which
meant the assumptions about
rapid initial elimination and slow “fix-
ing” of plutonium in the tissue were not
accurate. After roughly 20 to 30 days,
the excretion rate appeared to become
constant, but again, at much lower rates
(about 0.01 per cent in urine). The
total excretion rate (urinary and fecal)
at 21 days was about 10 times less than
that of radium.
The discovery that absorption of solu-
ble compounds of plutonium through
the gastrointestinal tract was very low
and essentially no absorption occurred
through the skin meant that the main
routes to internal deposition were ab-
sorption from contaminated wounds or
inhalation of dust particles. Such con-
siderations led Hamilton, on May 5,
1944, to suggest treatment for puncture
wounds.
Hamilton informed Stone that in acci-
dents involving intramuscular injec-
tion—such as might occur if closed
systems at high temperatures exploded
and shards punctured the worker’s
skin—absorption of plutonium would
be slow. Hamilton felt that “only a few
percent [of soluble product] would be
expected to be taken up within a matter
of an hour or so.” He realized “that
analogies are frequently dangerous for
the purposes of comparison, but the su-
perficial similarities . . . to snake bite
come to mind.” As a result, he sug-
gested a treatment that included, when
possible, the use of a tourniquet, which
“facilitates the washing out of the mate-
rial by bleeding and at the same time
retards absorption.”
Acute effects. By the end of 1945,
studies with rodents and dogs had
shown that the acute radiation effects of
plutonium were less “toxic” than highly
toxic chemicals (such as curare, strych-
nine, and botulinus toxin) but far ex-
ceeded any known chemical hazard of
heavy metals. The clinical picture of
acute plutonium toxicity in dogs was,
superficially at least, quite similar to the
effect of a single lethal dose of total-
body x rays. Although the initial vom-
iting and depression seen with x rays
were absent, weight loss and refusal of
food and water in the first days were
followed, around the tenth day, by the
final “shock” phase that included a rise
in body temperature, pulse rate, labored
breathing, and various hemorrhages.
Changes occurred in the blood as well,
including drops in white and red cell
counts. However, other animal species
showed certain dissimilarities between
acute plutonium toxicity and total-body
x rays.
The acute lethal dose for animals ap-
peared to be somewhere in the range
from 400 to 4000 micrograms of pluto-
nium per kilogram of body weight, de
pending on the species and, to a lesser
extent, on the chemical form of the plu-
tonium. Damage tended to occur more
specifically in the liver, kidneys, and
spleen and to red blood-cell production
in the bone marrow. In rats, about
60 per cent of the retained plutonium
ended up in the skeleton and 18 per
cent in the liver.
At that time, very little of the experi-
mental work extended over a period of
more than six or seven months, so the
picture of chronic plutonium toxicity
was essentially a guess. A few bone
tumors and one instance of bone thin-
ning had been observed in rats and
mice. It was not at all certain whether
the various effects, including those to
the blood, were progressive or whether
they could be extrapolated to lower
doses.
Certainly, extrapolating the results of
animal studies to humans had to be
done with caution. Experiments with
other toxic substances had shown in-
stances of dramatic differences between
animals and humans. Rats, for exam-
ple, will tolerate quantities of deposited
radium per unit of body weight that
would be lethal to humans, and various
inbred mice are capable of surviving
huge doses of external gamma radiation
compared to humans. Likewise, any
study involving skin was particularly
suspect because of the very great differ-
ences between human skin and those of
animals. Thus, the animal studies
could only be suggestive of what was
expected to happen in humans.
The Human Plutonium Injection Experiments
Number 23 1995 Los Alamos Science
189
Table 1. The Metabolic Behavior of Radium and Plutonium in Animals
Property
Radium
Plutonium
Initial excretion (rats)
urinary (first day)
~15 %
~0.7 %
fecal (first day)
~16 %
~2.3 %
Total excretion in 25 days (rats)
urinary
~23 %
~2.5 %
fecal
~32 %
~25.0 %
Overall deposition
bone
99 %
~50 %
liver
—
~30 %(at first)
Bone deposition
within the
surface of
mineralized bone
“active” bone
Planning for the Human
Injection Studies
By August 1944, despite the efforts of
a full-time chemist at Los Alamos and
another at Chicago, no satisfactory
method of analyzing excreta that could
consistently detect 1-microgram body
burdens had yet been devised (assum-
ing the 0.01-per-cent urinary excretion
rate suggested by the animal experi-
ments). An ion-exchange method de-
veloped by the Met Lab was satisfacto-
ry at the 5-microgram level, but
Hempelmann was convinced it was im-
portant to achieve even lower levels of
detectablility (see “Detection of Internal
Plutonium”).
