Prepared for the Hague Peace
Conference, May 1999
By Dr. Rosalie Bertell, Ph.D., G.N.S.H.
By Dr. Rosalie Bertell, Ph.D., G.N.S.H.
SOURCE: CCNR
Gulf War Veterans and Depleted
Uranium
Source of Exposure:
Uranium metal is autopyrophoric and can burn spontaneously at
room temperature in the presence of air, oxygen and water. At
temperatures of 200-400 degrees Centigrade, uranium powder may
self-ignite in atmospheres of carbon dioxide and nitrogen.
Oxidation of uranium under certain conditions may generate
sufficient energy to cause an explosion (Gindler 1973). Friction
caused by bullet or missile entry into a tank or armored car,
for example, can cause the uranium to ignite, forming a
concentrated ceramic aerosol capable of killing most personnel
in the vehicle. Depleted uranium was used extensively in place
of tungsten for ordnance by the US and UK in the Gulf War.
There is no dispute of the fact that at least 320 tons of
depleted uranium (DU) was "lost" in the Gulf war, and that much
of that was converted at high temperature into an aerosol, that
is, minute insoluble particles of uranium oxide, UO2 or UO3 , in
a mist or fog. It would have been impossible for ground troops
to identify this exposure if or when it occurred in war, as this
would require specialized detection equipment. However, veterans
can identify situations in which they were likely to have been
exposed to DU. Civilians working at military bases where live
ammunition exercises are conducted may also have been exposed.
Uranium oxide and its aerosol form are insoluble in water. The
aerosol resists gravity, and is able to travel tens of
kilometres in air. Once on the ground, it can be resuspended
when the sand is disturbed by motion or wind. Once breathed in,
the very small particles of uranium oxide, those which are 2.5
microns [ one micron = one millionth of a meter ] or less in
diameter, could reside in the lungs for years, slowly passing
through the lung tissue into the blood. Uranium oxide dust has a
biological half life in the lungs of about a year. According to
British NRPB [ National Radiation Protection Board ] experiments
with rats, the ceramic or aerosol form of uranium oxide takes
"twice as long" or about a two year biological half life in the
lungs, before passing into the blood stream. [Stradling et al
1988]
Because of coughing and other involuntary mechanisms by which
the body keeps large particles out of the lungs, the larger
particles are excreted through the gastro-intestinal tract in
feces. The uranium compounds which enter the body either through
the wall of the gastro-intestinal tract or the lungs, can be
broken down in the body fluids, and tetravalent uranium is
likely to oxidize to the hexavalent form, followed by the
formation of uranyl ions. Uranium generally forms complexes with
citrate, bicarbonates or protein in plasma, and it can be stored
in bone, lymph, liver, kidney or other tissues. Eventually this
uranium which is taken internally is excreted through urine.
Presence of depleted uranium in urine seven or eight years after
exposure is sufficient evidence to substantiate long term
internal contamination and tissue storage of this radioactive
substance.
Uranium is both a chemical toxic and radioactive hazard: Soluble
uranium is regulated because of its chemical toxicity, measured
by damage to the kidney and tubules. Uranium is a heavy metal,
known to cause uranium nephritis. Insoluble uranium, such as was
released in the Gulf War, is regulated by its radiological
properties, and not its chemical properties. Because of its slow
absorption through the lungs and long retention in body tissues,
its primary damage will be due to its radiological damage to
internal organs rather than chemical damage to the renal system.
Obviously, both types of damage occur simultaneously, therefore
it is a matter of judgment which severe damage, radiological or
chemical, occurs at the lowest dose level. However, with the
lengthening of the time during which the contaminant resides in
the body and the low overall dose, the risk of cancer death
becomes greater than the risk of significant damage to the renal
system.
Uranium decays into other radioactive chemicals with statistical
regularity. Therefore, in its natural and undisturbed state, it
always occurs together with a variety of other radioactive
chemicals, some of the best known being thorium, radium,
polonium and lead.
