DSHW-1995-002726 - 0901a0688013e568

DEFENSE AND LAUNCH VEHICLE DJ^ON
?.0. BOX 689
BRIGHAM CITY. UT 84302-0689
801-863-35n
DI^IOI THtOKOL
SPACE'DEFENSE'FASTENING SYSTEMS
',r^.s
16 May 1995 ..„„,„.
W300-FY95-141 "'" ''"••''
Document Processing Center (TS-790)
ATTN: FYI Coordinator
Office of Pollution Prevention
and Toxics
U. S. Environmental Protection Agency
401 M Street, S. W.
Washington, D. C. 20460
Re: Possible Adverse Bovine Effects from Molybdenum
Dear FYI Coordinator:
Thiokol Corporation is submitting the enclosed preliminary findings collected in a
recent investigation regarding possible adverse bovine health effects from
molybdenum (CAS 7439-98-7). This information is being submitted as an FYI notice
to apprise EPA of these findings. However, Thiokol does not believe this
information reasonably supports the conclusion that the substance involved presents a
substantial risk to human health or the environment.
As background, in 1956 Thiokol purchased approximately 10,000 acres of high desert
land in a remote area north of the Great Salt Lake for use as an industrial
manufacturing site for solid propulsion products. (The grazing rights to a majority of
these acres were, however, reserved to the rancher who sold the property to Thiokol.)
On this 10,000 acres, Thiokol has approximately 500 buildings, some of which are
used in manufacturing operations; others of which are used for office activities,
storage and testing. Two areas designated for thermal treatment of waste reactive
W300-FY95-141
15 May 1995
Page 3
Sincerely,
J. D. Thompson, Director
Safety, Environmental & Support Services
Thiokol Corporation
Mail Stop 300
P. O. Box 689
Brigham City, UT 84302-0689
Telephone [phone]
J. D. Thompson, Director
Safety, Environmental & Support Services
Enclosure
(jc£:. > Dennis R. Downs, Executive Secretary
Utah Department of Environmental Quality
Division of Solid and Hazardous Waste
'•SEUAlTNARV BINDINGS
"""'•"'e Adverse BoWne
May 2995
01 Investigation
The investigation into the dispersion of molybdenum is centered around M-
225. In order to characterize the extent of this molybdenum plume, grab
samples were collected at several sites around M-225, outlying areas and
background locations. In most cases, three samples of soil, forbes (bushes)
and annual plants, including grasses, were collected from each site. The
sample locations were pinpointed using a Global Positioning System (GPS)
and plotted on a site map. The samples were then analyzed at an EPA
certified CLP Laboratory using Inductively Coupled Plasma Atomic Emission
Spectroscopy (ICP) following EPA method 6010. The results were converted
to a dry weight basis. The cows' drinldng water sources surrounding M-225
were sampled and analyzed as well.
02 Results
Typical background levels for molybdenum in the area range from 2 to 5 ppm
in the grass, <2 to 3 ppm in the forbes, and <2 ppm in the soil. The highest
levels of molybdenum detected are approximately 2,930 ppm in the soil, 2,441
ppm in the grass and 1,949 ppm in the forbes, all of which are in areas directly
adjacent to M-225. These levels drop to approximately 78.6 ppm in the soils,
620 ppm in the grasses and 222 ppm in the forbes within a 1,000 foot circle of
M-225, with most measured levels decreasing rapidly outside of the circle as
distance increases. The grass molybdenum concentration in the affected areas
range from 10 ppm to 2441 ppm. No traces of molybdenum were detected in
the cows' drinking water sources.
03 Potential to Affect Human Health
Primary exposure to humans is low, since M-225 is in a remote location on a
10,000 acre industrial manufacturing site. The risk-based soil cleanup levels
for human exposure in an industrial location based on IRIS data are calculated
to be 10,000 ppm. Our maximum measured soil levels were 2,930 ppm, well
below that standard.
