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
Assessment Program.
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Pesticide
Information
Profile
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Imidacloprid
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TRADE OR OTHER NAMES
Imidacloprid is found in a variety of commercial insecticides. The
products Admire, Condifor, Gaucho, Premier, Premise, Provado, and Marathon all
contain imidacloprid as the active ingredient (1).
REGULATORY STATUS
Imidacloprid is a General Use Pesticide, and is classified by EPA as
both a toxicity class II and class III agent, and must be labeled with the
signal word "Warning" or "Caution" (1). There are tolerances for residues of
imidacloprid and its metabolites on food/feed additives ranging from 0.02 ppm
in eggs, to 3.0 ppm in hops (2).
INTRODUCTION
Imidacloprid is a systemic, chloro-nicotinyl insecticide with soil, seed
and foliar uses for the control of sucking insects including rice hoppers,
aphids, thrips, whiteflies, termites, turf insects, soil insects and some
beetles. It is most commonly used on rice, cereal, maize, potatoes,
vegetables, sugar beets, fruit, cotton, hops and turf, and is especially
systemic when used as a seed or soil treatment. The chemical works by
interfering with the transmission of stimuli in the insect nervous system.
Specifically, it causes a blockage in a type of neuronal pathway
(nicotinergic) that is more abundant in insects than in warm-blooded animals
(making the chemical selectively more toxic to insects than warm-blooded
animals). This blockage leads to the accumulation of acetylcholine, an
important neurotransmitter, resulting in the insect's paralysis, and
eventually death. It is effective on contact and via stomach action (3).
Imidacloprid based insecticide formu-lations are available as dustable
powder, granular, seed dressing (flowable slurry concentrate), soluble
concentrate, suspension concentrate, and wettable powder (1). Typical
application rates range from 0.05 - 0.125 pounds/acre. These application
rates are considerably lower than older, traditionally used insecticides. It
can be phytotoxic if it is not used according to manufacturer's
specifications, and has been shown to be compatible with fungicides when used
as a seed treatment to control insect pests (4).
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Imidacloprid is moderately toxic. The oral dose of technical grade
imidacloprid that resulted in mortality to half of the test animals (LD50) is
450 mg/kg body weight in rats (1), and 131 mg/kg in mice (3). The 24-hour
dermal LD50 in rats is >5,000 mg/kg. It is considered non-irritating to eyes
and skin (rabbits), and non-sensitizing to skin (guinea pigs) (3). Some
granular formulations may contain clays as inert ingredients that may act as
eye irritants. In acute inhalation toxicity tests with rats, the airborne
concentration of imidacloprid that resulted in mortality to half of the test
organisms (LC50) is > 69 mg/meters cubed air in the form of an aerosol, and
>5323 mg/meters cubed air in the form of dust. These values represent the
maximum attainable airborne concentrations (3).
Signs and Symptoms of Poisoning
Although no account of human poisoning was found in the literature, signs
and symptoms of poisoning would be expected to be similar to nicotinic signs
and symptoms, including fatigue, twitching, cramps, and muscle weakness
including the muscles necessary for breathing (5).
CHRONIC TOXICITY
A 2-year feeding study in rats fed up to 1,800 ppm resulted in a No
Observable Effect Level (NOEL) of 100 ppm (5.7 mg/kg body weight in males and
7.6 mg/kg in females). Adverse effects included decreased body weight gain in
females at 300 ppm, and increased thyroid lesions in males at 300 ppm and
females at 900 ppm. A 1-year feeding study in dogs fed up to 2,500 ppm
resulted in a NOEL of 1,250 ppm (41 mg/kg). Adverse effects included
increased cholesterol levels in the blood, and some stress to the liver
(measured by elevated liver cytochrome p-450 levels) (6).
Reproductive Effects
A three generation reproduction study in rats fed up to 700 ppm
imidacloprid resulted in a NOEL of 100 ppm (equivalent to 8 mg/kg/day) based
on decreased pup body weight observed at the 250 ppm dose level (6).
Teratogenic Effects
A developmental toxicity study in rats given doses up to 100 mg/kg/day by
gavage on days 6 to 16 of gestation resulted in a NOEL of 30 mg/kg/day (based
on skeletal abnormalities observed at the next highest dose tested of 100 mg/kg/day)
(4). In a developmental toxicity study with rabbits given doses of
imidacloprid by gavage during days 6 through 19 of gestation, resulted in a
NOEL of 24 mg/kg/day based on decreased body weight and skeletal abnormalities
observed at 72 mg/kg/day (highest dose tested) (6).
