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OCR for page 525
Uranium
Uranium is widely distributed throughout the world, with the average
concentration in the ea~th's crust being about 3 - ppm (Merritt, 1971~.
It does not occur in concentrated deposits, and much of the ore from
which uranium is recovered contains less than 0.1 percent uranium.
More than 100 minerals contain uranium as an important constituent,
with the primary minerals being uraninite and pitchblende, both of
which consist chemically of uranium oxide (UPON. Uranium occurs in
both North Carolina and Florida marine sedimentary phosphate
minerals and in igneous phosphate minerals from the western states in
concentrations up to 250 ppm. It appears to be present in the phosphate
minerals as an isomorphous substitution for calcium and is in tetra-
valent form. Uranium in some phosphate mining districts is presently
being extracted as a by-product of the fertilizer industry. Interest in the
effect of uranium on biological systems increased significantly during
World War II because of the need to process uranium-containing ores
for use in venous atomic energy projects.
ESSENTIALITY
There are several reports in the literature that uranium at very low
concentrations (0.002 to 0.2 ppm) has a positive effect on the growth of
plants and that it is a necessary nutrient in plant life (rinse, 19531.
Uranium has not been demonstrated to be essential in animals.
525
OCR for page 526
526 MINERAL TOLERANCE OF DOMESTIC ANIMALS
METABOLISM
Although uranium is not known to be essential for any metabolic func-
tion, a great deal of information is available on how uranium is metabo-
lized. When uranium enters the body, the urany! ion (UO2+2) is the only
stable form present in the oxidation-reduction system (Hodge, 1950~.
The urany! ion in the bloodstream or in the extracellular fluid combines
reversibly with serum albumin and forms strongly associated com-
plexes with bicarbonate and with a number of organic acids. Uranium
is transported to the tissues partly as a nondiffusable protein complex
and partly as a di~usable bicarbonate complex. Approximately 40 per-
cent of the uranium is present as the protein complex and 60 percent as
the bicarbonate complex.
When uranium enters the bloodstream, it is removed at two principal
sites: bone and kidney (Hodge, 1950; Durbin, 19601. This distribution
is rapid; within an hour about 30 percent of a parenteral dose of uranium
is deposited in the bone, about 15 percent in the kidney, and 20 percent
will already have appeared in the urine. After a period of about 1
month, most of the uranium initially found in the bone is still at this site.
The kidney may contain 1 or 2 percent of the original dose; the
remainder is accounted for in the urine. In the bone, uranium competes
with calcium for position on the mineral surface (Neuman et al., 1949~.
Each uranyl ion reacts with two adjacent surface phosphates with a
very stable linkage at sites formerly occupied by two calcium ions.
SOURCES
Very little information is available on the uranium content of animal
diets. The uranium concentration in soils is variable and dependent on
the parent geological material; however, most soils contain approxi-
mately 1 ppm uranium. Higher uranium concentrations in some soils
may result from the heavy usage of phosphate fertilizers (Menzel, 1968;
Spalding and Sackett, 1972~. Most plants are reported to contain 0.04
ppm or less (Bower, 1966) and it would appear that plant materials are
not a very significant source of uranium in animal diets. Because of the
occurrence of uranium in phosphate deposits, the phosphate supple-
ments used in animal feeds would probably be the major source of
uranium. Uranium levels in commercial feed grade phosphates contain-
ing 18.0 to 18.5 percent phosphorus range from 70 to 180 ppm uranium
(Reid et al., 1977~. A phosphate supplement of this concentration will
OCR for page 527
Uranium
527
be used in complete mixed feeds for farm livestock at a level of about
1 percent. This means that on the average phosphate supplements
contribute 0.7 to 1.S ppm uranium to animal diets.
Uranium compounds were found to have the following comparative
toxicities for the mouse when fed in the diet (Tannenbaum, 19511:
UO2, U3O'`: relatively nontoxic, even in large doses (> 100 mg ura-
nium per day)
U03, UC4: toxic in large doses (80 mg uranium per day)
U02(N03~' U04, N~U2O7: toxic in moderate doses (10 to 20 mg
uranium per day)
TOXICOSIS
Uranium is a highly toxic element when soluble salts are administered
by intravenous, subcutaneous, or intraperitoneal injection. The toxicity
is dependent upon and modified by many factors and most of the
reported studies have been conducted with laboratory animals, pri-
. -
man y mice.
The toxicological effect of uranium appears to be similar in all
animals studied (Tannenbaum, 19511. Most of the absorbed uranium is
excreted in the unne; however, some of the uranium reacts with the
protein of the surface of the columnar cells lining the renal tubule and
injures or kills these cells. With small or moderate doses, the distal
portion of the proximal convoluted tubule receives the severest injury.
