The health hazards of depleted uranium
For over two decades, there has been considerable public debate about the health effects
of depleted uranium (DU). Military services in many countries use depleted uranium in
munitions and to strengthen armour in vehicles. This is because uranium is a very dense metal
(approximately 70% more dense than lead), which is useful in a military context—and the chemical
and physical properties of natural uranium metal and DU metal are very similar. DU alloys are very
hard and pyrophoric, properties which make them superior to tungsten armour-piercing munitions.
DU armour-plating is also more resistant to penetration by conventional anti-tank munitions. DU
munitions were first used extensively in the First Gulf War (1991), in Bosnia (1995) and Kosovo (1999),
and continue to be used in Iraq since 2003 and perhaps in Afghanistan since 2002. Table 1 indicates
the amounts of DU used in recent wars by the United States (US) armed forces—the most frequent
user of DU munitions.
Table 1. Depleted uranium used by the United States in recent wars (metric tons)
First Gulf War
Second Gulf War
National Research Council, 2008, Review of Toxicologic and Radiologic Risks to Military Personnel from Exposure
to Depleted Uranium during and after Combat
, Washington, DC, National Academies Press, Tables 1–4.
On impact, DU may be dispersed as aerosols, which can be inhaled or ingested, or imbedded
in tissue as shrapnel. Frequent, continuing reports of illnesses suffered by combatants1 and civilians2
in these wars have resulted in speculation that these may be due to DU exposures. (See Box 1 for a
discussion of Gulf War Syndrome.)
DU is obtained as a waste product of nuclear power and of the manufacture of nuclear weapons.
It is a radioactive heavy metal that can be hazardous to humans in four ways:
Ian Fairlie is an independent consultant on radiation in the environment. He has degrees in chemistry and radiation
biology. He has worked for several UK Government departments and regulatory agencies, and currently advises
environmental NGOs, the European Parliament, and local authorities. Between 2001 and 2004, Dr Fairlie was Secretariat
to the UK Government's Committee Examining the Radiation Risks of Internal Emitters (CERRIE), which published its
report in October 2004. The author acknowledges the kind assistance of Professor D.G. Goodhead, Dr P. Day and
Dr A.C. Miller in reviewing this article. The author also thanks Dr K. Baverstock for his ideas in the section on human cell
evidence (in vitro
studies). Any errors remaining are, of course, the sole responsibility of the author.
• as a toxic heavy metal; • as a genotoxic (i.e. carcinogenic and mutagenic) agent from its chemical properties;• as a genotoxic agent from its radiation; and• as an endocrine disruptor.
Box 1. Gulf War Syndrome
Many soldiers and civilians from Gulf War areas have self-reported a variety of symptoms, often collectively termed
Gulf War Syndrome. The syndrome appears to be a complex, progressive, incapacitating multi-organ system disorder
whose symptoms can include fatigue, musculoskeletal and joint pains, headaches, neuropsychiatric disorders,
confusion, visual problems, changes of gait, loss of memory, swollen or enlarged lymph nodes, respiratory impairment,
impotence and urinary tract morphological and functional alterations.
Whatever the causes, it is clear that the suffering is widespread, measurable and real to those affected. Nearly 20%
of all US personnel deployed to the 1991 Gulf War were receiving some form of disability compensation due to these
effects by 2001.a A number of studies, summarized by Komaroff, have found that armed forces from several countries
deployed to the Persian Gulf region were statistically significantly more likely to report chronic, debilitating symptoms
than military personnel deployed to other areas.b Eisen et al. measured the prevalence of self-reported chronic illness
among Gulf War combatants compared to a control group of non-deployed veterans. They found that deployed
veterans reported dyspepsia, a group of common skin conditions (fibromyalgia), and chronic fatigue syndrome much
more often than the control group. The most striking association was chronic fatigue syndrome.c
Some authorsd have alleged these symptoms may be due, at least in part, to DU exposures. However, many soldiers
and civilians reporting these symptoms were clearly unexposed to DU, or were exposed to very small amounts, so the
single explanation of DU exposure is highly unlikely.
