uranium experiments. Therefore there will be significant bindingof the U-238 uranyl to the chromosomes resulting in destruction of wholechromosomes through the photoelectrons emitted throughout their length at
the binding sites of the U-238 atoms along the phosphate backbone. The U235 effects are then the normal alpha track high ionisation effect where achromosome is cut (double strand break) and recombines anomalously to givethe aberrations which are found. The authors (who are associated with the
French IRSN) point out that the aneuploidy produced by U-238 is associatedin other reports with cancer induction and they call for a reassessment of the
carcinogenicity of Uranium.
3.3. Reproductive and transgenerational genetic effects
The teratogenic effects of Uranium exposures have been reviewed by Hindin
et al (2005) who concluded from the evidence that Uranium represented a
teratogenic hazard. Certainly many reports have emerged from areas where
Uranium weapons have been employed showing that there follow major
increases in stillbirth, and congenital malformations of a particularly alarming
and unusual kind. Despite these, no credible western studies have beencommissioned or carried out. A case control study of UK Atomic Test
Veterans children and grandchildren identified a 9-fold excess of congenitalconditions in the children and an 8-fold excess in the grandchildren relative tonational controls (Busby and de Messieres 2007). These veterans were
exposed mainly to Uranium since their gamma film badge doses were in
general known and analysis showed the existence of significant quantities of
Uranium on the test sites.
A review of the reproductive toxicity of natural and depleted Uranium by
Domingo (2001) concluded that Uranium was a development toxicant when
given orally or subcutaneously to mice. Decreased fertility, embryo toxicity,
teratogenicity and reduced growth were shown to occur. Paternain et al (1989)
had already showed developmental and birth outcome effects in mice at doses
as low as 5mg/kg with no zero effect dose. A study of the effects of Uranium
on the hatching success, development and survival in early stages of zebrafish(danio rerio) was reported by Bourrachot et al (2008). The authors used levelsof depleted Uranium in the water of 200-500µg/l (about 3Bql-1) but also
employed a higher specific activity Uranium isotope U-233 to examine theeffects of what they believed to be chemical rather than radiological stress.
Both regimes showed significant developmental effects at the lowest
14

exposures. 250µgl-1 showed a 43% reduction in median hatching times
relative to a control. A 15 day exposure to this concentration of depleted
Uranium gave a 100% mortality at the pro-larval stage. The more radioactive
U-233 was more effective, but both isotopes showed the effects at this very
low concentration. The radiation doses at which this was occurring are
vanishingly small and would not be considered harmful on the basis of current
risk models.
Raymond-Whish et al (2007) found that drinking water below the US
EPA standard caused estrogen receptor dependent responses in female mice.
The authors exposed pregnant female mice to drinking water containing from
0.5 µgl-1 to 28mgl-1 and found estrogen receptor effects including selective
reduction of primary follicles, increased uterine weight, greater uterine
luminal epithelial cell height and other conditions. Mouse dams that drank the
Uranium containing water had morphologically normal pups but these had
fewer primary follicles than pups from dams that drank normal water.
3.4 Kidney
The kidney has been identified as a target for Uranium toxicity by manystudies; the early research is reviewed in the Royal Society reports (RS2001,
2002). More recently interest has followed concerns relating to weapons
exposures and research has focused on the levels needed to produce
nephrotoxic effects. A number of relevant studies are listed in Table 5.
A most relevant and interesting report by Ballardie et al 2008 presents theresults of a comprehensive medical and physical analysis of a veteran of theBalkans who presented with a range of kidney conditions and many Gulf war
syndrome conditions. Rather than assuming that this man’s spectrum ofconditions was a result of stress, a team of doctors and scientists at the
Manchester Royal Infirmary and the University of Sheffield set about
analyzing everything they could in order to try and discover the cause. By
biopsy analysis they discovered that his kidney was contaminated withenriched Uranium, which was uniformly disseminated throughout the
mitochondrial tissue. Treatment with heavy metal chelating agents effected acure. This is a major piece of evidence in the arguments which the Gulf War
and Balkans veterans have regarding the origin of their ill health and wassignificant in persuading the jury about causality in the above-mentioned
coroner’s inquest on Stuart Dyson who also suffered from Gulf War
syndrome before dying prematurely from colon cancer.

