Uranium poisioning


Material Information

Uranium poisioning
Series Title:
United States. Atomic Energy Commission. MDDC ;
Physical Description:
3 p. : ; 27 cm.
Wexler, Sol
University of California (1868-1952)
U.S. Atomic Energy Commission
Atomic Energy Commission
Place of Publication:
Oak Ridge, Tenn
Publication Date:


Subjects / Keywords:
Uranium -- Toxicology   ( lcsh )
Uranium compounds   ( lcsh )
federal government publication   ( marcgt )
bibliography   ( marcgt )
technical report   ( marcgt )
non-fiction   ( marcgt )


Includes bibliographical references (p. 3).
Date Declassified: June 16, 1947
Statement of Responsibility:
Sol Wexler.
General Note:
Manhattan District Declassified Code
General Note:
Date of Manuscript: July 9, 1942

Record Information

Source Institution:
University of Florida
Rights Management:
All applicable rights reserved by the source institution and holding location.
Resource Identifier:
aleph - 005024113
oclc - 465267923
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Full Text

MDDC 1054



Sol Wexler

University ol California
Radiation Laboratory

Date of Manuscript:
Date Declassified:

July 9, 1942
June 16, 1947

Issuance of this document does not constitute
authority for declassification of classified
copies of the same or similar content and tit
and by the same author.

Technical Information Branch, Oak Ridge, Tennessee
AEC, Oak Ridge, Tenn., 4-6-49--850-A4419

Printed in U.S.A.



Digitized by the Internel Archive
in 2011 with landing from
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hllp: www.archive.org details uraniumpoiSioninlOOuniv


By Sol Wexler


Poisoning from uranium may come about either through inhalation of uranium oxide dust (U30g,
UO2, or U03) or through contact with the soluble salts.
The pathological manifestation of uranium poisoning is nephritis, an inflammation of the kidney.
The intensity of the anatomical and functional lesion is the result of the accumulation of the metal in
the organ as a result of attempts at excretion.
Protection of the body against uranium involves protection of the hands and care to avoid in-
halation or ingestion. In the synthesis of uranyl nitrate, rubber gloves are recommended. Protection
against ingestion depends solely upon the worker; care must be exercised to prevent the taking of any
uranium by mouth during such operations as pipetting.

For more than one hundred years, uranium has been known to be poisonous to the animal
organism. As it is as toxic as arsenic, it is included in the official lists of poisons in Germany and
Russia. In particular, uranosic oxide, U308, is liberated as a dust in industries in v'hich uranium
is exposed to high temperatures and, without protection, may be inhaled and swallowed by workers.
Since U308 is soluble in gastric juice, ingestion of the oxide either directly or following inhalation
would probably lead to manifestations of poisoning. The symptoms are similar to those of other
heavy metal poisonings, especially those due to certain organic arsenic compounds. The poisonous
effect of uranium is usually ascribed to the action of the metal as such. Finally, uranium is not a
rapid poison, and the action of small and large doses is the same.
The first noticeable symptom of uranium poisoning is muscular weakness. Although no case of
glucose in the urine was observed, in a study of a group of four workers in a Belgian uranium salt
preparation factory, glycosuria is a symptom of uranium poisoning and is due to the lowered glucose
threshold of the kidneys. Furthermore, uranium salts, especially the nitrate, have an inhibitory ef-
fect on the activity of the digestive ferments, particularly fptylin and trypsin. In addition, the salts
check digestion, but apparently increase protein metabolism to a slight extent. Uranium increases
the output of carbon dioxide, raises the body temperature, and finally leads to emaciation. Being
an irritant poison, it produces gastro-intestinal disorder of greater or less intensity. Concentrated
solutions of uranium salts corrode the mucous membrane transforming the walls of the stomach
into a dead film of uranic albuminate.
The greatest pathological effect of uranium poisoning is nephritis, an inflammation of the kidney.
It is a diffuse, degenerative lesion affecting the renal parenchyma, the interstitial tissue, and the
renal vascular system. There are a number of types of nephritis depending on the part of the kidneys
attacked. Acute nephritis is the destruction of the renal tissue, similar to that produced by arsenic,
mercury, and phosphorus. Glomerular nephritis refers to inflammation of the glomeruli of the
kidneys. In interstitial and chronic nephritis, such as that due to lead poisoning and alcohol, the
kidneys become small, cystic, nodulated, and adherent to their capsules; furthermore, the interstitial
tissue is increased and there is a thickening of the vessel walls and the malpighian corpuscles.

