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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: 5/94


Trade names for the older compound fenvalerate included Ectrin, Sanmarton, Sumifly, Sumiflower, Sumitick and Pydrin. The trade name for the new product, esfenvalerate, is Asana XL. The compound may also be listed as S-fenvalerate.


Most products containing esfenvalerate are General Use Pesticides (GUP). The emulsified concentrate formulation is a Restricted Use Pesticide (RUP) because of possible adverse effects to aquatic organisms.


Esfenvalerate has replaced the compound fenvalerate for use in the United States. Much of the data for esfenvalerate is closely applicable to the pesticide fenvalerate because the two compounds contain the same components. The only difference in the two products is the relative proportions of the four separate constituents (isomers). Esfenvalerate has become the principal compound of the two because it results in lower application rates than fenvalerate, is less chronically toxic, and is a more powerful insecticide. The compound contains a much higher percentage of the one insecticidally active isomer (84% for esfenvalerate and 22% for fenvalerate).

Esfenvalerate is a synthetic pyrethroid insecticide which is used on a wide range of pests such as moths, flies, beetles, and other insects. It is used on vegetable crops, tree fruits, and nut crops. It may be mixed with a wide variety of other types of pesticides such as carbamate compounds or organophosphates.



Because esfenvalerate is a relatively new compound it has little usage history. Esfenvalerate is a moderately toxic pesticide and carries the signal word WARNING on the label. Because the two compounds, fenvalerate and esfenvalerate, are made up of the same four constituents (though, in different concentrations) some of the information gained from fenvalerate is applicable here. The bulk of evidence related to acute poisonings in humans due to fenvalerate comes from incidents in India, where nearly 600 cases of poisoning were reported between 1982 and 1988. These cases were due to improper handling of the pesticide. Acute toxic effects were observed in workers and among the general public. Symptoms of acute poisoning included dizziness, stimulation and itching of the skin from contact (which was worsened by sweating and washing). Severe cases of direct contact caused blurred vision, tightness in the chest, and convulsions. The symptoms appear to be reversible (6).

In rats, acute exposure to esfenvalerate produced muscle incoordination, tremors, convulsions, nerve damage and weight loss. The compound may produce nausea, vomiting, headache, temporary nervous system effects such as weakness, tremors and incoordination in domestic animals if accidentally ingested. Esfenvalerate is a strong eye irritant, producing tearing or blurring of vision (9).

The oral LD50 of esfenvalerate is 458 mg/kg in rats. The dermal LD50 is 2000 mg/kg for rabbits, indicating that esfenvalerate is moderately toxic by skin contact. The inhalation LC50 is greater than 2.93 mg/l for rats (9).


Rats and mice fed fenvalerate at concentrations from 0 to 50 mg/kg/day for two years had no compound-related effects except for significant reduction in body weight in rats (13, 14).

Reproductive Effects

In a three-generation rat study, low doses (up to 12.5 mg/kg) of fenvalerate produced no toxicity in offspring. Some maternal toxicity was noted in the second generation at the higher dose. There are no specific data available for esfenvalerate, but it is not expected to cause reproductive effects at low doses based on its similarity to esfenvalerate (9).

Teratogenic Effects

Fenvalerate doses up to 50 mg/kg/day did not produce any birth defects in fetuses when administered to pregnant rabbits on gestation days 6 through 18 and to mice on gestation days 6 through 15. Some maternal toxicity occurred in both rabbits and mice during these studies. It appears that the pesticide would not pose a serious threat to humans at low exposure levels (11, 12).

Mutagenic Effects

Esfenvalerate has no mutagenic effects. Numerous tests in hamsters, mice and rats show no signs of mutagenic activity associated with this compound (9). It is unlikely that it poses mutagenic risk to humans.

Carcinogenic Effects

Rats fed fenvalerate at doses up to 50 mg/kg/day for two years did not develop cancer (13). Another two year rat study conducted over a wide range of doses up to 75 mg/kg resulted in no evidence of cancer (15).

Mice which were fed diets containing small amounts of fenvalerate for two years did not show a significant increase in effects, including cancer (3). It appears that fenvalerate does not cause cancer. Based on the similarity of esfenvalerate to fenvalerate it is not expected to cause cancer (9).

Organ Toxicity

There is no mention of any dose related effects on internal organs of test animals or in human populations in any of the references used for this profile. Externally, contact with the compound may produce a tingling, itchy sensation.

Fate in Humans and Animals

When cows were treated with 0.1 g or 0.5 g of fenvalerate on their skin 0.03% to 0.06% of the applied chemical was found in their milk. When the cows received 5 and 15 mg/l of fenvalerate orally in their rations, the concentrations of fenvalerate in the whole milk increased to a maximum of 0.000048 mg/l and 0.000250 mg/l, respectively. Residues declined to non- detectable levels by day 7 and day 10, respectively. The total secretion of fenvalerate in the milk amounted to very little, 0.44% and 0.64%, of the total dose fed in the diet (2).

Fenvalerate does not appear to be metabolized by the bovine rumen, but is degraded further down the digestive tract. This happens rapidly since less than 0.02% of the parent compound is found in the urine. In addition, the major fenvalerate metabolite, 4-chloro-alpha-(1-methyl ethyl)-benzene acetic acid was not detected in urine. It was estimated that 25% of the parent compound was excreted in the feces (5).

While the data presented here are for fenvalerate, esfenvalerate behaves in a similar manner (10).


Effects on Birds

Esfenvalerate is moderately toxic to birds. Acute oral LD50 value for mallard ducks is 9,932 mg/kg. Dietary LC50 values for the technical material, fenvalerate, are >10,000 ppm in bobwhite quail and 5,500 ppm in mallard ducks (7).