Natural uranium in soil is about 1 to 3 parts per million,
whereas in uranium ore it is about 1,000 times more
concentrated, reaching about 0.05 to 0.2 percent of the total
weight. Depleted uranium concentrate is almost 100 percent
uranium. More than 99 percent of both natural and depleted
uranium consists of the isotope U-238. One gram of pure U-238
has a specific activity of 12.4 kBq, which means there are
12,400 atomic transformations every second, each of which
releases an energetic alpha particle. Uranium 238 has a half
life of 4.51 E+9 (or 4.51 times 10 to the 9thpower, equivalent
to 4,510,000,000 years).
Each atomic transformation produces another radioactive
chemical: first, uranium 238 produces thorium 234, (which has a
half life of 24.1 days), then the thorium 234 decays to
protactinium 234 (which has a half life of 6.75 hours), and then
protactinium decays to uranium 234 (which has a half life of
2.47E+5 or 247,000 years). The first two decay radioisotopes
together with the U 238 count for almost all of the
radioactivity in the depleted uranium. Even after an industrial
process which separates out the uranium 238 has taken place, it
will continue to produce these other radionuclides. Within 3 to
6 months they will all be present in equilibrium balance.
Therefore one must consider the array of radionuclides, not just
uranium 238, when trying to understand what happened when
veterans inhaled depleted uranium in the Gulf War.
It should be noted that uranium 235, the more fissionable
fraction which was partially removed in enrichment, makes up
only 0.2 to 0.3 percent of the depleted uranium, whereas it was
0.7 percent of natural uranium. It is this deficit which enables
one to use analytical methods to identify the uranium found in
veteran's urine as depleted and not natural uranium. The U 235
was extracted for use in nuclear weapons and nuclear reactor
fuel. Depleted uranium is considered nuclear waste, a by-product
of uranium enrichment.
The difference in radioactivity between natural and depleted
uranium is that given equal quantities, depleted uranium has
about half the radioactivity of the natural mixture of uranium
isotopes. However, because of the concentration of the uranium
in the depleted uranium waste, depleted uranium is much more
radioactive than uranium in its natural state.
Uranium and all of its decay products, with the exception of
radon which is a gas, are heavy metals. Unlike some other heavy
metals which are needed in trace quantities by the human body,
there is no known benefit to having uranium in the body. It is
always a contaminant. Ingesting and inhaling some uranium,
usually from food, is inescapable however, in the normal Earth
environment, and we humans basically take in, on average, 5 Bq
per year of uranium 238 in equilibrium with its decay products.
This gives an effective radiation dose equivalent to the whole
body of 0.005 mSv. Using a quantitative measure, we normally
ingest about 0.000436 g a year.[UNSCEAR 1988, 58-59] This is a
mixture of soluble and insoluble compounds, absorbed mostly
through the gut.
Regulatory limits recommended by the International Commission on
Radiological Protection [ICRP] assume that the maximum
permissible dose for members of the public will be the one which
gives the individual 1 mSv dose per year. This is in addition to
the natural exposure dose from uranium in the food web. Assuming
that this dose comes entirely from an insoluble inhaled uranium
oxide, and using the ICRP dose conversion factor for uranium 238
in equilibrium with its decay products, one can obtain a factor
of 0.84 mSv per mg, or a limit of intake of 1.2 mg (0.0012 g)
per year for the general public. This would give an added
radiation dose of 1.0 mSv from uranium, and an increase of
almost 2.75 times the natural uranium intake level. Nuclear
workers would be allowed by the ICRP maximum permissible level,
to reach an annual dose of 20 mSv, comparable to an intake of 24
mg of uranium, 55 times the normal yearly intake.
The US has not yet conformed to the 1990 international
recommendations which were used for this calculation, and it is
still permitting the general public to receive five times the
above general public amount, and the worker to receive 2.5 times
the above occupational amount. The US may have used its domestic
"nuclear worker" limits during the Gulf War, if it used any
protective regulations at all. The military manual discusses the
hazards of depleted uranium as less than other hazardous
conditions on an active battle field!