People in the Chemistry Division at
Los Alamos were concerned “about the
inability of the Medical Group to detect
dangerous amounts of plutonium in the
body.” They had already had instances
of significant inhalation exposures and
one accident in which a chemist inad-
vertently swallowed an unknown, but
small amount of plutonium solution
(see “A Swallow of Plutonium”). In
addition, there had been five accidents
involving wound exposures. They
could not afford to continue using
guesswork as the basis for transferring
skilled workers who had experienced
plutonium exposures away from priority
work.
As a result, on August 16, 1944,
Hempelmann proposed a new research
program to Oppenheimer. The first
order of business would be “develop-
ment of methods of detection of pluto-
nium in the excreta.” Hempelmann
also stressed the importance of deter-
mining “the factor by which the amount
of plutonium in the excreta must be
multiplied to ascertain the amount in
the body” and of developing “methods
of detection of plutonium in the lung.”
Oppenheimer authorized work on the
detection of plutonium in both excreta
and lungs, but he was concerned about
balancing priorities. He said, “in view
of the many urgent problems facing the
laboratory, it should be carried out with
as small an investment of personnel as
possible . . . fewer than ten people.” In
the same vein, he continued: “As for
the biological sides of the work, which
may involve animal or even human ex-
perimentation . . . it is desirable if these
can in any way be handled elsewhere
not to undertake them here.” Los
Alamos lacked the appropriate medical
research facilities, and Oppenheimer
suggested that Hempelmann and he
“discuss the biological questions with
Colonel Warren at a very early date.”
Warren, of course, had by now been in
charge of the medical programs for the
Manhattan Project for over a year. It
was logical that biological research
should be carried out at a site, such as
Rochester, which housed the appropri-
ate staff and facilities.
A three-part plan. Groves, informed
of the plutonium exposure problems,
apparently made sure that Warren was
in Los Alamos about a week later. On
August 29, Hempelmann summarized
The Human Plutonium Injection Experiments
190
Los Alamos Science Number 23 1995
A Swallow of Plutonium
On August 1, 1944, a sealed tube containing plutonium chloride solution
ejected part of its contents while being opened.* Gases had built up, most
likely from the dissociation of water by the alpha radiation, and some of the
solution shot through the narrow tube out against the wall when the pres-
sure was released and the gases “boiled.” Don Mastick, the young chemist
working with the plutonium, realized from the taste of acid in his mouth that
part of the solution must have bounced off the wall into his mouth.
It was estimated that about 10 milligrams of the material was lost, mostly on
the walls of the room, with some on Mastick’s face and some swallowed.
Although his face was thoroughly scrubbed, the skin remained contaminated
with about a microgram of plutonium. His mouth was also thoroughly
washed, but for many days afterwards, he could blow at an open-faced ion-
ization chamber across the room and cause the needle to go off-scale—the
level of contamination estimated to be about 10 micrograms. (This last fact
suggests that the plutonium solution may have had other radioactive conta-
minants in it since it was later found not to be possible to detect plutonium
deposited in the lungs through ionized air molecules.)
Hempelmann pumped out Mastick’s stomach to retrieve much of what had
been swallowed (analysis of the contents for plutonium registered 4098
counts per minute, which corresponds to only about 60 nanograms). Since
very little would have been absorbed through his gastrointestinal tract, Ma-
stick ended up with only a barely measurable body burden. His initial 24-
hour urine assays, when the excretion rate was highest, were only 5 to 7
counts per minute, which translates to well below a 1-microgram body bur-
den. Some plutonium was absorbed, of course, and improved assay meth-
ods available in the early seventies were able to detect small amounts of
plutonium in his urine thirty years later (hundredths of counts per minute).
*The 10 milligrams that were ejected in the accident were not “Los Alamos’ entire supply of pluto-
nium,” as reported elsewhere (for example, by Eileen Welsome in her 1993 articles in the
Albu-
querque Tribune and in the October 1995 Final Report of the President’s Advisory Committee on
Human Radiation Experiments). In March the first 1-gram reduction of plutonium to metal had
been performed at Los Alamos, and by the end of August, the Laboratory was working with over
50 grams of plutonium (5000 times more than the amount sprayed at the wall).