In addition, many Gulf War personnel were exposed to many substances that in theory could have produced
chronic tissue damage: solvents, insecticides, smoke and other combustion products, agents of chemical warfare
(irreversible anticholinesterase inhibitors, such as sarin), and pyridostigmine bromide (a reversible anticholinesterase
inhibitor taken to prevent the effects of sarin). Also, they received an intensive battery of simultaneously administered
immunizations, which some believea could have produced chronic debility.
In conclusion, although our understanding of the aetiologies of these symptoms remains poor to say the least, it is
difficult to ascribe anything more than a minor role to DU exposures.
a M. Davis, 2003, "Overview of Illnesses in Gulf War Veterans", in J.M. Colwill (ed.), Gulf War and Health. Volume 2:
Insecticides and Solvents,
Washington, DC, National Academies Press, pp. 533–561.
b A.L. Komaroff, 2005, "Unexplained Suffering in the Aftermath of War", Annals of Internal Medicine,
vol. 142, no. 11,
c S.A. Eisen et al., 2005, "Gulf War Veterans' Health: Medical Evaluation of a US Cohort", Annals of Internal Medicine,
vol. 142, no. 11, pp. 881 – 890.
d A. Durakovic, 2003, "Undiagnosed Illnesses and Radioactive Warfare", Croatian Medical Journal,
vol. 44, no. 5,
pp. 520–532; R. Bertell, 2006, "Depleted Uranium: All the Questions about DU and Gulf War Syndrome Are Not
Yet Answered", International Journal of Health Services,
vol. 36, no. 3, pp. 503–520.
DU has about 75% of the radioactivity of natural uranium (see below), and the same chemical
toxicity, endocrine disruptive property and mutagenicity as natural uranium.
Because of the controversy over DU, uranium is now one of the most studied radionuclides.
Over the past decade, there have been at least nine official reports on the toxicity and health effects
of uranium and DU.3 There have also been a number of informative reviews.4 Until the recent United
States' National Research Council (NRC) report, perhaps the most authoritative were the two reports
of the United Kingdom's Royal Society on chemically toxic risks and radiation risks, respectively.
These stated that there were legitimate concerns about the possible health consequences of using
a radioactive and chemically toxic material for munitions, but they concluded that the risks of DU
The health hazards of depleted uranium
munitions to soldiers were very low.5 However, since the Royal Society's reports, much new evidence
from radiation biology studies has emerged.
There are two main sources of information on DU health risks. The first is epidemiology studies—
i.e. studies of DU exposures and possible added risks to human populations. The second is radiation
biology studies in cells and animals. As we shall see, much more information on DU's health effects is
available from the latter than the former source.
What is depleted uranium?
Natural uranium (U) is a constituent of the Earth's crust at a concentration of about 3 parts per
million on average. Some uranium ore regions of the world contain much higher concentrations of
uranium—typically about 1,000 parts per million.
In the nuclear power fuel cycle, uranium ore is mined, and uranium is leached from ore and
refined to almost pure uranium dioxide (UO ) for use in nuclear fuel.6 This natural uranium consists of
three main isotopes, U-238, U-235 and U-234 (see Table 2). U-238 and U-235 are primordial—that
is, they were created at the same time as the Earth about 4.5 billion years ago. U-234, on the other
hand, is a decay product of U-238.
The vital consideration is that U-235 is fissile,
which means that it can maintain fission in nuclear
power stations and can be used in nuclear weapons. Most reactors are designed for uranium fuel that
has been slightly enriched in U-235. Typically, the U-235 concentration is required to be increased
from 0.7% to between 2% and 4%. This is known as low-enriched uranium (LEU). This concentration
is effected by the process of enrichment, whereby UO is converted to a gas (uranium hexafluoride,
UF ) and passed through gaseous diffusion or centrifuge facilities. U-235 is also a vital ingredient of
many nuclear weapons but here the enrichment required is to about 90% U-235. This is termed
highly enriched uranium (HEU).
The enrichment processes for nuclear weapons and nuclear fuel create about 7 metric tons of
depleted uranium for each metric ton of enriched uranium produced. The result is that very large
quantities of depleted uranium are produced as waste streams. In 1996, worldwide production of
DU was estimated by the European Parliament's Science and Technology Options Assessment (STOA)
panel at about 35,000 metric tons.7 As a result, it is estimated that over 1.2 million metric tons of DU
are currently stockpiled worldwide, mostly in the United States.8
DU is used in radiation screens and, in the past, has been issued in counterweights in aeroplane
wings; however these uses are small in comparison with the amounts generated each year. The largest
users of DU are military services, although the STOA report estimated that the total quantity of DU in
ammunition used in Iraq and Kosovo corresponded to only four days of DU production worldwide.