A secondary route of human exposure considered was the ingestion of beef
having elevated molybdenum levels. It is known, from the literature, that
molybdenum accumulates primarily in the liver and that muscle tissue has the
lowest levels of molybdenum accumulation (compared to all other tissue
types). Therefore, ingestion of bovine liver would provide the highest
potential dose of molybdenum. A tissue sample obtained by the rancher's
veterinarian from one of the dead cows which grazed on the area of highest
molybdenum concentration indicated a liver level of 23 ppm. IRIS data
establishes that the only measurable adverse effect from molybdenum
ingestion in humans is a rise in uric acid levels. The literature states that the
lowest level at which an observed adverse effect is seen is at ingestion levels of
10-15 ppm molybdenum/day which after many years of exposure may show a
manifestation of gout. However, the literature states that molybdenum does
not bio-accumulate and is quickly eliminated from cattle once they are taken
off the high molybdenum diet. In fact, the biological half life of molybdenum
is described in terms of hours. In order for an individual to have a potential
for a 10-15 ppm exposure, an individual would need to ingest at least a
kilogram of highly contaminated liver per day for many years. It is highly
unlikely that any individual would be exposed to such a dosage for several
reasons: 1) any cows that die on the pasture would never be used for human
consumption; 2) cattle are on this pasture for a few months in the spring and
fall (no long-term exposure); and 3) yoimg bulls are typically sold to a feed lot
for fattening in preparation for slaughter during which time any high liver
molybdenum levels would quickly be eliminated.
Based on this information, we believe there is no threat to human health.
04 Potential for Animal and Environmental Effects
Cattle are more susceptible to molybdenum exposure than any other animal.
From the literamre, Molybdenum levels in pastures in excess of 10 ppm dry
weight are known to cause a disease called teart, primarily characterized by
chronic severe scours, with anorexia, anemia, lameness and connective tissue
problems. Complex interactions occurring between copper and inorganic
sulfate also play a role in the severity of the symptoms. Little is known about
the mechanism of acute toxicity. Cattle grazing in the M-225 area have the
greatest potential for demonstrating these classical ill effects (scours, lameness,
anorexia, etc.); however, paradoxically, these cattle do not seem to exhibit
some of the classical signs of molybdenum toxicity. The only classical
symptom which they seem to exhibit is that of slight lameness or lethargy
which has only been noted during early spring grazing, not during fall grazing
in this same area, and could be a symptom of most any illness. An elevated
blood urea nitrogen level (BUN) and kidney damage were discovered in an
necropsy performed by the Utah State Diagnostics Laboratory on one of the
dead cows. The rancher's veterinarian also measured BUN levels on some of
the other ill and dead cattle and these were elevated as well. It was the
laboratory's opinion that the most likely cause of that cow's death was kidney
failure. Kidney failure has not been cited in the literature as an effect caused
by overexposure to molybdenum. It is, therefore, inconclusive as to what
extent the death or illness of the cattle is related to exposure to molybdenum.
Literature indicates that, unlike cattle, other ruminants (with the exception of
sheep) and non-ruminants are highly resistant to molybdenum toxicity.
Due to the desert environment, there are no lakes, streams or any other
receiving waters that are impacted by the minimal runoff from the site.
The most shallow aquifer at the treatment site is 620 feet below the surface.
This water source is used for manufacturing.
Molybdenum is an essential nutrient for plant growth; plants are not adversely
affected by high levels.
References
1. Eisler, R. 1989. Molybdenum Hazards to Fish, Wildlife and Invertebrates: A
Synoptic Review. Biological Report 85(1.19) U.S. Fish and Wildlife Service,
Patuxent Wildlife Research Center Laurel, MD.
National Research Center, 1980, Mineral Tolerance of Domestic Animals.
National Academy of Science, Washington D.C.
Friberg L. et al. 1979. Handbook on the Toxicology of Metals.
Elsevier/North-Holland Biomedical Press.