E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Publication Date: 9/93
TRADE OR OTHER NAMES
Commercial products containing the compound have trade names including
Grazon and Tordon. It may be used in formulations with other herbicides such
as bromoxynil, atropine, diuron, 2,4-D, MCPA, triclorpyr, and atrazine among
others. It is also compatible with fertilizers.
Picloram, in the pyridine family of compounds, is a systemic herbicide
used for general woody plant control. It also controls a wide range of broad-
leaved weeds excepting mustards (crucifers). Most grasses are resistant to
picloram so it is used in range management programs.
Picloram is formulated either as an acid (technical product) or as a
potassium salt. The materials in this document refer to the acid form unless
All uses of the pesticide except for the formulations in Tordon 101R and
Tordon RTU, are restricted by the EPA. Restricted Use Pesticides (RUP) may be
purchased and used only by certified applicators.
Picloram is a slightly toxic herbicide and therefore requires the signal
word CAUTION on its label. It is of moderate toxicity to the eyes and only
mildly toxic on the skin (9). There is no documented history of human
intoxication by picloram so symptoms of acute exposure are difficult to
characterize. A possible symptom from massive amounts would be nausea.
The oral LD50 for picloram is 8,200 mg/kg in rats, between 1,061-4,000
mg/kg for mice, between 1,922-3,000 mg/kg for guinea pigs, and between 2,000-
3,500 mg/kg for rabbits. The rabbit dermal LD50 is greater than 4,000 mg/kg,
a level which produced no mortality or toxic signs. Inhalation by a rat of a
formulated product failed to achieve an LC50 and no adverse effects were
observed for two weeks following the administration of the compound (7).
Mice fed large quantities (1,000 to 2,000 mg/kg/day) of picloram for 13
weeks experienced no clinical or blood changes. Females did show decreased
body weight and increased liver weights. Over a wide range of doses (30-1,000
mg/kg/day) for 32 days, no effects were seen in rat livers. Dogs, sheep and
beef cattle fed low levels of picloram for a month experienced no toxic
Multi-generation studies with pregnant rats exposed from gestation
through reproductive cycles to moderate levels (about 180 mg/kg) of picloram
produced no adverse effects on fertility. Pregnant mice fed small amounts of
the herbicide (15 mg/kg) for four days before and 14 days after mating showed
no adverse effect on fertility. While the evidence is limited, it does not
appear likely that the compound would have a significant adverse effect on
human reproduction at low levels of exposure.
No teratogenic effects were seen in the offspring of pregnant rats
exposed to high doses (1,000 mg/kg) during gestation. At even higher doses
(2,000 mg/kg), maternal toxicity was noted but did not induce malformation in
the pups (5). It is unlikely that the compound would pose a significant birth
defect threat in humans.
One test has shown that picloram is mutagenic (for the bacteria
Saccharomyces cerevisiae) and another test has shown that it is not mutagenic
(Ames test) (4). The results from these two experiments make any conclusion
about the mutagenic risks to humans impossible.
Mice fed average doses of 150 mg/kg or 250 mg/kg for 80 weeks and
observed for another ten weeks did not display any carcinogenic effects. Rats
fed 350 or 750 mg/kg for 80 weeks and observed for 33 weeks had no
carcinogenicity in the males. Females developed benign liver tumor nodules
(4). Several other tests have indicated an increased incidence of cancer
among animals treated with picloram. The EPA has determined that these
studies are inadequate based on two criteria. First they concluded that the
tests were not designed properly to fully assess the carcinogenicity of the
compound and second that all of the tests were conducted with picloram that
contained minor contaminants of HCB, a probable human carcinogen, that might
have skewed the results (10). The EPA has stated that the compound is not
classifiable as to its cancer effects in humans.
Mice and rats both had liver changes when fed high doses. Such changes
occurred at doses above 1,000 mg/kg for 13 weeks or 3,000 mg/kg for 32 days
and in rats at doses above 225 mg/kg for 90 days.
Fate in Humans and Animals
Low oral doses of 0.5 and 5 mg/kg were absorbed rapidly from the GI tract
of humans and excreted unchanged in the urine. Half of the product had been
excreted within a day or so. Skin absorbed only a very small amount of the
applied product (1).
Rats had a pattern much like the studies listed above for humans with
doses excreted virtually unchanged in urine and feces within 48 hours.
Picloram does not accumulate in fat and thus would tend not to significantly
accumulate in organisms.
An additive effect is seen when sheep are given moderate amounts of
picloram mixed with slightly larger amounts of 2,4-D over a five day period.
The combination was fatal even when picloram alone did not produce overt signs
of toxicity (4).