Therefore DU stockpiles worldwide are increasing at the rate of about 35,000 metric tons per year
and they pose serious disposal problems to governments involved with uranium enrichment.
How radioactive is DU compared to natural uranium?
This is an easy question to ask, but difficult to answer. Many reports state that DU has 60% of the
radioactivity of natural uranium. However, the correct figure is closer to 75% for two reasons:
enrichment facilities sometimes use reprocessed uranium (as opposed to 100% mined uranium), and
all forms of DU contain decay products.
Table 2. Main isotopes in natural and depleted uranium at the factory
Specific alpha activity
(Bq per gram)
Royal Society, 2001, The Health Hazards of Depleted Uranium Munitions: Part I,
The use of reprocessed uranium in du
Depleted uranium as used by the US military contains the isotope U-236 (see Table 2), which is not
present in natural uranium. This isotope arises only in nuclear reactors and its presence indicates that
the DU batch contains some uranium from the waste streams of reprocessing spent nuclear fuel—
carried out mainly by France, the Russian Federation, the United Kingdom and the United States.
Thus there are two types of depleted uranium—both come from the enrichment process, but one
includes small amounts of reprocessed uranium from spent nuclear fuel.
This is a problematic matter because reprocessed uranium is contaminated with the fission and
activation products of spent fuel. In particular, the fission product Tc-99 and the activation products
Np-237, Pu-238, Pu-239, Pu-240 and Am-241 are sometimes found in DU munitions.9 Depleted
uranium made with some reprocessed uranium is therefore more radioactive than the DU derived
solely from mining uranium ores.10 Most reports state that the amounts of contaminants in DU
munitions from spent nuclear fuel are low. According to the US Office of the Special Assistant for Gulf
War Illnesses, the dose from these contaminants amounts to less than 1% of the equivalent dose from
DU exposures, and the authors concluded that their risk impact was low.11 The Royal Society also
stated that these concentrations had been found to be low in the DU batches it had examined, but it
recommended continued vigilance on the matter.12
uranium decay producTs
Once DU has been made into munitions and placed in a warehouse, its U-238 and U-235 isotopes
decay and create various daughter products as shown in Tables 3 and 4, respectively. Within about six
months, these daughters are in secular equilibrium with their parents, i.e. the amounts of the daughters
being created by the parent are equal to the amounts of the daughters disintegrating. Therefore the
radiation from these decay products should be added when assessing the dangers of DU. The key
matter is that the decay products are beta emitters, especially Pa-234m, which emits very energetic
beta particles. As explained in the Royal Society report of 2001, these beta radiations may constitute
as much as 40% of the absorbed dose13 to tissues near embedded DU. It is important to realize that
this additional risk from the beta particles of decay products is currently not taken into account by the
International Commission on Radiological Protection (ICRP) in its dose coefficients (which estimate
the radiation doses from incorporated radioactive substances) for uranium isotopes.
The health hazards of depleted uranium
Bishop14 has estimated the total Table 3. U-238 decay seriesa
alpha, beta and gamma emissions per
year from 1g samples of natural uranium
and DU. He concluded that DU together
with its decay products in equilibrium are
75% as radioactive as natural uranium
plus its decay products. The report to the
European Parliament's STOA panel, using a
cruder method, estimated that DU is 80%
as radioactive as natural uranium. This a
truncated after U-234 because its very long half-life ends the decay
means that the adjective "depleted" may chain for practical purposes.
give a misleading impression: a more Table 4. Truncated U-235 decay series
accurate description would be the phrase
"slightly less radioactive".
Pathways for DU exposures
du in The environmenT
DU exposures can occur via several pathways. One is external radiation, whereby beta radiation (and,
to a much lesser degree, gamma radiation) from the decay products of DU irradiate the body, but in
most cases such exposures are very small. More important are the internal exposures resulting from
inhalation of DU aerosols and dusts, from ingestion of DU-contaminated water and food, and from
wounds, i.e. inoculation by DU shrapnel.
