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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.


Publication Date: 9/95


The active ingredient deltamethrin (NRDC 161 and RU 22974) is found in a variety of commercial insecticide products. Trade names for products containing deltamethrin include Butoflin, Butoss, Butox, Cislin, Crackdown, Cresus, Decis, Decis-Prime, K-Othrin, and K-Otek (1, 4, 7, 8, 20).


Deltamethrin is used in the U.S. in the Environmental Health Market. It is being sold in many countries for agricultural, public health and livestock applications (7, 20).


Deltamethrin is a pyrethroid insecticide that kills insects on contact and through digestion. It is used to control apple and pear suckers, plum fruit moth, caterpillars on brassicas, pea moth, aphids (apples, plums, hops), winter moth (apples and plums), codling and tortrix moths (apples). Control of aphids, mealy bugs, scale insects, and whitefly on glasshouse cucumbers, tomatoes, peppers, potted plants, and ornamentals. It also controls numerous insect pests of field crops. Formulations include emulsifiable concentrates, wettable powders, ULV and flowable formulations and granules. There are no known incompatibilities with other common insecticides and fungicides (1, 4, 5, 7).

Deltamethrin is a synthetic insecticide based structurally on natural pyrethrins, which rapidly paralyze the insect nervous system giving a quick knockdown effect (13). Deltamethrin has a rapidly disabling effect on feeding insects and for this reason there is hope that it may be useful to control the vectors of "non-persistent" viruses (viruses that can be passed on by the vector within a few minutes of starting to feed on the plant) (3). Deltamethrin's mode of action is thought to be mainly central in action, or at least originate in higher nerve centers of the brain. Death of insects seems to be due to irreversible damage to the nervous system occurring when poisoning lasts more than a few hours (11). Deltamethrin poisoning occurs through cuticular penetration or oral uptake. The susceptibility of insects is dependent on a variety of factors and can vary, as with many insecticides, according to the environmental conditions. Flies are most susceptible to pyrethroid poisoning shortly before dawn. The LD50 drops by the factor of 2 as compared to full daylight activity (13, 20).

Many pyrethroids are not very active against cattle ticks, but some alpha cyano compounds (of which deltamethrin is one) have higher activity than organophosphates or amidines, the former standard compounds for this purpose (13). Deltamethrin has very good residual activity for outdoor uses (field crops, cattle dip, tsetse) and for indoor uses (mosquitoes, stable flies, horsefiles, fleas, cockroaches, stored product insects) (9, 20). Deltamethrin has very broad spectrum control. It is considered the most powerful of the synthetic pyrethroids. It is up to three orders more active than some pyrethroids (14, 20).



Deltamethrin produces typical type II motor symptoms in mammals (16). Type II symptoms include a writhing syndrome in rodents, as well as copious salivation (3). The acute oral LD50 in male rats ranged from 128 mg/kg to greater than 5,000 mg/kg depending on the carrier and conditions of the study (2, 10); the LD50 for female rats was 52 mg/kg and other published values range from 31 to 139 mg/kg. Values ranging from 21 to 34 mg/kg were obtained for mice; while dogs had a reported LD50 of 300 mg/kg. The intravenous LD50 in rats and dogs was 2 to 2.6 mg/kg, and the dermal LD50 was greater than 2,940 mg/kg (1, 4, 16). The acute percutaneous LD50 for rats was reported to be greater than 2,000 mg/kg; greater than 10,000 mg/kg for quail; and greater than 4,640 mg/kg for ducks (2, 13). The acute dermal LD50 for rabbits was greater than 2,000 mg/kg (1, 4). No skin irritation and slight eye irritation were reported (1). Another study indicated skin irritation in rats and guinea pigs (13).

The signs of poisoning produced in rats by deltamethrin are not the same as those produced by other pyrethroids. Especially characteristic are rolling convulsions. The site of action is considered to be central with little or none of the peripheral component demonstrated for other pyrethroids. The sequence of signs is clearly defined, progressing from chewing, salivation, and pawing to rolling convulsions, tonic seizures, and death. Blood pressure begins to drop promptly, but slowly; it tends to normalize about the time choreoathetosis (abnormal movements of the body of a combined choreic and athetoid pattern) begins but falls precipitously prior to death. The early signs, including choreoathetosis, are reversible, but rats that exhibit a tonic seizure and shock almost always die promptly (18).