The maximum dose per year from anthropogenic sources can be
converted to the maximum concentration permissible in air using
the fact that the adult male breathes in about 23 cubic metres
of air in a day [ICRP 1977]. The maximum permissible
concentration in air for the general public would be: 0.14
microgram per cu metre, and for workers: 2.9 micrograms per cu m
assuming the Gulf War situation of continuous occupancy rather
than a 40 hour work week, and an 8 hour day. It is common in the
US and Canada to refer to 2000 pounds as a "ton", whereas the
British "ton" is 2240 pounds. Both are roughly 1000 kg. Just in
order to understand the scale of the ceramic uranium released in
Desert Storm, at least 300 million grams were "lost", and
breathing in only 0.023 g would be equivalent to the maximum
permissible inhalation dose for a nuclear worker to receive in a
year under the 1990 recommendations of ICRP.
Medical Testing for Depleted Uranium Contamination:
Potential testing includes:
chemical analysis of uranium in urine, feces, blood and hair;
tests of damage to kidneys, including analysis for protein,
glucose and non-protein nitrogen in urine;
radioactivity counting; or
more invasive tests such as surgical biopsy of lung or bone
marrow.
Experience with Gulf War veterans indicates that a 24 hour urine
collection analysis shows the most promise of detecting depleted
uranium contamination seven or eight years after exposure.
However, since this test only measures the amount of depleted
uranium which has been circulating in the blood or kidneys
within one or two weeks prior to the testing time, rather than
testing the true body burden, it cannot be directly used to
reconstruct the veteran's dose received during the Gulf War.
However, this seems to be the best diagnostic tool at this time,
eight years after the exposure.
Feces tests for uranium are used for rapid detection of intake
in an emergency situation, and in order to be useful for dose
reconstruction, must be undertaken within hours or days of the
exposure. Blood and fecal analysis are not advised except
immediately after a known large intake of uranium.
Whole body counting for uranium, using the sodium iodide or
hyper pure germanium detectors, is designed to detect the
isotope uranium 235, the isotope of uranium partially removed
from depleted uranium. For lung counting, again it is the
uranium 235 which is detected, and the minimum detection limit
is about 7.4 Bq or 200 pCi. Since normally humans take in only 5
Bq per year, this is not a very sensitive measure. Seven or
eight years after the Gulf War exposure, this method of
detection is most likely useless for veterans.
Routine blood counts shortly after exposure, or during a
chelating process for decontamination of the body are useful.
This is not a search for uranium in blood, but rather a complete
blood count with differential. This is done to discover
potentially abnormal blood counts, since the stem cells which
produce the circulating lymphocytes and erythrocytes are in the
bone marrow, near to where uranium is normally stored in the
body. The monocyte stem cells in bone marrow are known to be
among the most radiosensitive cells. Their depletion can lead to
both iron deficient anemia, since they recycle heme from
discarded red blood cells, and to depressed cellular immune
system, since monocytes activate the lymphocyte immune system
after they detect foreign bodies.
Hair tests need to be done very carefully since they tend to
reflect the hair products used: shampoos, conditioners, hair
coloring or permanent waves. Pubic hair would likely be the best
material for analysis. I am not aware of good standards against
which to test the Uranium content of hair, or how the analysis
would differentiate between the various uranium isotopes.
Testing of lymph nodes or bone on autopsy would be helpful.
However, invasive biopsies on live patients carry no benefit for
the patient and are usually not recommended because of ethical
considerations about experimentation on humans. If a veteran is
recommended for bronchoscopy for medical reasons, it would be
advisable to also take tissue samples for analysis for depleted
uranium.
When chelation processes have been initiated the rate of
excretion of uranium in urine will be increased and there is a
risk of damage to kidney tubules. Therefore careful urine
analysis for protein, glucose and non-protein nitrogen in
important. Some researchers have also reported specifically
finding B-2-microglobulinuria and aminoaciduria in urine due to
uranium damage.