When DU projectiles penetrate armoured vehicles, their occupants are often injured by DU
shrapnel, which can remain in the body for lengthy periods. When tanks are struck by DU projectiles,
depending on the material and thickness of their armour, about 10%15 is volatilized into an aerosol
that immediately burns to form poorly soluble uranium oxides that may remain in high concentrations
in enclosed spaces, i.e. tanks and bunkers. These aerosols can contain very small particles of uranium
oxide of between 0.1 and 10 microns16 in diameter, which can be inhaled and deposit in the lungs.
White blood cells scavenge these particles and transport them to tracheobronchial lymph nodes for
lengthy periods. These particles are usually insoluble, and are unlikely to be detected in urine samples.
Therefore the practice of routine urine sampling of returning soldiers may be ineffectual at detecting
uranium oxide exposure.
Initial distribution of uranium compounds strongly depends on their solubility and absorption route.
Large fractions of administered soluble uranium compounds are absorbed. For example, 20% to 30%
was found in the bones of male rats within 2.5 hours of uranium administration, and 90% of the
uranium remaining after 40 days was in the bone.17
Uranium compounds are distributed to all tissues, preferentially bone, kidneys, liver and testes.18
Rats implanted with DU pellets also show uranium concentrations in the heart, lung tissue, ovaries
and lymph nodes.19 Like many heavy metals, uranium reacts with DNA and ions and blood proteins
to form compounds (called complexes). Uranium can cross the placenta and the blood–brain barrier
and accumulate in the brain. Soluble uranium compounds are cleared more rapidly than insoluble
compounds: two-thirds of uranium in blood is excreted in urine over the first 24 hours. Elimination of
soluble uranium is primarily by the kidneys and urine. The release of DU from embedded particles in
shrapnel is slow: it takes 1.5 years for 80–90% of uranium in bone to be excreted.20
Health effects of DU
Since the Second World War, it has been known that uranium, a radioactive heavy metal, is hazardous
to humans in at least two ways. Like other heavy metals, such as chromium, lead, nickel and mercury,
uranium is chemically toxic to kidneys, the cardiovascular system, liver, muscle and the nervous
system. Also, since all uranium isotopes are radioactive, they emit radiation—a known carcinogenic
agent. This was thought to be of concern mainly when uranium was inhaled as aerosols or dusts
because their long residence times in the lung could result in lung cancers.
This means that, in the United States, which perhaps has the most detailed regulations covering
uranium, uranium exposures are regulated by radiation protection and chemical regulation authorities
in two different ways: by maximum doses from uranium radiation exposures to the lung via insoluble
uranium particles; and by maximum concentrations of soluble uranium chemicals, particularly in the
kidney.21 Uranium's chemical toxicity effects generally occur at lower uranium concentrations than its
chemical carcinogeniciTy of du
Scientists are increasingly aware that uranium and DU are hazardous to humans in a third way: they
are chemically (as well as radiologically) carcinogenic. This considerably increases our perception of
the hazards of DU and natural uranium because low concentrations of soluble uranium throughout
the body—previously considered to be harmless (and therefore
Low concentrations of soluble
neglected)—may be carcinogenic without threshold. In other words,
uranium throughout the body—
no matter how low the DU or uranium concentration, a small risk
previously considered to be harmless—
of chemical carcinogenesis remains. However, Taylor and Taylor
may be carcinogenic.
estimated that these risks were very low.23
The Royal Society's report of 2001 discussed the emerging evidence of DU's chemical
carcinogenicity, and suggested that uranium's chemical and radiation effects may act synergistically,
that is, their effects may need to be multiplied together rather than added together. More recently, the
NRC report examined uranium's chemical carcinogenicity and expressed variable views. For example,
chapter 7 called for research on "whether" a chemical mechanism of uranium carcinogenesis existed.