15

Table 5 Recent studies of relevance to the effects of Uranium on kidney
structure and function
Study

Results

Prat et al 2005

Identified a set of 18 genes which were deregulated following
exposure to Uranium; the Calcium pathway is heavily
implicated; nephroblastoma genes implicatedRats exposed to 40mg/l DU in water for 9 months. Kidney
deterioration and lower red blood cell counts (renal anemia).
Investigated effects of DU on rat kidney brush border vesicles.
Uranyl at 140µg /mg protein reduced ability to transport
glucose.
Effects of embedded fragments of DU (shrapnel) in rodents.
Uranium from implanted fragments found in bone, kidney,muscle and liver distant from the site of implant.
Alters neurophysiological parameters in rat hippocampus,
crosses the placental barrier, enters foetal tissue. Decreased
rodent litter size when animals bred 6 months after
implantation. No kidney effects found suggesting adaptation.
Toxicity and biochemical markers in rats exposed to Uranium
at 0.2, 1 or 2µg/g animal. Measurable changes in manymarkers in bone and kidney at the lowest doses.
Renal dysfunction after long term chronic exposure to
Uranium pieces surgically implanted in rats.
Clinical chemistry and microscopic renal effects in rats
exposed to single injection IM of 0.1, 0.3 and 1.0 2µg/g
animal. Nephrotoxocity seen at all doses.

Berradi et al 2008
Goldman et al 2006
McClain et al 2002

Fukuda et al 2006
Zhu et al 2008
Zimmerman et al
2007

3.5 Brain
The effects of Uranium on the brain have only recently emerged. As alreadyoutlined above, the studies by Haley demonstrated a link between lower brain
function and the spectrum of conditions which make up Gulf War syndrome.
Inhalation of Uranium nanoparticles from the weaponised aerosols provides a
direct route to the lower brain through the physiological connections with thenasal passages and olfactory bulb. The French (IRSN and other) studies wereperhaps the first to show the accumulation of Uranium in nervous tissue, towhich it seems to have an affinity, probably because of the similarity of theuranyl ion to Ca++. Monleau et al (2005) of the IRSN laboratory in France
showed that Uranium concentrations in the brains of rats exposed byinhalation were as follows: olfactory bulb> hippocampus> frontal cortex>
cerebellum. Uranium is normally excluded from the overall system by a low
gut transfer factor. Evolutionarily there will never have been a period whenaerosols of pure Uranium existed in the environment and even Uranium
miners will not be exposed to the same extent since the dusts in the mines
have very low Uranium content. A list of recent studies is given in Table 6.
It is clear from the results of Lestaeval et al 2005 that at levels where
there is no nephrotoxicity, there are measurable changes in behaviour in rats

16

exposed to 144µg/kg. by injection. Taken together, these studies strongly
suggest that Gulf War syndrome is an effect of inhalation of micrograms of
Uranium and draw attention to the extraordinary neurotoxicity of the material.
Table 6 Recent studies of neurological effects of Uranium
Study
Monleau et al
2005
IRSN, France
Barillet et al
2007
IRSN, France

Results
Inhalation of Uranium by rats. Uranium concentration inbrain: Olfactory bulb> hippocampus> frontal cortex>
cerebellum. Behavioural changes shown
Oxidative stress and neurotoxicity in adult male zebrafish
exposed to U-238 and U-233 in water. Oxidative stressand neurophysiological changes (increase in ACh) in
exposures to both isotopes
Pellmar et al
Depleted Uranium fragments implanted in rats and caused
1999
electrophysiological changes in hippocampal slices
McDiarmid et al Gulf war veterans studied found subtle effects on
1999
reproductive and central nervous system function
Briner andRats exposed to drinking water containing 75 or 150mg/l
Murray 2005
DU. Behavioural changes after 2 weeks; increased lipidoxidation
Lestaeval et al
The brain is a target organ after depleted Uranium
2005
exposure. 144µg/kg injection in rats caused at kidney
IRSN France
levels of 2.6 µg/g. This level would be normally seen as a
sub toxic dose to the kidney. However, this was associatedwith decrease in food intake and sleep wake cycle
disturbance.
Barber et al
Short term kinetics of Uranium in rat brain after2005
intraperitoneal injection 1µg/g animal. Uranium entered
the brain rapidly and was initially concentrated in the
hippocampus and striatum. Clearance was slow; contentsof hippocampus, cerebellum and cortex was still high after
7 days4 Animal studies, cell cultures and mechanisms