If death ensues, it follows a typical uremia caused by kidney dysfunc-
tion; if the animal survives, cellular regeneration restores much of the
kidney tissue and function.
One-year feeding experiments on dogs have shown that a level of 100
mg of uranyl nitrate hexahydrate per kilogram of body weight per day
did not affect body weight (Hodge, 1953~. Levels as low as 20 mg/kg of
body weight per day of the same compound produced the characteristic
histological kidney changes associated with uranium toxicosis.
Tannenbaum and Silverstone (1944) reported on studies in which
uranium in the form of uranyl nitrate hexahydrate was fed to mice at
levels ranging from 2 to 2,370 ppm in the diet. Over the period (48
weeks) studied, there was no definite indication of toxicosis at any of
the levels fed, but there was a decrease in growth in the groups receiv-
ing the highest levels.
When mice were fed moderately toxic doses of uranium (1 percent
uranyl nitrate hexahydrate~,740 ppm uranium), the following ob-
OCR for page 528
528 MINERAL TOLERANCE OF DOMESTIC ANIMALS
servations were made (Tannenbaum and Silverstone, 19441: After
ingesting the diet for a few days, the animals ate less food, either failed
to grow or lost weight, were cold to the touch, huddled together, and
had need fur and arched backs. When necropsied during the second
or third week, the kidneys were enlarged, pink-gray, and exhibited
microscopically an acute necrotizing nephrosis. Some animals died in
this period, however, those mice that survived the acute reaction re-
covered and proceeded to grow at a normal or near-normal rate. This
was accompanied by regeneration of the tubular epithelium and a return
to normal size and appearance of the kidneys. The striking features of
this recovery are: (1) that it occurs despite the continued daily ingestion
of the same dose of urany} nitrate that caused the original acute reaction
and (2) that uranium continues to accumulate in the bones and kidneys,
reaching levels far in excess of the levels found in these tissues during
the acute reaction. These observations and other data tend to support
the view that animals acquire a tolerance to uranium. If mice are started
on diets containing nontoxic levels of uranyl nitrate hexahydrate (1,422
ppm uranium) and the uranyl nitrate is increased gradually over a
period of time, the dose may be increased to a level that would ordi-
narily cause 100 percent mortality in previously unexposed mice. The
preexposed mice do not exhibit the acute reaction clinically or mo~pho-
logically, but they do proceed to decline in weight and eventually die
from the chronic poisoning. The principal morphological changes ob-
served during the chronic poisoning are also renal (Tannenbaum, 1951~.
Hodge (1953) reported on a 1-year feeding test utilizing rats in which
three dietary levels of uranyl nitrate hexahydrate were fed (474, 2,370,
and 9,480 ppm uranium). The rats maintained on the 474 ppm level grew
practically as well as the control rats, and there was no difference in
mortality in this group, as compared to the controls. At the 2,370 ppm
level, a slight depression in body weight was observed; however, the
mortality was no different than the control group. At the 9,480 ppm
level, there was a marked reduction in growth and a high mortality
during the first month of the study. Animals that survived the initial
period showed partial recovery.
The solubility of the uranium compound and its rate of absorption
from the gastrointestinal tract are probably the most important factors
in determining its relative toxicity. Since uranium is a toxic element
once it gets into the body tissues and since relatively large amounts of
uranium compounds must be ingested to produce toxicosis (in compari-
son with subcutaneous doses), it is apparent that only a small percent-
age of an ingested uranium compound is absorbed from the gastroin-
OCR for page 529
Uranium
529
testinal tract. It has been estimated that even for a soluble compound
such as urany} nitrate hexahydrate less than 0.5 percent of the amount
ingested is absorbed (Tannenbaum, 1951~.
TISSUE LEVELS
The most extensive studies on the distribution of uranium in tissues
have been performed on animals injected subcutaneously with soluble
uranium salts (Ferretti and Schwartz, 1946; Tannenbaum and Silver-
stone, 1951; Hodge, 19531. Sufficient data have been gathered on mice
fed uranium compounds to suggest that the same generalizations as
were made for injected animals hold true for those ingesting the ma-
tenal in the diet (Tannenbaum, 19511. Bone and kidney are the principal
sites of concentration of uranium following an intake either by subcuta-
neous injection or the oral route. The liver and spleen contain consider-
ably lower concentrations of uranium than the kidney, yet the concen-
tration in these tissues is higher than in other soft tissues.