Acute exposure effects in humans include the following: ataxia, convulsions leading to muscle fibrillation and paralysis, dermatitis, edema, diarrhea, dyspnea, headache, hepatic microsomal enzyme induction, irritability, peripheral vascular collapse, rhinorrhea, serum alkaline phosphatase elevation, tinnitus, tremors, vomiting and death due to respiratory failure. Allergic reactions have included the following effects: anaphylaxis, bronchospasm, eosinophilia, fever, hypersensitivity pneumonia, pallor, pollinosis, sweating, sudden swelling of the face, eyelids, lips and mucous membranes, and tachycardia (17).

Studies have shown many cases of dermal deltamethrin poisoning after agricultural use with inadequate handling precautions, and many cases of accidental or suicidal poisoning by the oral route at doses estimated to be 2- 250 mg/kg. Oral ingestion caused epigastric pain, nausea, vomiting and coarse muscular fasciculations. With doses of 100-250 mg/kg, coma was caused within 15-20 minutes (16).


In 2-year feeding trials, the reported NEL (no effect level) was 12 mg/kg diet for mice; and 2.1 mg/kg diet for rats. The dose without activity in rats over a 90-day period was 10 mg/kg/day (1, 2).

Suspected chronic exposure effects in humans include the following: choreoathetosis, hypotension, prenatal damage and shock (17). Workers exposed to deltamethrin during its manufacture over 7-8 years experienced transient cutaneous and mucous membrane irritation, which could be prevented by use of gloves and face masks. No other ill effects were seen (16).

Reproductive Effects

A reproductive 3-generation study in rats reported a reproductive NOEL to be greater than 2.5 mg/kg/day. Levels tested were 0, 0.1, 1.0 and 2.5 mg/kg/day (19). Oral administration of deltamethrin to mice on days 7 to 16 of gestation produced a dosage-related reduction of weight gain but no effect on the number of implants, fetal mortality, fetal weight or malformations (18).

Teratogenic Effects

There were no reported teratogenic effects in mice, rats and rabbits (1). Deltamethrin has no teratogenic activity (16).

Mutagenic Effects

There were no mutagenic effects in mice, rats and rabbits (1). Deltamethrin has no mutagenic activity (16).

Carcinogenic Effects

No information was available.

Organ Toxicity

Deltamethrin is hydrolyzed by liver microsomal enzymes to 3- (2,2dibromovinyl) 2,2-cyclopropane carboxylic acid and 3-phenoxybenzaldehyde (3).

Fate in Humans and Animals

Elimination of the compound in the rat occurs within 2-4 days of administration (1). Pyrethroid-poisoned mice and rats die during seizures within one or two hours after treatment (11). Metabolites of the cyano substituent are eliminated more slowly, and tissue levels remain relatively high, especially in the skin and stomach. Deltamethrin at an oral dosage of 50 mg/kg produces a marked increase of cGMP but not cAMP in the brain of rats (18). Metabolism of deltamethrin in rats involves rapid ester cleavage and hydroxylation. Deltamethrin has a half-life in the rat brain of 1 to 2 days, but it is more persistent in body fat, with a half-life of 5 days (16).

In mammals, the point of death from deltamethrin poisoning is sharply defined by respiratory or cardiac failure (11). Rats and dogs given oral doses of 10 mg/kg/day for 13 weeks exhibited some motor symptoms but no fatalities or pathological changes. The dogs exhibited diarrhea and vomiting. In another study, rats given 15 daily oral doses of 10 mg/kg showed severe motor symptoms, but a full neuropathological examination of the central nervous system showed no pathological changes (16).

Physical signs of deltamethrin poisoning can include dermatitis after skin contact; exposure to sunlight can make it worse. Severe swelling of the face including lips and eyelids can occur. Symptoms and consequences of poisoning include: sweating, fever, anxiety and rapid heartbeat. If swallowed, symptoms are likely to include feeling sick, vomiting, diarrhea, twitching of arms and legs, and convulsions if poisoning is severe (12).

