SWRHL-114r
THE JANUARY 1971 SHEEP DEATH INCIDENT NEAR
GARRISON, UTAH
by
Radiological Research Program.
Western Environmental Research Laboratory"
ENVIRONMENTAL PROTECTION AGENCY
Published November 1971
This research was performed as a part of the Radiation
Effects Program and was supported by the U. S. Atomic
Energy Commission under
Memorandum of Understanding No. SF 54 373
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This reoort was prepared as an account of work sponsored
by the United States Government. Neither the United
States nor the United States Atomic Energy Commission,
nor any of their employees, nor any of their contractors,
subcontractors, or their employees, makes any warranty,
express or implied, or assumes any legal liability or
responsibility for the accuracy, completeness or useful-
ness of any information, apparatus, product or process
disclosed, or represents that its use would not infringe
privately-owned rights.
Available from the National Technical Information Service,
U. S. Department of Commerce,
Springfield, VA. 22151
Price: paper copy $3.00; microfiche $.95.
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THE JANUARY 1971 SHEEP DEATH INCIDENT NEAR
GARRISON, UTAH
by
Radiological Research Program
Western Environmental Research Laboratory*
ENVIRONMENTAL PROTECTION AGENCY
Published November 1971
This research was performed as a part of the Radiation
Effects Program and was supported by the U. S. Atomic
Energy Commission under
Memorandum of Understanding No. SF 54 373
*Formerly Southwestern Radiological Health Laboratory, part of the U. S.
Department of Health, Education, and Welfare, Public Health Service,
Environmental Health Service, Environmental Control Administration,
Bureau of Radiological Health.
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The January 1971 Sheep Death Incident Near Garrison, Utah
ABSTRACT
The acute death near Garrison, Utah, in January, 1971, of some 1,250
sheep from a flock of 2,600 was the object of national attention.
The implied cause of either nerve gas from Dugway Proving Grounds
or radiation from the Nevada Test Site was the principal newsworthy
ingredient used to focus national interest and was the reason used to
initiate several investigations to determine the true cause of the
deaths.
Based on early accounts of the incident, scientists from the Western
Environmental Research Laboratory postulated that weed poisoning, probably
Halogeton glomeratus, was a probable cause of death. This postulate
was subsequently confirmed by the field and laboratory results of
several investigative groups. The findings of the investigation in
which the Western Environmental Research Laboratory scientists participated
are presented and discussed.
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TABLE OF CONTENTS
Page
ABSTRACT i
LIST OF FIGURES AND TABLE ħħħ
PREFACE iv
INTRODUCTION 1
DESCRIPTION OF HALOGETON 2
FIELD EVALUATION 4
RESULTS AND DISCUSSION 9
REFERENCES 11
ii
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LIST OF FIGURES AND TABLE
Figure Page
1. Close-up view of Halogeton glomeratus on the sheep 3
range at Garrison, Utah.
2. Plant populations on the Garrison range. 5
3. Garrison sheep range strewn with carcasses. 7
4. Dead sheep showing blood-tinged frothy exudate 8
from the nose.
Table
1. Analytical results of rumen contents from 10
three sheep.
iii
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PREFACE
A rapid response to situations involving potential radiation exposures
is often decisive in reducing such exposures or in minimizing the
apprehension of the general population. Recognizing this fact, the
Radiological Research Program of the Western Environmental Research
Laboratory has developed and maintains an ad_ hoc investigative capability
which has been used effectively in past incidents. An adjunct capability
is contained within the Animal Investigation Program which investigates
alleged radiation illness in domestic and game animals.
The investigation described in this report resulted from the application
of these capabilities to an incident which occurred in Utah where a large
number of sheep had died. The circumstances surrounding the deaths
indicated that radiation was not the most probable cause, but prudence
required an exact determination.
The contributions of Dr. R. E. Stanley, Mr. K. W. Brown, Mr. E. M. Daley,
Mr. D. N. McNelis and Dr. S. C. Black to the success of this study are
greatly appreciated.
Special acknowledgement is given to Mr. J. J. Davis for providing the
photographs used in this report.