Relating Depleted Uranium Contamination with Observed
Health Effects in Veterans:
There are two ways of documenting the radiological health
effects of a veteran's exposure to depleted uranium. The first,
and the one usually attempted in a compensation argument, would
be to reconstruct the original dose and then appeal to
regulatory limits or dose-response estimates available in the
scientific literature. This methodology is not recommended for
the Gulf War veterans, because the uranium excretion rate seven
or eight years after exposure cannot be used to estimate the
original lung and body burden of depleted uranium. Moreover, no
dose-response estimates for the chronic health effects of such
exposure are available from the literature, as will be seen
later in this paper. Recognized dose-response estimates for
radioactive materials are unique to fatal cancers (and even
these are disputed). It is not clear whether regulatory limits
for exposure to ionizing radiation apply in a war situation, or,
if they do, whether the veteran should be considered to have
been "general public" or a "nuclear worker". Beyond this, the
question of whether international or US standards should be used
for a multinational situation needs to be addressed.
The second methodology would require ranking veterans on an
ordinal scale for their original exposure, based on their
current excretion rate of depleted uranium. This involves the
reasonable assumption that the original contamination, although
not precisely measurable, was proportional to the current
excretion rate. The analysis of a 24 hour urine sample, for
example, could be rated on a specific research scale as having
"high", "medium" or "low" quantities of the contaminate. By
collecting detailed health and exposure data on each veteran,
one can use biostatistical methods to determine firstly, whether
any medical problems show an increase with the ordinal scale
increase in exposure, determined through urine analysis; and
secondly, whether there is a correlation between the descriptive
accounts of potential depleted uranium exposure and the assigned
ordinal scale determined on the basis of the urine analysis.
Using Non-Parametric Statistics one could determine the
statistical significance of various medical problems being
depleted uranium exposure related. This would undoubtedly
eliminate some medical problems from consideration and highlight
others. It could point to future research questions. It could
also provide a fair method of dealing with the current suffering
of the veterans using the best scientific methodology available
at this time. Risk estimates based on radiation related cancer
death are obviously unable to provide a reasonable response to
current veteran medical problems.
K
nown Occupational Health Problems Related to Uranium
Exposure:
In Volume 2 of the Encyclopaedia of Occupational Health, under
uranium alloys and compounds, page 2238, it reads:
"Uranium poisoning is characterized by generalized health
impairment. The element and its compounds produce changes in the
kidneys, liver, lungs and cardiovascular, nervous and
haemopoietic systems, and cause disorders of protein and
carbohydrate metabolism.......
Chronic poisoning results from prolonged exposure to low
concentrations of insoluble compounds and presents a clinical
picture different from that of acute poisoning. The outstanding
signs and symptoms are pulmonary fibrosis, pneumoconiosis, and
blood changes with a fall in red blood count; haemoglobin,
erythrocyte and reticulocyte levels in the peripheral blood are
reduced. Leucopenia may be observed with leucocyte disorders
(cytolysis, pyknosis, and hypersegmentosis).
There may be damage to the nervous system. Morphological changes
in the lungs, liver, spleen, intestines and other organs and
tissues may be found, and it is reported that uranium exposure
inhibits reproductive activity and affects uterine and
extra-uterine development in experimental animals. Insoluble
compounds tend to be retained in tissues and organs for long
periods."
Human and Animal Studies on Uranium Exposure:
In a study of uranium toxicity by the US Agency for Toxic
Substances and Disease Registry [ATSDR 1998], released for
public review and comments by 17 February 1998, exposure times
were divided into three categories: acute, less than 15 days;
intermediate, 15 to 365 days; and chronic more than a year. Most
of the Gulf War Veterans would have had chronic duration
exposure from the point of view of the length of time the
material remained in the body. However, this ATSDR division was
based of the duration of the presence of the external source of
contamination, not its residence time in the body, therefore it
would, in most cases be considered intermediate duration
exposure. There is very little human research available to
clarify the effects of intermediate duration exposure to humans.
It should not be assumed that lack of research implies lack of
effect on that particular system. It should also be noted that
although one or more papers may exist for acute and chronic
duration exposures, these do not necessarily cover the questions
which one might like to raise. No comments on the quality or
extent of the research is implied by this table.
Health Effects which have been
associated with inhalation of uranium:
The more soluble compounds of uranium, namely, uranium
hexafluoride, uranyl fluoride, uranium tetrachloride, uranyl
nitrate hexahydrate, are likely to be absorbed into the blood
from the alveolar pockets in the lungs within days of exposure.
