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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.



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).


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).


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).



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).


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).


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).


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).


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)


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


  1. Meister, R.T. (ed.). 1995. Farm Chemicals Handbook '95. Meister Publishing Company. Willoughby, OH.
  2. U.S. Environmental Protection Agency. 1995. Imidacloprid; Pesticide Tolerance and Raw Agricultural commodities. 40 CFR Part 180 Section 472.
  3. Kidd, H. and D. James (eds.). 1994. Agrochemicals Handbook. Third Edition. Royal Society of Chemistry. Cambridge, England.
  4. 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.
  5. 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.
  6. Federal Register. Imidacloprid; Pesticide Tolerances. July 5, 1995. 60(128): 34943-24945.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. Placke, F.J. and E. Weber. 1993. Method of Determining Imidacloprid Residues in Plant Materials. Pflanzenschutz-Nachrichten Bayer. 46(2): 109-182.