The ICRP-based desk analyses (Royal Society, WHO, SHER, RAND,
ATSDR etc.) which employ absorbed dose and use risk factors for cancer
culled from the Japanese A-Bomb cohorts do not predict the observations andmust now be abandoned. Clearly Uranium exposure is much more hazardous.
Cell culture and animal experiments have provided useful information fordeveloping and understanding of the mechanism involved. What all thesestudies seem to show, is that internal Uranium exposure, to particles but also
to ionic forms, seems to be acting as if it were considerably more radioactive
than it is on the basis of its intrinsic radioactivity. Thus U-238 exposure
causes oxidative stress, genomic instability, chromosome damage,
micronuclei formation, all consequences of ionizing radiation exposure, yet in17some experiments the concentration is so low that there is stochastically noradiation exposure because there are too few decays. This finding has beenvariously interpreted as suggesting a chemical mutagenic effect, a heavy
metal effect, or a synergy between radiation and chemistry. Of course, one rediscovery is the affinity of Uranium for DNA phosphate. The affinity of theuranyl ion, UO 2++ for Calcium Ca ++ sites was known in the 1960s when thesubstance began to be employed as an electron microscope stain. The affinity
constant was measured in an elegant flow experiment by Nielsen et al in 1992
and was of the order of 1010M-1. This would suggest, in mass-action
equilibrium terms, that at quite low concentrations (100ng/l) there is asignificant amount of Uranium bound to the phosphate backbone of the DNA.
This seems to agree with the experimental observations of biological effects
reviewed here. The ECRR model is particularly concerned with radionuclides
which bind to DNA (Strontium-90, Barium-140) since these beta emitters
decay into the DNA and also change their charge and transmute into aradioactive daughter producing an ion and perhaps Auger electrons. The
charge change alone will cause an ionization on the DNA. It seems that
Uranium is therefore in this category, which would result in a weighting (seeChapter 6).
But there is also the fact that Uranium has a high atomic number andwould therefore amplify natural background gamma radiation (and also thephoton radiation which it, itself, produces, in addition to any photon radiationfrom other Uranium isotopes present in any mixture. The conclusion of theCommittee is that such a mechanism is capable on its own of explaining themany anomalous findings reviewed in this chapter and in this section. The
extent of the enhancement must await experimental investigation, but theseexperiments are straightforward, involving simultaneous exposure to Uranium
and to X-rays of various energies. The use of dilute uranyl salts as anenhancing agent for X-ray targeted radiotherapy for cancer was suggested in a
British Patent Application in 2007 (Busby 2008). It is clear from the studies
that significant binding in vitro occurs at 200µM or 84ng/l. This concentration
is not currently considered toxic but is in the same range as that found inmany drinking waters and in the urine of Gulf veterans.
A list of some studies which bear on the issue of the mechanism for the
anomalous enhancement of Uranium both as ionic and as particulate is given
in Table 7.

18

Table 7. Studies of Uranium effects in cell culture and in animals which
reveal information on possible mechanisms for its anomalous hazard.
Study

ResultGueguen et al 2007

Drug metabolism is altered following exposure of DU torats; induces expression of CYP enzymes
Leukemic transformation of haematopoietic cells in miceinternally exposed to DU pellets.
Transformation of human osteoblast cells to tumorigenic
type after exposure to DU; 0.0014% cells were hit by alphaparticles. Suggests no radiation effect.
Showed both Uranium and tungsten capable of causing
micronuclei in human osteoblast system and tumorigenictransformations.
Malignant transformation of human bronchial epithelial cellby exposure to Uranium; DU shows carcinogenesis in vitro
Depleted Uranium induces apoptosis in mouse macrophages
Hepatic effects of Uranium on liver metabolism enzymes
Uranium causes oxidative stress in lung epithelial cells

Miller et al 2005
Miller et al 1998
Miller et al 2002
Yang et al 2002
Kalinich et al 2002
Gueguen et al 2006
Pariyakaruppan et al
2006
Grignard et al 2008
Tissandie et al 2006
Yazzie et al 2003
Busby 2005a
Busby 2005b
Stearns et al 2005
Busby and Schnug
2008
Elsaesser et al 2007
Wan et al 2006