Although inhalation products also are transported through
coughing and mucocilliary action to the gastro-intestinal tract
only about 2 percent of this fraction is actually absorbed into
the body fluids through the intestinal wall. Therefore all of
the research papers on acute effects of uranium refer to these
soluble uranium compounds via inhalation. The main acute effect
of inhalation of soluble uranium compounds is damage to the
renal system, and the main long term storage place of these
compounds in the body is bone.
These research findings do not apply easily to the insoluble
uranium compounds to which the Gulf Veterans were exposed when
the depleted uranium ordnance was used in battle.
The uranium compound used for ordnance was uranium 238 and
limited amounts of its decay products. Particles of these
compounds smaller than 2.5 microns are usually deposited deep in
the lungs and pulmonary lymph nodes where they can remain for
years. According to research done in the UK by the NRPB, ceramic
uranium is formed when uranium ignites through friction, as
happened in the Gulf War. In this form, it is twice as slow to
move from the lungs to the blood than would be the non-ceramic
uranium. Of the portion of inhaled uranium which passes through
the gastro-intestinal tract, only 0.2 percent is normally
absorbed through the intestinal wall. This may be an even
smaller portion for ceramic uranium. This fraction of the
inhaled compound can, of course, do damage to the GI tract as it
passes through because it emits damaging alpha particles with
statistical regularity. The residence time of the insoluble
uranium compounds in the GI tract (the biological half life) is
estimated in years. [ibid.]
The chemical action of all isotopic mixtures of uranium
(depleted, natural and enriched) is identical. Current evidence
from animal studies suggests that the chemical toxicity is
largely due to its chemical damage to kidney tubular cells,
leading to nephritis.
The differences in toxicity based on the solubility of the
Uranium compound (regardless of which uranium isotope is
incorporated in the compound) are more striking: water soluble
salts are primarily renal and systemic chemical toxicants;
insoluble chemical compounds are primarily lung chemical
toxicants and systemic radiological hazards. Once uranium
dioxide enters the blood, hexavalent uranium is formed, which is
also a systemic chemical toxicant.
It is important to note that there is no scientific evidence
which supports the US Veteran Administration claim that the
insoluble uranium to which the Gulf War Veterans were exposed
will be primarily a renal chemical toxicant. Yet this is the
criteria which the VA proposes for attributing any health
problems of the Veteran to depleted uranium. Intermediate and
chronic exposure duration to insoluble uranium is regulated in
the US by its radiological property. The slow excretion rate of
the uranium oxide allows for some kidney and tubule repair and
regeneration. Moreover, because of the long biological half
life, much of the uranium is still being stored in the body and
has not yet passed through the kidneys. The direct damage to
lungs and kidneys by uranium compounds is thought to be the
result of the combined radiation and chemical properties, and it
is difficult to attribute a portion of the damage to these
separate factors which cannot be separated in life.
There is human research indicating that inhalation of insoluble
uranium dioxide is associated with general damage to pulmonary
structure, usually non-cancerous damage to alveolar epithelium.
With acute duration exposure this can lead to emphysema or
pulmonary fibrosis (Cooper et al, 1982; Dungworth, 1989;
Saccomanno et al, 1982; Stokinger 1981; Wedeen 1992). Animal
studies demonstrate uranium compounds can cause adverse
hematological disturbances (Cross et al. 1981 b; Dygert 1949;
Spiegel 1949; Stokinger et al 1953).
Important information from a chart developed by ATSDR
[referenced earlier] is reproduced here, the reader will find
all of this information and the references in the original
document.