However, chapter 8 recommended that studies be conducted to determine the relative contributions
of the chemical and radiological mechanisms of uranium carcinogenesis.24
uranium as an endocrine disrupTor
Recent evidence from the United States suggests that DU may be hazardous to humans in a fourth
way: it may act as an endocrine disruptor, that is, a substance that interferes with hormones. A number
of studies have indicated that heavy metals may act as endocrine disruptors.25 For example, cadmium
stimulates the proliferation of human breast cancer cells,26 interacts with estrogen receptors27 and
stimulates estrogenic responses in vivo
Raymond-Whish et al. tested whether depleted uranium added to drinking water caused
responses in the female mouse reproductive tract like those caused by the estrogen diethylstilbestrol.
The health hazards of depleted uranium
concluded that uranium is an endocrine-disrupting chemical and that populations exposed to
environmental uranium (including indigenous populations in the United States living near uranium
mine tailings) should be examined for increased risk of fertility problems and reproductive cancers. 29
Cell, animal, human and epidemiological studies
human cell evidence (in vitro
A comprehensive body of research indicates that the exposure of human cells in vitro
to DU results
in genotoxic effects and induces cell phenomena closely associated with carcinogenesis. These cell
phenomena include the following:
• genomic instability—a process involved in carcinogenesis;30 • transformation to a tumorigenic state, whereby affected cells grow as cancers when injected
• induction of mutations whose presence characterizes most cancers;32• DNA oxidative damage;33• activation of gene expression pathways;34 • formation of DNA-U adducts;35• induction of dicentrics in chromosomes—a radiation-specific change in human cells;36
• chromosomal damage.37
animal evidence (in vivo
Long-term studies in monkeys of uranium oxide (i.e. insoluble) inhalation indicate the carcinogenicity
to the lung of this kind of exposure and possibly its involvement in non-Hodgkins lymphoma.38
Monleau et al. measured the induction of DNA double strand breaks by inhaled DU in rats.39 Hahn
et al. found an elevated risk of cancer in rats implanted with small DU foils. They concluded that DU
fragments embedded in muscle tissue were carcinogenic if large enough; however, they stated the
mechanism was unclear.40
After mice were exposed to embedded DU for 3 months then injected with progenitor cells,
Miller et al. found that 75% of mice developed leukaemia (compared with 10% in control mice). In
addition, mice showed changes in the musculoskeletal system, i.e. bone formation and remodelling,
after oral, intraperitoneal, intravenous and implantation uranium exposure.41
studies with embedded DU pellets in animals showed aberrant expression of oncogenes
and tumour suppressor genes associated with carcinogenesis.42 Although these effects may be caused
by DU radiation, there are many reasons suggesting that its chemical effects predominate. In the in
transformation and sister chromatid exchange studies, induced effects were very much more
frequent than expected from the very small number of cells hit by an alpha particle (1 in 100,000 cells
from a 10µm-sized particle of DU). In addition, similar transformation frequencies were observed with
the non-radioactive heavy-metal carcinogens nickel and lead; it was speculated that DU's genotoxicity
may be due to uranyl ions acting to produce free radicals, especially if the ions are effectively chelated
to DNA like other metal ions.43
Uranium is a well-established nephrotoxin (i.e. it is toxic to kidneys) in humans, the primary target
being the proximal tubule. Damage occurs when uranium forms complexes with the phosphate
ligands and proteins in tubular walls, which impair kidney function. Biomarkers of these tubular effects
include enzymuria and increased excretion of small proteins, amino acids and glucose. Uranium is
also a bone seeker and is incorporated into the bone matrix by displacing calcium to form complexes
with phosphate groups.44
McDiarmid et al. observed a statistically significant increase in mutations in peripheral
lymphocytes in three US Gulf War veterans with embedded DU fragments reflected in measurements
of uranium in urine. However, their continuing surveillance (for 14 years) has yielded no evidence of
reproductive system dysfunction in males, abnormalities in sperm or alterations in neuroendocrine
function.45 Nevertheless, it should be recalled that soldiers are a healthy subset of the wider population,
and the numbers of exposed soldiers in these studies are relatively small. Monleau et al. found that
repeated uranium inhalations tended to potentiate, that is, increase the effect of or act synergistically
with uranium's genotoxic effects.46 Zaire et al. observed the induction of chromosome aberrations in
uranium mineworkers in Namibia.47 Such rearrangements of genetic material in chromosomes are
involved in the carcinogenic process.