Pattison et al 2008
Hahn et al 2002
Darolles et al 2010

Contamination with depleted or enriched Uranium
differently affects steroid metabolism in rats
Short term DU exposure affects vitamin D metabolism inrats
Uranyl acetate causes DNA single strand breaks in vitro in
the presence of ascorbate. Suggests that affinity for DNA isgreater than affinity for ascorbate.
Suggests and attempts to quantify secondary photoelectron
effect for Uranium bound to DNA phosphate. Draws
attention to affinity of Uranyl for DNA.
As above for Uranium particles
Induction of hprt mutations and DNA adducts in Chinese
Hamster ovary cells at 200 µM (80ng/l).
Discusses SPE for Uranium in ionic form as explanation forobserved effects
Monte Carlo simulations of Uranium, Gold and water
nanoparticles of different sizes confirm the enhancements
due to SPE
In vitro immune toxicity of depleted Uranium: effects on
mouse macrophages. At 50 and 100µM. Macrophageactivity altered at 200µM for 2 h.
Monte Carlo simulation of Uranium particles in tissue
confirm SPE effect is ‘significant’ but lower than suggested
by Busby.
Implanted DU fragments cause soft tissue sarcomas in themuscles of rats.
Different toxicological profiles of depleted and enricheduranium: U235 causes chromosome aberrations (alpha)
U238 causes aneuploidy (photoelectron toxicity explains
this spectrum)19

5 Conclusions
It is necessary to conclude that Uranium represents a perfect example of the
problem resulting from the physics-based approach to radiation risk which
ECRR2003 drew attention to. When doses are calculated in terms of absorbed
dose following ICRP, the quantities of Uranium usually found in theenvironment confer very small doses compared with natural backgroundgamma radiation, and even smaller when compared with the levels of dose
which correlated with cancer in the A-Bomb groups. But it is clear that thisapproach is massively in error, since it has avoided or, more accurately,
knows nothing about, chemistry, biology, physiology and pharmacology.
These sciences were historically considered of less importance than physics
and mathematics, in some deeply felt (by the physicists anyway)philosophical and emotional way. This is the flaw in rational analysis: it is
only as good as its data, and if, in order to solve a problem, it has to be
reduced to the level where a solution can be claimed, the answer is often
wrong.
The Committee has had to deal with this very real problem bypresenting a real solution; in this case the solution is to weight Uranium
exposures by a factor of 1000 at normal background gamma photon levels(100nGy/h). This will be modified when experimental results of Secondary
Photoelectron effects become available. It is clear that the effects of Uranium
are wide ranging, and so to consider only genetic effects from Uranium
exposure would be quite wrong. In addition, different types of exposure willcause different spectra of conditions.
In the case of conventional estimates of risk from internal Uranium,
which essentially compare it with external doses, the errors are arguably
greater than for any other material. There is now sufficient evidence to treat
Uranium aerosols as if they had infinite biological effectiveness. The
Committee therefore believes that using a risk factor to assess causality in
Uranium-exposed populations or individuals should be done with extreme
caution, even if that risk factor has been modified by application of aweighting that approximates observation.. If a disease or condition or genetic
heritable effect of any kind is seen to increase after exposure to Uranium,
causality should not be ruled out whatever the dose differential between a
population before and after the exposure, or between exposed populations
relative to unexposed controls.
The dose coefficients for uranium exposures are given in Table 8 below.
Table 8. Dose coefficients for uranium weapons exposures (from ECRR2010)
Isotope (form)

Half life

U-238 inhalation
U-238 µ particle
U-238 ingestion

4.5 E+9
4.5 E+9
4.5 E+9ak(0-1)Sv/Bq
2.5 E-3
2.5 E-2
2.5E-420

k(1-14)Sv/Bq
1.2 E-3
1.2 E-2
1.2E-4k(adult)
Sv/Bq
8.4 E-4
8.4 E-3
8.4E-5

The committee believes to employ a risk factor, even one elevated by theweighting, to attempt to assess causality in uranium exposed populations or
individuals should be done with extreme caution. There is now sufficientevidence to treat uranium aerosols as if they had infinite biologicaleffectiveness since a single nanoparticle, if trapped in a biological replicating
system may cause genomic amplification of damage over time. If a disease orcondition or genetic heritable effect of any kind is elevated after exposure touranium, or in those exposed to uranium relative to unexposed controls,causality should not be ruled out whatever the differential dose.

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