No measurable residues were found in milk from cows fed small amounts of
the herbicide in their diets. At higher levels of exposure, milk levels of
picloram were low (0.05 to 0.29 ppm) and declined rapidly upon withdrawal of
picloram from the diet.
Ducks, pheasant, and quail had picloram related LD50 values of greater
than 2,000-5,000 mg/kg, with no mortality seen at even the highest levels.
This indicates that the compound is practically non-toxic to wildfowl (7).
Picloram is moderately to slightly toxic to fish. Rainbow trout had a
picloram related 96-hour LC50 of 19.3 mg/l, while it was 6.3 mg/l for the
technical material in channel catfish (10). The isooctylester was more toxic.
The LD50 for the isooctylester in rainbow trout is 4 mg/l, and in channel
catfish is 1.4 mg/l (5). With LC50 values ranging from 10 to 68 mg/l,
picloram is only slightly toxic to aquatic invertebrates The compound is non-
toxic to bees (9).
The U.S. Fish and Wildlife service has determined that the compound,
because of its persistence, mobility and toxicity to plants, may pose a threat
to endangered plant species. The EPA is developing guidelines to reduce the
potential of affecting these plants (10).
In heavy clay soil, picloram has a half life of slightly over two months.
However, when more organic material is present, the half life of the compound
nearly doubles. Breakdown by soil microorganisms occurs slowly, resulting in
the formation of carbon dioxide (CO2) and the release of a chloride ion (5).
The compound is mobile and relatively persistent in soil and can therefore
leach to groundwater. Picloram has been detected in the groundwater of seven
In water, the action of sunlight is an important mechanism leading to the
breakdown of the product. Herbicide levels in farm ponds which were 1 ppm at
the time of spraying reached 10 ppb in 100 days primarily due to dilution and
the action of sunlight. The movement of picloram in runoff after heavy
rainfall may occur.
Picloram is readily absorbed by plant roots, less so by the foliage, and
is readily translocated throughout plants. It remains stable and intact in
PHYSICAL PROPERTIES AND GUIDELINES
|NOEL: ||(dog) 7 mg/kg/day animal: 150 mg/kg/day, based on multiple effects
|DWEL: ||2 mg/l
|HA: ||0.5 mg/l (lifetime)
|TLV-TWA: ||10 mg/m3
|ADI: ||0.07 mg/kg/day (10)
|RfD: ||0.07 mg/kg/day (EPA)
|LEL: ||35 mg/kg/day (dog)
|CAS #: ||1918-02-1
|Chemical name: ||4-amino-3,5,6-trichloro-2-pyridinecarboxylic acid
|Chemical class/use: ||chlorobenzoic acid herbicide
|Solubility in water: ||430 mg/l (salt. 200,000 mg/l)
|Solubility in other solvents: ||acetone 1.98 g/100 g; ethanol 1.05 g/100 g; benzene 0.02 g/100 g
|Melting Point: ||218-219 degrees C
|Vapor Pressure: ||6.16 x 10 to the minus 7 mm Hg at 35 degrees C
Dow Chemical Company
PO Box 1706
Midland, MI 48640
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received: December, 1992
Newton, Michael and Frank N. Dost, (1984). Biological and Physical
Effects of Forest Vegetation Management. Washington Dept of Natural
Resources, Olympia, WA.
Witt, James M. and Peter C. Scott (No date). A Chemical
Classification of Pesticides, A Technical Regional Training Program in the
Proper and Safe Use of Pesticides. Dept of Agricultural Chemistry, Oregon
State University, Corvallis, OR.
Trabalka, J.R. and C.T. Garten, Jr. (No date). Development of
Predictive Models for Xenobiotic Bioaccumulation in Terrestrial Ecosystems.
Environmental Sciences Div. Publication No. 2037, Oak Ridge National
Laboratory, Oak Ridge, TN.
National Research Council (1983). Drinking Water and Health, Volume
5. Board on Toxicology and Environmental Health Hazards, Commission on Life
Sciences, Safe Drinking Water Committee, National Academy Press, Washington,
National Library of Medicine (1992). Hazardous Substances Databank.
TOXNET, Medlars Management Section, Bethesda, MD.
Beste, C.E., Chairman (1983). Herbicide Handbook of the Weed Science
Society of America. Weed Science Society of America, Champaign, IL.
Forest Service. (1984). Pesticide Background Statements, Vol. I
Herbicides. United States Department of Agriculture, Agriculture Handbook No.
U. S. Environmental Protection Agency (1987). Health Advisory, Office
of Drinking Water.
The Agrochemicals Handbook. (1991). The Royal Society of Chemistry.
Walker, Mary M. and Lawrence H. Keith. (1992). EPA's Pesticide Fact
Sheet Database. Lewis Publishing. Chelsea, MI.
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are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
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