Availability of Human or Animal Data for the Presence of a
Particular Health Effect after Exposure via Inhalation to
Insoluble Uranium Effect on body system studied: Effects of
acute duration exposure (less than 15 days) Effects of
intermediate duration exposure (15 days to 1 year) Effects of
chronic duration exposure (more than 1 year)
Respiratory Human Studies:
rales, slight degeneration in lung epithelium; hemorrhagic lungs
[1]
Animal Studies:
severe nasal congestion, hemorrhage; gasping in 100 percent [2]
Animal Studies:
slight degenerative changes in lung;[3] pulmonary edema;
hemorrhage; emphysema; inflamation of the brochi; bronchial
pneumonia; alveoli and alveolar interstices; edematous alveoli;
hyperemia and atelectasis.; lung lesions; minimal pulmonary
hyaline fibrosis and pulmonary fibrosis. [2]
Animal Studies:
minimal pulmonary fibrosis [3] Lung cancer in dog [3]
Hepatic
Animal Studies:
moderate fatty livers in 5 of 8 animals that died; focal
necrosis of liver.[3]
Animal Studies:
increased bromo-sulfalein retention [2]
Hematological
Animal Studies:
increased macrophage activity; increased plasma prothrombin and
fibrinogen.[3] A (increased percentage myeloblasts and lymphoid
cells in bone marrow; decreased RBC; increased plasma
prothrombin and fibrinogen; increased neutrophils ; decreased
lymphocytes) Animal Studies:
lengthened blood clotting time, decreased blood fibinogen [2]
Gastro-intestinal Human Studies:
anorexia, abdominal pain, diarrhea, tenesmus or ineffective
straining, and pus and blood in stool [1]
anorexia; vomited blood; ulceration of caecum.[1],[6]
Renal Human Studies:
proteinuria, elevated levels of NPN, aminoacid nitrogen/creatinine,
abnormal phenol-sulfonphthalein excretion. Increased urinary
catalase; diuresis.[1]
Animal Studies:
Proteinuria, glucosuria and polyuria; severe degeneration of
renal cortical tubules 5-8 days post exposure. [2]
Animal Studies:
diuresis, mild degeneration in glomerulus and tubules. [3]
proteinuria, increased NPN.[3] minimal microscopic lesions in
tubular epithelium [1]
Animal Studies:
slight azotemia [4] slight degenerative changes [3] minimal
microscopic lesions [1], [5],[6] tubular necrosis and
regeneration [6]
Cardiovascular Musculo-skeletal Animal Studies:
severe muscle weakness; lassitude [3 with F].
Endocrine
Metabolic
Dermal
Ocular Animal Studies:
conjunctivitis [2]
Animal Studies:
eye irritation [2]
Body Weight Animal Studies:
26 percent decrease inMetabolicght; 14 percent decrease at 22 mg
/ cu m air; [1], [3] 12 percent decrease at 2.1 mg/cu m air.[2]
2.9 to 27.9 percent decreased body weight guinea pig [6]
Other Systemic Animal Studies:
weakness and unsteady gate, [1] minimal lymph node fibrosis.[3]
rhinitis [1]
Animal Studies:
minimal lymph node fibrosis [3] lung cancer (dog) [3]
Mortality Animal Studies:
20 percent for dogs at 2 mg per cu. m air [2] Animal Studies:
10 percent rat and guinea pig [4] 17 percent dog [4] 60 percent
rabbits [3]
67 percent rabbits [4]
Animal Studies:
4.5 percent mortality dog [3]
Uranium tetrafluoride, UF4 , insoluble in water.
Uranium hexafluoride, UF6 , soluble in water, highly chemically
toxic.
Uranium dioxide, UO2 , insoluble in water, highly toxic and
spontaneously flammable, used in ordnance in place of lead in
the Gulf War. (Also called uranium oxide.)
Uranium trioxide, UO3 , insoluble in water, poisonous,
decomposes when heated. (Also called uranium oxide.)
Uranyl Chloride, UO2Cl2 , uranium oxide salt.
Uranium Nitrate, UO2(NO3)2.2H2O , soluble in water, toxic and
explosive.
With respect to ORAL exposure, there is no human data but a
great deal of animal data. This was not as likely a pathway in
the Gulf War as was inhalation, but possible contamination of
food and water can not be totally ignored.
DERMAL exposure was researched in humans only in the acute
duration of exposure case. Animal studies on dermal exposure
include acute, intermediate and chronic duration of exposure,
and immunologic/lymphoreticular and neurologic effects.
Mortality Within 30 Days of Exposure:
The lowest acute duration lethal dose observed, with exposure to
the soluble uranium hexafluoride, was 637 mg per cu metre of
air. No acute dose deaths were found using insoluble compounds.