A. A. Moghissi
Chief, Radiological
Research Program,
Western Environmental
Research Laboratory
lv
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INTRODUCTION
On January 21, 1971, several news agencies reported that more than a
thousand sheep had died suddenly in western Utah, near the small town of
Garrison. The news releases implied the possibility of nerve gas or
radiation as etiological agents. Because of these implications and the high
incidence of sheep loss, the State of Utah, through the State Department
of Agriculture, initiated a comprehensive investigation of the cause of the
reported losses. In addition to the official investigation by the Utah
Department of Agriculture, several other investigative groups were
permitted to observe the incident and to conduct independent investigations
on a non-interference basis. The findings reported herein are from a
limited independent investigation conducted by scientists from the Western
Environmental Research Laboratory of the Environmental Protection Agency.
The speculation by the news agencies of the possible connection with
environmental contamination by nerve gas or radioactive materials was based
on two prior incidents. In 1968, about 6,500 sheep died in Utah following
a nerve gas testing operation at the Army's Dugway Proving Grounds. However,
nerve gas testing at Dugway was officially stopped later in 1968. On
December 18, 1970, an underground test at the Nevada Test Site, code-named
Baneberry, accidentally vented and released radioactive material to the
atmosphere. While some radioactive material was deposited on certain parts
of Utah, the amount measured was several orders of magnitude below that
required to produce acute mortality in sheep. Hence, neither of the two
causes speculated appeared plausible, so other possible causes were considered
by the Western Environmental Research Laboratory scientists. Based on a
knowledge of the ecology of the area, the type of livestock involved, and the
season of the year, it was suspected that a poisonous plant (Halogeton
glomeratus) could be the cause of death.
Because of repeated speculation in the press that the sheep could have been
killed by radiation, the Nevada Operations Office of the Atomic Energy
Commission (NVOO/AEC) decided to offer assistance with the investigation
and requested the participation of Western Environmental Research Laboratory
scientists. The Western Environmental Research Laboratory provided a veteri-
narian and a botantist to the five-man team which was to be sent to the site.
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Other members of the team were from the AEC and included an
environmental scientist, a health physicist and public information
officer.
The team was instructed to observe the investigation conducted by the
Utah Department of Agriculture, obtain all pertinent facts surrounding
the incident, and to offer any appropriate assistance required to expeditiously
investigate the incident and determine the cause of death. Upon arrival
at Garrison on January 7, 1971, the team met with a team of investigators
from the University of Utah. The two groups proceeded to the site, a sheep
range in Antelope Valley some 18 miles southeast of Garrison, Utah.
DESCRIPTION OF HALOGETON
Halogeton glomeratus is a member of the Goosefoot family. It is an
annual, growing to a height of 5 to 60 cm. The plant resembles young
Russian thistle (Salsola kali var. tenuifolia). The leaves are generally
smooth, fleshy and sausage shaped. They are usually from 0.5 to 2 cm long,
with a solitary white-colored hair about 3 mm long growing out of the
extreme tip.
Young halogeton plants are dark green to blue-green with red stems. Follow-
ing fall and winter frosts the plant fades and becomes straw colored. Plants
growing in dense stands may attain a height of only a few cm as shown in
Figure 1; whereas widely spaced plants under favorable moisture conditions
may reach a height of 30 - 60 cm. Regardless of its height this plant
produces viable seed in relative abundance.
Halogeton thrives in both saline and non-saline soils of semiarid regions.
Heavy infestations of halogeton occur in areas where the soil has been
disturbed. Prime areas of growth are overgrazed ranges, sheep trails,
along railroad beds, road margins, burned-over areas, and abandoned farm
lands.
Halogeton probably originated as a contaminant in agricultural seeds
which were imported from Russia. It was first recorded in the mid-
thirties in Nevada. Since then it has spread over approximately two
million acres in Nevada, Utah, Idaho, Wyoming, and Montana. Some
occurrences have also been reported in California, Oregon, and Colorado.
2
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Figure 1. Close-up view of Halogeton glomeratus on the sheep
range at Garrison, Utah. With the exception of the
one horsebrush plant in the left background, the
remainder of the plants shown are halogeton. The
halogeton plants in this area did not exceed a height
of 20 cm.
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The toxicity of halogeton is based on its oxalate content. This plant
becomes more toxic as the growing season advances, and is most toxic
when it is frozen and dry, primarily because of the increase in concen-
tration of oxalates particularly in the form of soluble oxalic acid.
It is unpalatable while green but it is apparently acceptable to animals
during fall and winter.
Sheep are the most frequently poisoned livestock from halogeton, although
cattle have been occasionally affected. Losses occur mostly when
hungry animals are trailed through or grazed on heavily infested areas.