Few human epidemiology studies have showed convincing effects from DU exposures. The Royal
Society examined 14 epidemiological studies of occupational uranium exposures to workers engaged
in the extraction, milling and machining of uranium.48 These showed no sign of excess deaths due
to cancer or kidney disease related to inhaling or ingesting uranium. However, the report stressed
that these studies should be interpreted with care. First, there were few reliable data on uranium
exposure levels to workers, especially in the early years of uranium processing, when exposures due
to inhalation of uranium-containing dust were thought to be high. In addition, smoking was a powerful
confounder, causing approximately 90% of lung cancers, and information on smoking habits was not
available for any of the studies. Another problem was the healthy worker effect, which meant that risk
comparisons should be made with other workers and not the general population. The report stressed
that these types of epidemiological studies are not able to detect small increases in risk, although a
twofold increase might have been detectable.
In addition, a cardinal rule in epidemiology is that absence of evidence in a study should not
be used to allege evidence of absence.49 It many cases, it may mean that the study was not powerful
enough to detect an increased risk.
A number of studies have examined health effects in military personnel,50 but their brief exposures
to uranium dusts and aerosols have been much lower than those experienced by uranium mining and
milling activities. Unfortunately, very few studies have been made of the many civilians exposed to
DU in various conflicts.51 Those carried out raise as many questions as answers, especially on the
unusually low incidence rates of congenital malformations in Iraq pre-1990.52 Hindin et al. carried
out an extensive literature review of congenital malformations following DU exposures in US military
personnel and concluded that the human epidemiological evidence was consistent with increased risk
of birth defects in offspring of persons exposed to DU.
The health hazards of depleted uranium
ossible synergism between radiation effects and chemical effects
Many studies clearly indicate that DU has both chemically induced and radiation induced effects. An
important question is whether synergism exists between these two effects, i.e. whether they potentiate
one another. There is suggestive evidence for this:
• synergistic responses when nickel exposures are combined with gamma radiation;53• bystander cells (i.e. unirradiated) are vulnerable to both radiation-induced and chemical-
A number of authors have theorized that synergism may occur. For example, Miller et al.
specifically proposed that DU's radiological and chemical effects might play tumour-initiating and
tumour-promoting roles.55 If this were the case, it would be a clear example of synergism.
In addition, the Royal Society stated:
One could speculate … that the potential for synergistic effects between the radiation and
chemical actions of DU would be greatest in the vicinity of particles or fragments of DU,
from which essentially all the surrounding cells are chemically exposed and may thereby be
sensitized to the occasional radioactive decay particle.56
It concluded that further studies were required to examine the possibility of synergy between
the chemical effects and radiation effects of DU. The NRC report also recommended that studies
be conducted to determine the relative contribution of chemical and radiological mechanisms of
uranium carcinogenesis. It added that if the chemical contribution were found to be substantial,
studies should then be undertaken to calculate cancer risks resulting from DU's combined chemical
and radiological effects.
Despite the existence of many reports on DU, it remains difficult to assess whether (and if so to what
degree) DU exposures have caused increased incidences of ill health among exposed soldiers and
others. This is because of the inconclusive findings of some of the reports; the large uncertainties
in the assessed doses and risks from DU exposures; the possible presence of confounders; and the
paucity of data from battlefield and other exposures. In other words, the available epidemiological
data are sparse and inconclusive.
However, as shown above, we have two main sources of data to derive uranium's risks—animal
and cell studies as well as epidemiological studies. In fact, uranium's chemical risks are derived
from the former for safety regulation purposes. In general terms, the risks of almost all chemicals
are based on the concentrations found not to be harmful in animals. These concentrations are
divided by safety factors of 10 to 1,000 then applied to humans, i.e. acceptable concentrations for
humans are 10 to 1,000 times safer than those in animals. This rather simple system works well and
is clearly precautionary.
With radionuclides, this precautionary approach is not used. Instead, radiation scientists insist
that human data (i.e. from epidemiology studies) must be used to derive risks. Many may think that
these are a better source because humans are different from animals and cells, and in theory this
is correct. But in practice it is less clear cut: there are a large number of practical difficulties with
epidemiology studies. In essence, they are a blunt tool for investigating risks, and insisting on using
such studies alone rather than relying on cell and animal studies as well means that we might be
underestimating DU risks.