MDDC 1054 1

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In addition, the heart becomes hypertrophied, and the valls of the small arteries thicken. Nervous
symptoms, such as loss of sight and coordinating power, sometimes predominate as a result of the
coagulating action of uranium salts on albumin. Albumin in the urine albuminuriaa) is the earliest
indication of renal irritation, which functionally at least is the earliest demonstrable stage of
Whereas uranium as a poison produces widespread lesions from the functional point of view,
there is no doubt that anatomically its most marked effect is on the kidney. Experiments show a
marked tendency for the deposition of uranium in the kidneys, with no detectable amounts in any
of the other organs; the deposition is exclusively in the renal cortex and not in the medullary
portion of the kidneys. The fact that this deposition occurs in living animals and not in excised
kidneys would indicate that it has to do with living processes. This raises the question as to
whether it is due to a special lack of resistance of the kidney to the poison, a special affinity for
the poison, or the attempted excretion through the kidneys. It appears, as a result of experimental
uranium nephritis, that the intensity of the anatomical and functional lesion is not to be attributed
to a susceptibility of this organ for the poison, but is the result of the accumulation of the metal
in the organ as a result of attempts at excretion. This would result in a vicious circle in which
increased attempts at excretion result in increased concentration of the poison because of de-
creased effectiveness of excretion.
In the study of four Belgian workers, two of whom worked with soluble and two'with insoluble
uranium salts, it was shown that there was a decrease in the nitrogen and a large increase in the
chlorine content of the urine. Furthermore, a small amount of uranium was found in the urine. A
small dose of uranium increases the volume of urine. However, it is well known that in uranium
poisoning there is, in general, a considerable reduction in the urine output, which may go on to
complete suppression, this process going hand in hand with degenerative processes in the renal
epithelium and later alterations in the glomerulus. This can be explained at least in part by the
early collection of uranium in the kidney, the uranium operating by its coagulative effect on the
epithelial protoplasm producing haemorrhages in the kidney.
Accompanying nephritis is an acid intoxication which may be reduced by the administration
of sodium bicarbonate. Also concurrent are marked changes in the parathyroid and thyroid glands.
In the study of the four Belgian uranium workers it has been found that the uranium salts
under consideration (sodium uranate and uranyl nitrate) clearly have an effect upon the blood
forming processes, resulting in every case in a considerable decrease in the leucocyte content.
This was particularly marked in the two workmen handling insoluble salts, their skin and mucous
membrane having come in contact with large quantities of uranium. The blood of these workers
also showed a decrease in the hematin content, with signs of anemia, those who handled the soluble
salts being the more affected in this way. A worker who handled the salts six months exhibited
purpling of the hands, this being the result of alteration in the red blood corpuscles. This pale color
showed anemia, the confirmation of which was given by the results of the blood and urine analysis.
Examination showed that the red blood cell counts for the four workers were not equal. Some cells
of the soluble salt workers were deformed; in the case of one of the workers there was a deformation
of the red blood cell nuclei. On the other hand, the corpuscles of the insoluble salt workers were
Lastly, it must be mentioned that the salts deposited on the skin and mucous membrane are
also radioactive poisoning agents. The pathological effects and methods of protection have been
described in the report "Radium: Pathological Effects and Protection." However, because of the
very long half-life of uranium (106 years), its rate of bombardment is not very large, and, con-
sequently, the danger from this source is much less than in the case of radium.
Protection of the body against uranium involves protection of the hands and protection against
ingestion and inhalation, especially of U308. In the synthesis of uranyl nitrate, rubber gloves are

MDDC 1054

recommended. Protection against ingestion depends solely upon the worker; care must be taken to
prevent the taking of any uranium by mouth during such operations as pipetting. It is recommended
that masks with breathing screens be worn during boiling or grinding of uranium salts, it being
advisable that the mask cover the entire face of the worker. It is practically impossible to have no
contact with uranium. However, it has been shown that absorption of uranium salts by the skin is
extremely small.


1. Eitel, H., Arch.exp. Path. Pharmakol., 135:188 (1928).

2. In, N. and G. J. Ryo, Chosen Med. Assoc., 29:1459 (1939).
3. Karsner, H. J., S. P. Riemann, and S. C. Brooks, J. Med. Res., 39:163 (1918).

4. de Leat, M. and C. Meurice, Ch. Ing. Chim., 9:247 (1925).

5. MacNider, W., J. Exp. Med., 23:171 (1916).
6. Mellor, J. W., A Comprehensive Treatise on Inorganic and Theoretical Chemistry, Vol. XII, 32,
Longman, Green, and Sons, New York, 1922.

7. Stedman, Medical Dictionary, 14th ed., William Wood and Company, 1939.
8. Weekers, R., Arch.intern. Pharmaco-dynamie, 54:423 (1936).


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