The amount of halogeton that will kill a sheep varies according to the
condition of the plant and is reported to be from 340 to 500 grams.
Animals fasted for a day or longer are poisoned by smaller amounts than
sheep that have been feeding on other forage. The first symptoms of
halogeton poisoning may occur in four to six hours after an animal
eats a lethal amount. Poisoned animals have difficulty in breathing,
appear weak and drowsy, show drooling and white froth about the mouth,
have nasal discharge (usually bloody), lapse into a coma, and die
within a few hours.
FIELD EVALUATION
The vegetation of the area was juniper and sagebrush with large stands of
halogeton throughout. In certain areas of the range, more than 60 percent
of the vegetation present was halogeton. Figure 2 shows a panoramic view of
the area and illustrates the vegetation characteristics. The vegetation in
the foreground is predominantly halogeton. The light colored areas which are
more distant are also halogeton. Of the various ecological factors which
could have resulted in excessive halogeton population of the area, overgrazing
appeared to be the most probable cause. Apparently, past grazing practices
had been sufficient to produce the necessary soil disturbance and to limit
the population of competitive non-toxic plants.
Another factor of undefined significance was the limited availability of
water. The sheep satisfied their need for water by grazing near the snow
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Figure 2. Plant populations on the Garrison range. Halogeton
dominates the population in the immediate foreground,
with juniper and sage appearing more distant.
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line and eating snow. While this is not an unusual range practice, it
may be a contributing factor during times of significant nutritional
stress.
The dead sheep, pregnant Columbia ewes, presented several consistent
external signs. Most died in a position of sternal recumbency with
little evidence of severe pain prior to death. Figure 3 shows the
carcasses strewn throughout the area. Occasionally some would present
evidence of contraction of the neck muscles, since the head was
drawn back. All the dead animals had reddish froth from the nose as
shown in Figure 4. Interspersed among the carcasses were several animals
in various stages of morbidity. All morbid animals exhibited dyspnea.
Several were able to walk, but were unsteady and exhibited flexure of the
distal joints in both front and rear legs. Other animals in recumbent
positions were unable to stand. Although they would attempt to rise with
prodding, they would fall before attaining a full standing position. Upon
talking with the owner, it was learned that no deaths had occurred prior to
January 21. About noon of January 22, approximately 1,250 of the original
flock of 2,600 were dead.
Permission was requested and obtained from the owner to collect tissue
and ingesta samples from the dead animals. Although the number of samples
collected was less than intended, some useful information was obtained.
While the history and symptoms along with the widespread distribution
of halogeton throughout the area were almost conclusive enough for a diagnosis,
an examination of rumen contents further enhanced this viewpoint. Prior
to laboratory analysis of the samples gross observation indicated the
halogeton content of the engorged rumen to be about 50 percent.
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Figure 3. Garrison sheep range strewn with carcasses,
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Figure 4. Dead sheep showing blood-tinged frothy exudate from the nose.
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RESULTS AND DISCUSSION
Analytical results of the rumen contents collected from the three sheep
are shown in Table 1, indicating an average halogeton content of 44 percent.
It may be of interest to calculate the halogeton content of the rumens
of these sheep for comparison to the amount reported as fatal for sheep.
If the capacity of the sheep stomach is assumed to be approximately 15 liters
and the capacity of the rumen alone is 80 percent of this value, or 12 liters,( ^
the halogeton content of the entire stomach would have been 6.6 kg, with 5.3 kg
contained in the rumen. As mentioned the lethal amount varies according to a
number of parameters and is reported to be 340 - 500 g. If 420 g is
assumed as an average amount to produce acute lethality, these animals had
an average rumen content which was about 12 times this amount.
The one thyroid collected weighed 7 grams and contained 350 pCi I/g as
of January 22. Using reported values for I in sheep thyroid; namely,
(1) peak activity is attained in 12 - 15 days of daily ingestion, and (2)
the effective half-life is about six days; the calculated peak concentration
would be about 3,500 pCi/g. This calculated value is in agreement with
other thyroid measurements made at a similar time on other animal thyroids
collected from the off-site area.
The observations and findings reported here indicate the probable cause
of death to be oxalate poisoning resulting from ingestion of fatal amounts
of halogeton. This diagnosis was in agreement with that contained in
the final report issued by the Utah Department of Agriculture. In the Utah
report, "Halogeton Poisoning in Sheep, Antelope Valley (near Garrison),
Utah, January 1971," Dr. F. James Schoenfeld, Utah State Veterinarian, and others,
detailed all necropsy and laboratory findings and concluded that the cause of
death was halogeton poisoning.