The problem is that sole reliance on epidemiological data tends to downplay the substantial
body of radiobiological evidence that overwhelmingly points to DU as a very hazardous substance.57
This evidence points to DU being:
• a chemical carcinogen mutagen and teratogen;• a radiological carcinogen mutagen and teratogen;• a chemical toxin with pronounced effects on kidneys and other organs; and• an endocrine disruptor.
Indeed, continued reluctance to act on the many research findings from radiobiology could be
considered a breach of the precautionary principle in law.58
Given the preponderance of cell and animal studies indicating
Sole reliance on epidemiological
that DU is a very hazardous substance, the safest approach would
data tends to downplay the substantial
be to seek a moratorium on its use. It is notable that, in December
body of radiobiological evidence that
2007, the UN General Assembly carried a motion by 136 votes to 5,
overwhelmingly points to DU as a very
recognizing the health concerns over the use of uranium weapons
and requesting that states report to the Secretary-General on the
matter.59 Also in May 2008, the European Parliament carried a motion that strongly reiterated its call
on all European Union member states and North Atlantic Treaty Organization countries to impose a
moratorium on the use of depleted uranium weapons and to redouble efforts toward a global ban.
The resolution was adopted with 491 votes in favour, 18 against and 12 abstentions.60
It is recommended that, for practical purposes, DU should be treated as being equally as radioactive
as natural uranium. As regards the dose coefficients for DU and uranium, a precautionary approach
would be to assume that their uranium isotopes coexist in equilibrium with their main decay
products (the ICRP assumes the opposite). This means that the dose coefficients for U-238 should be
increased by about 40%. This would result in uranium and DU doses (and risks) being increased by
It is also recommended that isotope surveillance should be maintained on new batches of DU to
ensure that reprocessed DU is not being added to DU obtained from uranium ore.
There have been many attempts in the literature to assess likely exposures and risks to military
personnel from Gulf War operations and correspondingly few among civilians. Most military studies
have concluded that the estimated exposures and resulting risks are minor and too small to be detected
in epidemiology studies among the relatively few DU-exposed soldiers. In light of this, further studies
of military personnel do not seem to be merited. Instead, research should be carried out on the health
impacts among the tens of thousands of Iraqi civilians estimated to have been exposed to DU and
their offspring. Populations exposed to DU and natural uranium should be examined for increased
risk of fertility problems and reproductive cancers.
It is also recommended that further radiobiological research be carried out into possible synergistic
effects of DU exposures. Finally, further research should investigate the properties of DU as a possible
The health hazards of depleted uranium
1. See, for example, Naomi Harley et al., 1999, A Review of the Scientific Literature as It Pertains to Gulf War Illnesses,
Volume 7: Depleted Uranium,
Santa Monica, CA, RAND Corporation.
2. See, for example, M. Aitken, 1999, "Gulf War Leaves Legacy of Cancer", British Medical Journal,
August, vol. 319,
3. National Research Council, 2008, Review of Toxicologic and Radiologic Risks to Military Personnel from Exposure to
Depleted Uranium during and after Combat
, Washington, DC, National Academies Press;
M.A. Parkhurst et al., 2004,
Depleted Uranium Aerosol Doses and Risks: Summary of U.S. Assessments,
Battelle Press; Royal Society, 2001, The
Health Hazards of Depleted Uranium Munitions: Part I,
London; Royal Society, 2002, The Health Hazards of Depleted
Uranium Munitions: Part II,
London; World Health Organization, 2001, Depleted Uranium: Sources Exposures and
WHO document WHO/SDE/PHE/01.1, Geneva; Carolyn E. Fulco et al. (eds), 2000, Gulf War and
Health, Volume 1: Depleted Uranium, Sarin, Pyridostigmine Bromide, Vaccines,
Washington, DC, National Academies
Press, chapter 4; Office of the Special Assistant for Gulf War Illnesses (OSAGWI), 2000, Environmental Exposure
Report: Depleted Uranium
; Harley et al., op. cit.; Agency for Toxic Substances and Disease Registry, US Department
of Health and Human Services, 1999, Toxicological Profile for Uranium,
4. D.M. Taylor and S.K. Taylor, 1997, "Environmental Uranium and Human Health", Reviews on Environmental Health,
vol. 12, no. 3, pp. 147–157; S. Fetter and F.N. von Hippel, 1999, "The Hazard Posed by Depleted Uranium
Munitions", Science & Global Security,
vol. 8, no. 2, pp. 125–161; D. Brugge et al., 2005, "Exposure Pathways
and Health Effects Associated with Chemical and Radiological Toxicity of Natural Uranium: A Review", Reviews on
vol. 20, no. 3, pp. 177–193; A.C. Miller (ed.), 2007, Depleted Uranium: Properties, Uses, and
Boca Raton, FL, CRC Press.