A health survey of 199 workers who repacked pyrethroid insecticides into boxes by hand indicated that about two-thirds of the workers had a burning sensation and tightness and numbness on the face, while one-third had sniffs and sneezes. Abnormal sensations in the face, dizziness, tiredness and red rashes on the skin were more common in summer than in winter. Workers did not wear protective gloves in summer because of the heat. The symptoms usually occurred thirty minutes after exposure to the pyrethroids and rarely lasted more than 24 hours (12).

Cold burning and numbness of the skin occurred to two-thirds of humans in a Chinese factory exposed to about 5-12 mg deltamethrin per cubic meter of air. The other third suffered from sneezing and eye-watering. In addition, headache, heartburn and skin spots were reported, and these symptoms were dependent on the time of the year (13).

A study was conducted of pesticide workers (one mixer, one bagger, and three spraymen) who applied 5% deltamethrin to the inside walls of houses at an active ingredient rate of 0.05 g/m2. The work lasted two days. Each man wore overalls (washed daily), shoes, and a hat. The mixer wore a cartridge- type respirator and rubber gloves. The bagger wore the same, plus an apron. The spraymen did not wear masks. All practiced good personal hygiene. No complaints were received from the workers and no effect of exposure was detected by clinical examination (18).

A second trial lasting about five weeks involved three baggers, two mixers, two helpers, and nine spraymen. Conditions, including protective equipment, were the same except that all spraymen wore disposable face masks. Six of the nine spraymen, all baggers, and one of two mixers complained of "heat around the eyes," "heat in the face," or "heat in the face and upper shoulders" plus "burning of the eyes" and tiredness. Complaints lasted until evening of each work day. There were no positive clinical signs of exposure to deltamethrin by any of the workers (18).


Effects on Birds

The reported 8-day LC50 for ducks was greater than 4,640 mg/kg diet; and greater than 10,000 mg/kg diet for quail (2).

Effects on Aquatic Organisms

As is common with many pyrethoids, deltamethrin has a high toxicity to fish under laboratory conditions. However, in field conditions under normal conditions of use, fish are not harmed. Deltamethrin had an impact on aquatic herbivorous insects. This impact led to an increase of algae. Although the fish (fathead minnows) accumulated the deltamethrin, no mortality could be observed (13, 20).

In laboratory trials, the LC50 for fish was 1-10 micrograms/l. Aquatic fauna, particularly crustacea, may be affected, but fish are not harmed under normal conditions of use (2).

Effects on Other Animals (Nontarget species)

Deltamethrin is considered toxic to bees (1). The 24 hour oral LD50 for technical deltamethrin fed to bees was 0.079 micrograms ai/bee; and the 24 hour oral LD50 for the EC formulation of deltamethrin was equal to or greater than 0.4 micrograms ai/bee (11). The reported contact LD50 for bees is 0.05 micrograms ai/bee, but with a field rate of only 12 g ai/ha, the hazard ratio is very low (240). A hazard ratio is defined as exposure (g ai/ha) divided by intrinsic toxicity (LD50 in micrograms ai/bee). The hazard ratio is a risk estimate, or an indicator of the level of mortality that is to be expected in the field. A ratio of greater than 50 indicates the chemical is not dangerous to bees. A ratio between 50 and 2,500 indicates a field test is needed, and over 2,500 indicates the compound is considered dangerous to bees. Although the intrinsic toxicity of deltamethrin is similar to that of organophosphates such as azinphos-methyl, the low rate of use of deltamethnn makes its hazard ratio considerably lower (the azinphos-methyl hazard ratio is 8937) (15).

Deltamethrin is very toxic over long periods to the predatory mite Typhodromum pyri. The parasitic wasp Encarsia formosa, released in greenhouses to combat whitefly, is too sensitive to allow a treatment with deltamethrin against excessive outbreaks of whiteflies (13). Deltamethrin had little or no effect on adults or cocoons of Apanteles plutellae, a parasite of the diamond back moth in India. Spiders were also indicated to be strongly affected in field investigations (3, 15).


Breakdown of Chemical in Soil and Groundwater

In soil, degradation occurs within 1-2 weeks (1).