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Table 1. Analytical Results of Rumen Contents from Three Sheep
Sheep #1
Scientific Name
Artemisia arbuscula
Halogeton glomeratus
Unidentified grass
Cowania stansburiana
Herbaceous Fragments
Common Name
Black sagebrush
Halogeton
Grass
Cliffrose
Plant Parts
Stems-Leaves
Stems-Leaves-Seeds
Stems-Leaves
Stems-Leaves
Fragments
Composition
67
21
10
1
1
Total 100 %
Sheep #2
Scientific Name
Halogeton glomeratus
Artemisia arbuseula
Unidentified grass
Atriplex oonfertifolia
Herbaceous fragments
Artemisia tridentata
Unidentified shrub
Common Name
Halogeton
Black sagebrush
Grass
Shadscale
Big sagebrush
Plant Parts
Stems-Leaves
Stems-Leaves
Stems-Leaves
Stems-Leaves
Fragments
Leaves
Leaves
Composition
47
45
5
2
1
Trace
Trace
Total 100 %
Sheep #3
Scientific Name
Halogeton glomeratus
Artemisia arbuscula
Unidentified grass
Cowania stansburiana
Ephedra
Juniperus osteosperma
Unidentified shrub
Common Name
Halogeton
Black sagebrush
Grass
Cliffrose
Mormon tea
Utah juniper
Plant Parts
Stems-Leaves-Seeds
Stems-Leaves
Stems-Leaves
Stems-Leaves
Stems
Leaves
Leaves
Composition
63
33
3
1
Trace
Trace
Trace
Total 100
10
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REFERENCES
1. J. M. Fenley, How to Live with Halogeton by Limiting Its Spread,
Agricultural Extension Service, University of Nevada Bulletin-106,
1952.
2. C. W. Cook and L. A. Stoddart, The Halogeton Problem in Utah:,
Bulletin 364, Agricultural Experiment Station, Utah State Agri-
cultural College, November 1953.
3. K. W. Brown and D. D. Smith, The Poisonous Plants of the U. S. Atomic
Energy Commission's Nevada Test Site, Nye County, Nevada. SWRHL-33r.
December 1966.
4. Poisonous Grassland Plants, Section 4 of a series -- Pasture and Range
Plants, Phillips Petroleum Company, Copyright 1957.
5. Farmers' Bulletin No. 2106, United States Department of Agriculture,
16 Plants Poisonous to Livestock in Western States, prepared by
the Animal Disease and Parasite Research Division and the Crops
Research Division, Agricultural Research Service, Washington, D. C.,
1951. Revised June 1963. Slightly revised August 1964. Available
from U. S. Government Printing Office.
6. J. D. Grossman and S. Sisson, The Anatomy of th'e Domestic Animals,
W. B. Saunders Company, Philadelphia and London, 1948.
7. L. K. Bustad, E. E. Elefson, E. C. Watson, D. H. Wood, H. A. Ragan,
I 131 in the Thyroid of Sheep and in Food, Thyroid, and Milk of Dairy
Cows, Hanford Biology Research Annual Report for 1962, HW-76000, p. 60-62,
Hanford Atomic Products Operation, Richland, Wash., 1963.