Since there were acute deaths in the Iraqi tanks in persons not
directly hit, one can assume concentrations of uranium aerosol
were greater than this amount. It should also be noted that it
was the radiation protection units of the military which
designated these contaminated tanks off bounds. They were acting
because of radiological (not chemical) properties of the
aerosol.
The intermediate duration exposure, 15 to 365 days, dose level
for mortality with insoluble uranium oxide, was 15.8 mg per cu
metre of air. With soluble uranium hexachloride it was much
lower, 2 mg per cu metre air.
The dose resulting in lung cancer in the dog study, with chronic
duration inhalation of the insoluble uranium oxide, was 5.1 mg
per cu metre air, for 1 to 5 years, 5 day a week and 5.4 hours a
day.
Systemic Damage:
Damage to body organs occurred with intermediate or chronic
exposure at doses as low as 0.05 mg per cu metre air. A
generally sensitive indicator of exposure seems to be loss of
body weight. However this finding is somtimes attributed to the
unpleasant taste of the uranium laced food given to animals.
There is also damage to the entrance portals: respiratory and
gastro-intestinal systems; and the exit portals: intestinal and
renal systems. Uranium oxide was associated with fibrosis and
other degenerative changes in the lung. It was also associated
with proteinuria, and increased NPN (non-protein nitrogen) and
slight degenerative changes in the tubules. The more severe
renal damage was associated with the soluble compounds uranium
tetrafluoride and uranium hexafluoride (not thought to have been
used in the Gulf War ordnance).
Focal necrosis of the liver was only associated with uranium
oxide. This may be a clue to one of its storage places in body
tissue. Uranium oxide is also associated with hematological
changes, lymph node fibrosis, severe muscle weakness and
lassitude at intermediate or chronic dose rates in 0.2 to 16 mg
per cu metre air. None of the uranium research dealt with the
synergistic, additive or antagonistic effects potentially
present in the Gulf War mixture of iatrogenic, pathological,
toxic chemical and electromagnetic exposures.
Potential US Government administration of
radio-protective substances to combat military:
It is obvious that the US had some expectation of the health
effects related to using depleted uranium ordnance in the Gulf
War. This is evident based on military research and manuals.
They would also have had access to information on chemical and
biological agents which could protect against some of the
harmful side effects. These agents might also "confuse" the
toxicology of this exposure. Some potential radio-protective
agents are thiols (also called mercaptans, these are
organosulfur compounds that are derivatives of hydrogen
sulfide), nitroxides (used as a food aerosol and an anesthetic),
cytokines (non-antibody proteins released by one cell
population, e.g T-lymphocytes, generating an immune response),
eicosanoids (biologically active substances derived from
arachidonic acid, including the prostaglandins and leukotrienes),
antioxidants and modifiers of apoptosis (fragmentation of a cell
into small membrane bound particle which are then eliminates by
phagocytes).
Just in case this is the reality and not merely a suspicion, it
would be good to examine the after effects of exposure to
ceramic depleted uranium in Iraqi veterans and in the survivors
of the El Al crash at Shipol Airport, Amsterdam. It is unlikely
that these two populations were given any protective agents.
Proposal for assisting the Gulf War veterans:
In keeping with the above findings, it is proposed to undertake
an analysis of both questionnaire and clinical data for a sample
of each of the following populations: US, Canadian and British
Gulf War veterans or civilian base workers exposed to DU; US,
Canadian and British military personnel not exposed to DU; Iraqi
Veterans exposed to DU; Iraqi Veterans not exposed to DU; and
firemen and civilians exposed to the El Al crash.
Sampling strategy and sample size to be determined:
Each participant should complete a questionnaire [See draft
questionnaire in Appendix A] covering general background
variables, exposure profile and medical problems and symptoms.
Each participant will agree to collect a 24 hour urine sample
for analysis, and to take 500 mg blue-green algae (Spirulina) 48
hours before beginning the collection. This is a mild chelating
agent. Each participant will agree to the analysis of this data
for the benefit of all exposed persons, and to the release of
the results of the analysis without identifying characteristics
for individuals.