Mutagenic Effects
Imidacloprid may be weakly mutagenic. In a battery of 23 laboratory
mutagenicity assays, imidacloprid tested negative for mutagenic effects in all
but two of the assays. It did test positive for causing changes in
chromosomes in human lymphocytes, as well as testing positive for genotoxicity
in Chinese hamster ovary cells (6).
Carcinogenic Effects
Imidacloprid is considered to be of minimal carcinogenic risk, and is
thus categorized by EPA as a "Group E" carcinogen (evidence of
noncarcinogenicity for humans). There were no carcinogenic effects in a 2-year
carcinogenicity study in rats fed up to 1,800 ppm imidacloprid (2).
Organ Toxicity
In short-term feeding studies in rats, there were thyroid lesions
associated with very high doses of imidacloprid (6).
Fate in Humans and Animals
Imidacloprid is quickly and almost completely absorbed from the
gastrointestinal tract, and eliminated via urine and feces (70-80% and 20-30%,
respectively, of the 96% of the parent compound administered within 48 hours).
The most important metabolic steps include the degradation to 6-chloronicotinic
acid, a compound that acts on the nervous system as described
above. This compound may be conjugated with glycine and eliminated, or
reduced to guanidine (3).
ECOLOGICAL EFFECTS
Effects on Birds
Imidacloprid is toxic to upland game birds. The LD50 is 152 mg/kg for
bobwhite quail, and 31 mg/kg in Japanese quail (1, 3). In studies with red-
winged blackbirds and brown-headed cowbirds, it was observed that birds
learned to avoid imidacloprid treated seeds after experiencing transitory
gastrointestinal distress (retching) and ataxia (loss of coordination). It
was concluded that the risk of dietary exposure to birds via treated seeds was
minimal. Based on these studies, imidacloprid appears to have potential as a
bird repellent seed treatment (7, 8).
Effects on Aquatic Organisms
The toxicity of imidacloprid to fish is moderately low. The 96-hour
LC50 of imidacloprid is 211 mg/l for rainbow trout, 280 mg/l for carp, and 237
mg/l for golden orfe. In tests with the aquatic invertebrate Daphnia, the 48-
hour EC50 (effective concentration to cause toxicity in 50% of the test
organisms) was 85 mg/l (3). Products containing imidacloprid may be very
toxic to aquatic invertebrates.
Effects on Other Animals (Nontarget species)
Imidacloprid is highly toxic to bees if used as a foliar application,
especially during flowering, but is not considered a hazard to bees when used
as a seed treatment (3).
ENVIRONMENTAL FATE
Breakdown of Chemical in Soil and Groundwater
The half-life of imidacloprid in soil is 48-190 days, depending on the
amount of ground cover (it breaks down faster in soils with plant ground cover
than in fallow soils) (9). Organic material aging may also affect the
breakdown rate of imidacloprid. Plots treated with cow manure and allowed to
age before sowing showed longer persistence of imidacloprid in soils than in
plots where the manure was more recently applied, and not allowed to age (10).
Imidacloprid is degraded stepwise to the primary metabolite 6-chloronicotinic
acid, which eventually breaks down into carbon dioxide (11). There is
generally not a high risk of groundwater contamination with imidacloprid if
used as directed. The chemical is moderately soluble, and has moderate
binding affinity to organic materials in soils. However, there is a potential
for the compound to move through sensitive soil types including porous,
gravelly, or cobbly soils, depending on irrigation practices (12).
Breakdown of Chemical in Surface Water
The half-life in water is much greater than 31 days at pH 5, 7 and 9.
No other information was found.
Breakdown of Chemical in Vegetation
Imidacloprid penetrates the plant, and moves from the stem to the tips
of the plant. It has been tested in a variety of application and crop types,
and is metabolized following the same pathways. The most important steps were
loss of the nitro group, hydroxylation at the imidazolidine ring, hydrolysis
to 6- chloronicotinic acid and formation of conjugates (3).
Analytical Methods
Methods are available for determining imidacloprid residues (the 6-
chloropicolyl moiety) in plant materials using HPLC with u.v. detection (13).