Breakdown of Chemical in Surface Water

Deltamethrin in pond water was rapidly adsorbed, mostly by sediment, in addition to uptake by plants and evaporation into the air (13).

Breakdown of Chemical in Vegetation

About 10 days after use, there are no deltamethrin residues observed on plants. There is no known phytotoxicity to crops (1, 5).


There is no degradation of deltamethrin in storage for 6 months at 40[ring]C. It is extremely stable to atmospheric oxygen. Under UV irradiation and in sunlight, a cistrans isomerization, splitting of the ester bond, and loss of bromine occur (1). Deltamethrin is noncorrosive to metals (1). By contrast with natural pyrethrins, it is stable to air and sunlight (7, 14). When exposed to air and light, deltamethrin remains unchanged after two years at 40[ring] C. It is considered stable when exposed to air and sunlight, and more stable in acid than alkaline media (9).

Deltamethrin is a lipophilic compound of high molecular weight and consequent low volatility. It is not used for soil application in agricultural practice because it moves neither in the vapor nor water phase and has no systemic action (11, 20).

Exposure Guidelines:

ADI: 0.01 mg/kg (9)

Physical Properties:

Appearance: colorless crystalline powder (9); white or slightly beige powder (16)
Molecular weight: 505.24 (9)
Molecular formula: C22H19Br2NO3 (6, 9, 16)
CAS No.: 52918-63-5 (1)
Chemical names: cyano(3-phenoxy-phenyl)methyl; 3-(2,2dibromoethenyl)-2,2-dimethylcyclopropanecarboxylate (CA); [partial diff]-cyano-m-phenoxybenzyl, (1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethyl -cyclopropanl-carboxylate, (S)-[partial diff]-cyano-3-phenoxybenzyl (1R)-cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane-carboxylate (IUPAC) (1)
Chemical Class/Use: pyrethroid/contact and stomach poison insecticide (2)
Solubility in water: less than 0.1 mg/l (1) Insoluble: < 1 ppm at room temperature (8). 0.002 mg/l at 20 degrees C (9). Almost insoluble (3)
Solubility in other solvents: in kerosene and isoalkanes, less than 0.5, isopropanol 0.6, ethanol 1.5, xylene 25, methylene chloride 70 (all in g/100 g at 20 degrees C) (1). In acetone 500g/1, benzene 450 g/l, dimethyl sulfoxide 450 g/l, cyclohexanone 750 g/l, dioxane 900 g/l all at room temperature (9), toluene 250 g/l (18)
Melting point: 98-101 degrees C (1, 2, 4)
Boiling point: Decomposes on distillation (1)
Vapor pressure: 2 x 10 to the minus 8 mbar at 25 degrees C (1). Non-volatile: <1 x 10 to the minus 7 mmHg (8). 1.5 x 10 to the minus 8 mmHg at 25 degrees C (14)


AgrEvo Environmental Health, Inc.
95 Chestnut Ridge Rd.
P.O. Box 30
Montvale, NJ 07645
Telephone: 201-307-9700
Fax: 201-307-3281

Reviewed by Basic Manufacturer:

Comments solicited: October, 1994
Comments received: February, 1995


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  12. Hurst, Peter, Alistair Hay and Nigel Dudley. 1991. The Pesticide Handbook. Journeyman Press. London, Concord, MA.
  13. Haug, G. and H. Hoffman (eds). 1990. Chemistry of Plant Protection 4: Synthetic Pyrethroid Insecticides: Structures and Properties. Springer-Verlag. Berlin, Heidelberg, New York.
  14. Spencer, E. Y. 1981. Guide to the Chemicals Used in Crop Protection. 7th edition. Publication 1093. Research Branch. Agriculture Canada.
  15. Elzen, G. W. 1989. Sublethal Effects of Pesticides on Beneficial Parasitoids. In: Pesticides and Non-target Invertebrates. Ed. by Paul C. Jepson. Intercept Ltd. Dorset, England. pp 129-150.
  16. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Classes of Pesticides, Vol. 2. Academic Press, Inc., NY.
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  20. Review by AgrEvo. February, 1995.