5. The report stated that "Exposure to sufficiently high levels might be expected to increase the incidence of some
cancers, notably lung cancer, and possibly leukaemia, and may damage the kidneys". Using a worst-case scenario,
they estimated an extra 1.2 deaths per 1000 from lung cancer among those with the highest exposure (e.g. surviving
personnel in a vehicle struck by a depleted uranium penetrator) (Royal Society, 2001, op. cit., p. 21).
6. Uranium mining is highly destructive of local environments and uranium refining creates large quantities of radioactive
tailings, which continue to release large quantities of the radioactive gases radon and thoron for millennia.
7. Science and Technology Options Assessment, 2001, Depleted Uranium: Environmental and Health Effects in the Gulf
War, Bosnia and Kosovo
, document STOA 100 EN.
8. Wise Uranium Project, Depleted Uranium Inventories,
at <www.wise-uranium.org/eddat.html>, last updated 21
9. Royal Society, 2002, op. cit.; R.K. Bhat, 2000, Tank-Automotive and Armaments Command (TACOM) and Army
Material Command (AMC) Review of Transuranics (TRU) in Depleted Uranium Armor
, Memorandum, Fort Belvoir, VA,
Army Test Measurement and Diagnostic Equipment Activity.
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Used in Armor-piercing Munitions", op. cit.
The health hazards of depleted uranium
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in Ministry of Higher Education and Scientific Research Republic of Iraq, Selected Research Works on the Effect of
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Munitions", op. cit., p. 275.
54. Ibid., p. 277.
55. Miller et al., 2004, op. cit., p. 254.
56. Royal Society, 2001, op. cit., p. 69.
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and in vivo
Studies", Reviews on Environmental Health,
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58. E. Hey, 1995, "The Precautionary Principle. Where Does It Come from and Where Might It Lead in the Case of
Radioactive Releases to the Environment", in IAEA, Proceedings of an International Atomic Energy Agency Symposium
on the Environmental Impact of Radioactive Releases
, Vienna, document IAEA-SM-339/195.
59. UN General Assembly resolution 62/30 of 5 December 2007, UN document A/RES/62/30, 10 January 2008.
60. European Parliament resolution of 22 May 2008 on (depleted) uranium weapons and their effect on human health
and the environment – towards a global ban on the use of such weapons, document P6_TA(2008)0233.
PERIODICO D'INFORMAZIONE DELL'UNIONE ITALIANA DEI CIECHI E DEGLI IPOVEDENTI ONLUS – SEZIONE PROVINCIALE DI TRENTO Anno I - Numero 0 - OTTOBRE 2011 - Trimestrale La prima Presidente La nuova sede Gruppo sportivo non donna dell'UIC di Trento dell'Unione Ciechi vedenti di Trento
SIRT1 Regulates Circadian Clock GeneExpression through PER2 Deacetylation Gad Asher,David Gatfield,Markus Hans Reinke,Charna Florian Kreppel,Raul Mostoslavsky,Frederick W. Alt,and Ueli 1Department of Molecular Biology, Sciences III, University of Geneva, 30, Quai Ernest Ansermet, CH-1211 Geneva-4, Switzerland2Division of Gene Therapy, University of Ulm, Helmholtzstrasse 8/1, D-89081 Ulm, Germany3Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA4Howard Hughes Medical Institute, Children's Hospital, Center for Blood Research, and Department of Genetics,Harvard University Medical School, Boston, MA 02115, USA*Correspondence: DOI 10.1016/j.cell.2008.06.050