PHYSICAL PROPERTIES AND GUIDELINES
Exposure Guidelines:
| RfD: | 0.057 mg/kg/day (2) |
| NOEL: | 5.7 mg/kg/day (2) |
| LEL: | 16.9 mg/kg/day |
| TMRC: | 0.002594 mg/k/day (2) |
| MOE: | 2,500 |
Physical Properties:
| Molecular formula: | C9H10ClN5O2 |
| Molecular weight: | 255.7 |
| CAS #: | 13826-41-3 |
| IUPAC name: | 1-(6-chloro-3-pyridylmethyl)-N-nitroimidazolidin-2-ylideneamine. |
| C.A. name: | 1-[(6-chloro-3-pyridinyl)methyl]-N-nitro-2-imidazolidinimine. |
| Form: | Colorless crystals with a weak characteristic odor. |
| Melting point: | 143.8 degrees C (crystal form 1) 136.4 degrees C (crystal form 2) |
| Solubility in water: | 0.51 g/l (20 degrees C) |
| Solubility in other solvents @ 20 degrees C: | dichloromethane - 50.0 - 100.0 g/l; isopropanol - 1.0-2.0 g/l; toluene - 0.5-1.0 g/l; n-hexane - <0.1 g/l; fat - 0.061 g/100g |
| Vapor pressure: | 0.2 uPa (20 degrees C) (1.5 X 10 to the minus 9 mmHg) |
| Specific gravity/density: | 1.543 (20 degrees C) |
| Stability: | Stable to hydrolysis at pH 5-11. |
| Melting point: | 136.4-143.8 degrees C. |
| Kow log p: | 0.57 (22 degrees C). (3) |
BASIC MANUFACTURER
Bayer Agricultural Products
P. O. Box 4913
Kansas City, MO 64120
Review by Basic Manufacturer:
Comments solicited: May and October, 1995
Comments received: not received
REFERENCES
Meister, R.T. (ed.). 1995. Farm Chemicals Handbook '95. Meister
Publishing Company. Willoughby, OH.
U.S. Environmental Protection Agency. 1995. Imidacloprid; Pesticide
Tolerance and Raw Agricultural commodities. 40 CFR Part 180 Section 472.
Kidd, H. and D. James (eds.). 1994. Agrochemicals Handbook. Third
Edition. Royal Society of Chemistry. Cambridge, England.
Pike, K.S., G.L. Reed, G.T. Graf and D. Allison. 1993. Compatibility
of Imidacloprid with Fungicides as a Seed-Treatment Control of Russian Wheat
Aphid (Homoptera: Aphidae) and Effect on Germination, Growth, and Yield of
Wheat Barley. J.Econ.Entomol. 86(2): 586-593.
Doull, J., C.D. Klassen, and M.O. Amdur (eds.). 1991. Cassarett and
Doull's Toxicology. The Basic Science of Poisons. Fourth Edition. Pergamon
Press, Elmsford, NY.
Federal Register. Imidacloprid; Pesticide Tolerances. July 5, 1995.
60(128): 34943-24945.
Avery, M.L., D.G. Decker and D.L. Fischer. 1994. Cage and Flight Pen
Evaluation of Avian Repellancy and Hazard Associated with Imidacloprid-Treated
Rice Seed. Crop Protection 13(7): 535-540.
Avery, M.L., D. Decker, D.L. Fischer and T.R. Stafford. 1993.
Responses of Captive Blackbirds to a New Seed Treatment. J. Wildl. Manage.
57(3): 652-656.
Scholz, K., and M. Spiteller. 1992. Influence of Groundcover on the
Degradation of 14C-Imidacloprid in Soil. Brighton Crop Protection Conference.
Pests and Diseases. pp. 883-888.
Rouchard, J., F. Gustin and A. Wauters. 1994. Soil Organic Matter
Aging and its Effect on Insecticide Imidacloprid Soil Biodegradation in Sugar
Beet Crop. Toxicol. Environ. Chem. 45(3-4): 149-155.
Hellpointer, E. 1994. Degradation and Translocation of Imidacloprid
(NTN 33893) Under Field Conditions on a Lysimeter. Miles Report No. 106426,
pp. 1-71. Miles Inc., Agricultural Division, PO Box 4913, Kansas City, MO.
Jenkins, J.J. 1994. Use of Imidacloprid for Aphid Control on Apples in
Oregon. Potential for Ground and Surface Water Contamination. Department of
Agricultural Chemistry. Oregon State University, Corvallis, OR.
Placke, F.J. and E. Weber. 1993. Method of Determining Imidacloprid
Residues in Plant Materials. Pflanzenschutz-Nachrichten Bayer. 46(2): 109-182.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
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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