Garner (1963) discussed the toxicity of uranium to livestock and its
potential transfer to humans via food products. He concluded that it is
not accumulated to any appreciable extent in edible tissues or secreted
in significant amounts into milk. Chapman and Hammons (1963) indi-
cated that in the dairy cow, milk received only 0.2 percent of the
estimated uranium intake per day, whereas greater than 99 percent of
the estimated daily intake appeared in the feces.
MAXIMUM TOLERABLE LEVELS
Although uranium is a toxic element when soluble salts are ad-
m~nistered by injection, the amount of dietary uranium that is absorbed
from the gastrointestinal tract is very low. The animal can tolerate
much higher dietary levels of the element as compared to those ad-
m~nistered by injection. Because there are so many factors that in-
fluence the toxicity of uranium and all combinations of factors have not
been studied, even for a single species, it is difficult to set a safe upper
limit for dietary uranium levels. There is very little, if any, information
available on the toxicity of uranium in farm livestock. A dietary level
of 400 ppm uranium appears to be safe for rats, even when the uranium
is present in a highly soluble form such as uranyl nitrate hexahydrate.
Except for an inadvertent direct contamination of livestock diets or
OCR for page 530
530 MINERAL TOLERANCE OF DOMESTIC ANIMALS
feed ingredients with a uranium compound, uranium toxicosis does not
appear to be a practical problem. Total uranium content of animal diets
probably does not exceed 3 - ppm.
SUMMARY
Uranium is widely distributed throughout the world, but it does not
occur in concentrated deposits. Although uranium is not known to be
essential for any metabolic function in animals, a great deal of informa-
tion is available on how uranium is metabolized. Me toxicological
effect of uranium appears to be similar in all animals studied and is
characterized by kidney dysfunction due to damage of the cells lining
the renal tubule. Although uranium is a toxic element when soluble
salts are administered by injection, the amount of dietary uranium that
is absorbed from the gastrointestinal tract is very low. A dietary level
of 400 ppm uranium appears to be safe for rats, even when the uranium
is present in a highly soluble form.
OCR for page 531
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OCR for page 533
Uranium
REFERENCES
533
Bowen, H. J. M. 1966. Trace Elements in Biochemistry. Academic Press, New York.
Chapman, T. S., and S. Hammons, Jr. 1963. Some observations concerning uranium
content of ingesta and excrete of cattle. Health Phys. 9:79.
Dense, A. G. 1953. Effects of uranium on plants, pp. 2257-2269. In C. Voegtlin and
H. C. Hodge (eds.). Pharmacology and Toxicology of Uranium Compounds. McGraw-
Hill Book Co., New York.
Durbin, P. W. 1960. Metabolic characteristics within a chemical family. Health Phys.
2:225.
Ferretti, R. J., and S. Schwartz. 1946. Uranium distribution studies, pp. 247-282. In A.
Tannenbaum, ed. Toxicology of Uranium. McGraw-Hill Book Co., New York.
Garner, R. J. 1963. Environmental contamination and grazing animals. Health Phys.
9:597.
Hodge, H. C. 1950. Pharmacologic tools in the study of the mechanics of uranium
poisoning. Arch. Ind. Hyg. Occup. Med. 2:300.
Hodge, H. C. 1953. In C. Voegtlin and PI. C. Hodge, eds. Pharmacology and Toxicology
of Uranium Compounds, McGraw-Hill Book Co., New York.
Menzel, R. G. 1968. Uranium, radium and thorium content in phosphate rocks and their
possible radiation hazard. J. Agric. Food Chem. 16:231.
Merritt, R. C. 1971. The Extractive Metallurgy of Uranium. Colorado School of Mines
Research Institute, Atomic Energy Commission.
Neuman, W. F., M. W. Neuman, E. R. Main, and B. J. MuLyan. 1949. The disposition
of uranium in bone. VI. Ion composition studies. J. Biol. Chem. 179:341.
Reid, D. F., W. M. Sackett, and R. F. Spalding. 1977. Uranium and radium in livestock
feed supplements. Health Phys. 32:535.
Spalding, R. F., and W. M. Sackett. 1972. Uranium in runoff from the Gulf of Mexico
distributive province: Anomalous concentrations. Science 175:629.
Tannenbaum, A., ed. 1951. Toxicology of Uranium. McGraw-Hill Book Co., New York.
Tannenbaum, A., and H. Silverstone. 1944. Some aspects of the toxicology of uranium
compounds, pp. 59-96. In A. Tannenbaum, ed. Toxicology of Uranium. McGraw-Hill
Book Co., New York.
Tannenbaum, A., and H. Silverstone. 1951. Distribution in tissues and excretion of
uranium, pp. 1~21. In A. Tannenbaum, ed. Toxicology of Uranium. McGraw-Hill
Book Co., New York.
Representative terms from entire chapter:
uranyl nitrate