11
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DISTRIBUTION
1 20 WERL, Las Vegas, Nevada
21 Robert E. Miller, Manager, NVOO/AEC, Las Vegas, Nevada
22 Robert H. Thalgott, NVOO/AEC, Las Vegas, Nevada
23 Thomas H. Blankenship, NVOO/AEC, Las Vegas, Nevada
24 Henry G. Vermillion, NVOO/AEC, Las Vegas, Nevada
25 Donald W. Hendricks, NVOO/AEC, Las Vegas, Nevada
26 Elwood M. Douthett, NVOO/AEC, Las Vegas, Nevada
27 Jared J. Davis, NVOO/AEC, Las Vegas, Nevada
28 Ernest D. Campbell, NVOO/AEC, Las Vegas, Nevada
29 - 30 Technical Library, NVOO/AEC, Las Vegas, Nevada
31 Chief, NOB/DNA, NVOO/AEC, Las Vegas, Nevada
32 Joseph J. DiNunno, Office of Environmental Affairs, USAEC, Washington, D.C.
33 Martin B. Biles, DOS, USAEC, Washington, D.C.
34 Roy D. Maxwell, DOS, USAEC, Washington, D.C.
35 Assistant General Manager, DMA, USAEC, Washington, D.C.
36 Gordon C. Facer, DMA, USAEC, Washington, D.C.
37 John S. Kelly, DPNE, USAEC, Washington, D.C.
38 Fred J. Clark, Jr., DPNE, USAEC, Washington, D.C.
39 John R. Totter, DBM, USAEC, Washington, D.C.
40 John S. Kirby-Smith, DBM, USAEC, Washington, D.C.
41 L. Joe Deal, DBM, USAEC, Washington, D.C.
42 Charles L. Osterberg, DBM, USAEC, Washington, D.C.
43 Rudolf J. Engelmann, DBM, USAEC, Washington, D.C.
44 Philip W. Allen, ARL/NOAA, Las Vegas, Nevada
45 Gilbert J. Ferber, ARL/NOAA, Silver Spring, Maryland
46 Stanley M. Greenfield, Assistant Administrator for Research § Monitoring,
EPA, Washington, D.C.
47 Joseph A. Lieberman, Deputy Assistant Administrator for Radiation Programs,
EPA, Rockville, Maryland
48 Paul C. Tompkins, Act. Dir., Div. of Criteria £ Standards, Office of
Radiation Programs, EPA, Rockville, Maryland
49 50 Charles L. Weaver, Act. Dir., Div. of Surveillance § Inspection,
Office of Radiation Programs, EPA, Rockville, Maryland
51 Ernest D. Harward, Act. Dir., Div. of Technology Assessment, Office of
Radiation Programs, EPA, Rockville, Maryland
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Distribution (continued)
52 William A. Mills, Dir., Twinbrook Research Laboratory, EPA, Rockville, Md
53 Gordon Everett, Dir., Office of Technical Analysis, EPA, Washington, D.C.
54 Bernd Kahn, Radiological Engineering Lab., EPA, Cincinnati, Ohio
55 Regional Admin., Region IX, EPA, San Francisco, California
56 Eastern Environmental Radiation Laboratory, EPA, Montgomery, Alabama
57 William C. King, LLL, Mercury, Nevada
58 Bernard W. Shore, LLL, Livermore, California
59 James E. Carothers, LLL, Livermore, California
60 Roger E. Batzel, LLL, Livermore, California
61 Howard A. Tewes, LLL, Livermore, California
62 Lawrence S. Germain, LLL, Livermore, California
63 Paul L. Phelps, LLL, Livermore, California
64 William E. Ogle, LASL, Los Alamos, New Mexico
65 Harry J. Otway, LASL, Los Alamos, New Mexico
66 George E. Tucker, Sandia Laboratories, Albuquerque, New Mexico
67 Wright H. Langham, LASL, Los Alamos, New Mexico
68 Harry S. Jordan, LASL, Los Alamos, New Mexico
69 Arden E. Bicker, REECo., Mercury, Nevada
70 Clinton S. Maupin, REECo., Mercury- Nevada
71 Byron F. Murphey, Sandia Laboratories, Albuquerque, New Mexico
72 Melvin L. Merritt, Sandia Laboratories, Albuquerque, New Mexico
73 Richard S. Davidson, Battelle Memorial Institute, Columbus, Ohio
74 R. Glen Fuller, Battelle Memorial Institute, Las Vegas, Nevada
75 Steven V. Kaye, Oak Ridge National Lab., Oak Ridge, Tennessee
76 Leo K. Bustad, University of California, Davis, California
77 Leonard A. Sagan, Palo Alto Medical Clinic, Palo Alto, California
78 Vincent Schultz, Washington State University; Pullman, Washington
79 Arthur Wallace, University of California, Los Angeles, California
80 Wesley E. Niles, University of Nevada, Las Vegas, Nevada
81 Robert C. Pendleton, University of Utah, Salt Lake City: Utah
82 William S. Twenhofel, U. S. Geological Survey, Denver, Colorado
83 Paul R. Fenske, Desert Research Institute, University of Nevada,
Reno, Nevada
84 John M. Ward, President, Desert Research Institute, University of
Nevada, Reno, Nevada
85 - 86 DTIE, USAEC, Oak Ridge, Tennessee (for public availability)
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