All questionnaire data will be entered into computer using
Epi Info Software (WHO) and transferred on disc to the
Biostatistical Support Unit of the University of Toronto for
analysis.
Research Hypotheses to be tested:
(to be written as a null hypothesis)
There will be a high correlation between the questionnaire
exposure estimates and the level of depleted uranium found in
urine. Medical problems related to damage of the blood and/or
hepatic systems will show an association with exposure data and
urine sample analysis for depleted uranium.
Preliminary work to be accomplished:
Identification of principal investigators for each identified
study group.
Development of a Grant Proposal, including the null hypotheses
and protocols.
Development of a budget for each population study group.
Agreement of the Research team to undertake the study.
Raising of funds or assignment of costs for the study.
Identification and training of data entry processors for each
group.
Benefits for Participants:
In addition to the general benefits to be obtained by clarifying
the health effects of exposure to this toxic material,
especially in the ceramic form experienced in the Gulf War, each
participant testing positive for DU in a urine analysis will be
assisted to enter a chelating process to remove as much as
possible of the contaminant from the body.
References:
ATSDR 1998: "Toxicological Profile for Uranium" Draft for Public
Comment, US Department of Health and Human Services, Public
Health Service, Agency for Toxic Substances and Disease Ragistry,
September 1997.
Cooper JR, Stradling GN, Smith H, et al 1982. "The behaviour of
uranium 233 oxide and uranyl 233 nitrate in rats. International
Journal of Radiation Biology and Related Studies in Physics,
Chemistry and Medicine. Vol 41(4): 421-433.
Cross FT, Palmer RF, Busch RH et al, 1981. "Development of
lesions in Syrian golden hamsters following exposure to radon
daughters and uranium dust". Health Physics Vol 41:1135-153.
Dungworth DL. 1989 "Non-carcinogenic responses of the
respiratory tract to inhaled toxicants." In: Concepts in
Inhalation Toxicology. Editors: McClellan RO, and Henderson RF.
Hemisphere Publ. Corp. New York NY.
Dygert HP 1949. Pharmacology and Toxicology of Uranium
Compounds. Pages: 647-652, 666-672, and 673-675. McGraw Hill
Books Inc.
Encyclopaedia of Occupational Health and Safety, Third (Revised)
Edition. Technical Editor: Dr. Luigi Parmeggiani, published by
the International Labour Organization in 1983 (ISBN:
92-2--103289-2) Geneva, Switzerland.
Gindler JE, 1973. "Physical and Chemical Properties of Uranium."
In: Uranium, Plutonium and Transplutonic Elements" Editors:
Hodge et al. New York NY: Springer Verlag; 69-164.
ICRP 1991: Recommendations of the International Commission on
Radiological Protection. Publication, accepted in 1990 and
reported in Publication 60. Pergamon Press, UK.
Saccamanno G, Thun MJ, Baker DB, et al 1982. "The contribution
of uranium miners to lung cancer histogenesis renal toxicity in
uranium mill workers". Cancer Research Vol. 82 43-52.
Spiegel CJ, 1949. Pharmacology and Toxicology of Uranium
Compounds. McGraw Hill Book Co.Inc.
Stokinger HE, Baxter RC, Dygent HP, et al 1953. In: Toxicity
Following Inhalation for 1 and 2 Years. Editors: Voegtlin C and
Hodge HC.
Stokinger HE, 1981. Uranium. In: Industrial Hygiene and
Toxicology. Vol 2A, 3rd Edition. Editors:Clayton CD and Clayton
FE. John Wiley and Sons, New York NY, 1995-2013.
Stradling GN, Stather JW, Gray SA, et al. "The metabolism of
Ceramic Uranium and Non-ceramic Uranium Dioxide after Deposition
in the Rat Lung." Human Toxicology 1988 Mar 7; Vol 7 (2):
133-139.
UNSCEAR: United Nations Scientific Committee on the Effects of
Atomic Radiation reports to the UN General Assembly.
Wedeen RP, 1992. "Renal diseases of Occupational Origin".
Occupational Medicine Vol 7 (3):449.
Search Engine Optimization and SEO Tools