Effects on Aquatic Organisms

Fish are very sensitive to esfenvalerate with 96-hour LC50s of 0.00026 mg/l for bluegill, 0.00026 mg/l for rainbow trout, 0.00134 mg/l for carp, and 0.0019 mg/l for killifish. Daphnia magna, an aquatic invertebrate, has an LC50 of 0.00024 mg/l. The pesticide is very highly toxic to these species. These values are based on laboratory tests with the technical material. Water turbidity, such as would be found in the field, tends to reduce the toxicity of this compound (9).

Bioaccumulation factors in rainbow trout are about 400 times the background (ambient water concentration of the pesticide) levels (7).

Effects on Other Organisms (Nontarget species)

Esfenvalerate is also highly toxic to bees. The compound tends to repel bees for a day or two after application, causing bee visitations to drop during that time (4). Since most intoxicated bees die in the field before they can return to contaminate the hive, the brood is not exposed except by direct spray. Dried spray residues are not expected to pose a significant threat to bees (9).


Breakdown of Chemical in Soil and Groundwater

Under field conditions, fenvalerate has a half-life ranging from about 15 days to 3 months depending on soil type. In a soil laboratory study, soil maintained under aerobic conditions have a half-life ranging from 65 days to 8 months, and soil maintained under anaerobic conditions have a half-life of approximately 6 months (7).

Esfenvalerate and its breakdown products are relatively immobile in soil and thus pose little risk to groundwater (7). The compound's ability to bind to soil increases with increasing organic matter. It is very insoluble in water. Fenvalerate has not been found in groundwater at over 100 groundwater supply sites (8).

Breakdown of Chemical in Surface Water

Esfenvalerate will hydrolyze and photodegrade in water. The half-life of fenvalerate in natural water has been reported to range from 4 to 15 days (16).

Breakdown in Plants

No information was available about the breakdown of this compound in plants.


Esfenvalerate is a colorless, crystalline compound with a molecular mass of 419.9 g/mol. The technical material is amber colored. Formulations include emulsifiable concentrates, suspension concentrates, and ULV liquid.

Exposure Guidelines:

RfD: N/A

Physical Properties:

CAS #: 66230-04-4 (1)
Chemical name: (s)-cyano(3-phenoxy phenyl)methyl (s)-4-chloro-alpha-(1-methyl ethyl)benzene acetate
Solubility in water: < 0.02 mg/l @ 20 degrees C (calculated)
Solubility in other solvents: hexane 77 g/l; acetone, chloroform, methanol > 450 g/l @ 20 degrees C
Melting Point: clear viscous liquid at 23 degrees C
Vapor Pressure: 0.067 mPa @ 25 degrees C
Partition Coefficient (octanol/water) (log): 6.22
Adsorption Coefficient: 5248
Chemical class/use: synthetic pyrethroid insecticide


Du Pont Agricultural Products
Walker's Mill, Barley Mill Plaza
P.O. Box 80038
Wilmington, DE 19880-0038
Toll free: (800) 441-7515
Emergency: (800) 441-3637

Review by Basic Manufacturer:

Comments solicited: April, 1993
Comments received: May, 1993


  1. The Agrochemicals Handbook: Third Edition. (1991). The Royal Society of Chemistry, Unwin Brothers Ltd., Surrey, England.
  2. Frank, R., H.E. Braun, L.A. Miller, and G.W. Allan. (1984). Fenvalerate Residues in Milk Following Topical Treatments to Dairy Cows. Pesticide Science, 15: 600-604.
  3. Food and Agriculture Organization of the United Nations. (1981). Pesticide Residues in Food - 1981. FAO Plant Production and Protection Paper 42.
  4. Shell Chemical Company. (1982). Pydrin Insecticide. Technical Manual ADP82-015.
  5. Wszolek, P.C., N.A. LaFaunce, T. Wachs, and D.J. Lisk. (1981). Studies of Possible Bovine Urinary Excretion and Rumen Decomposition of Fenvalerate Insecticide and a Metabolite. Bulletin of Environmental Contamination and Toxicology, 26: 262-266.
  6. Ecobichon, Donald J. (1991). Toxic Effects of Pesticides. In Casarett and Doull's Toxicology, The Basic Science of Poisons: Fourth Edition. Curtis D. Klaassen, Mary O. Amdur, and John Doull, Editors. Macmillan Publishing Company, New York.
  7. Walker, Mary M. and Lawrence H. Keith. (1992). EPA's Pesticide Fact Sheet Database. Lewis Publishers, Chelsea, MI.
  8. Williams, W. Martin, Patrick W. Holden, Douglas W. Parsons, and Matthew N. Lorber. (1988). Pesticides in Ground Water Data Base; 1988 Interim Report. U. S. Environmental Protection Agency. Office of Pesticide Programs. Environmental Fate and Effects Divisions.
  9. Asana XL Technical Bulletin. (no date). Du Pont Chemical Corp.
  10. O'Neal, Frederick O. (1991). Summary of Toxicological Studies Supporting Safety Assessment of Du Pont "Asana" XL Insecticide. Du Pont Report Number ESFE/GEN 1. Du Pont Chemical Corp.
  11. Shell Chemical Company. (1975). Teratogenic study of fenvalerate with rabbits. Unpublished study, MRID No. 00071664.
  12. Shell Chemical Company. (1976). Teratogenic study of fenvalerate with mice. Unpublished study, MRID No. 00064329.
  13. Shell Chemical Company. (1978a). Oncogenicity study of fenvalerate with rats over a two-year period. Unpublished study, MRID Nos. 00082007, 00082244.
  14. Shell Chemical Company. (1978b). Oncogenicity study of fenvalerate with mice over a two-year period. Unpublished study, MRID No. 00079876.
  15. Shell Chemical Company. (1981). Oncogenicity study of fenvalerate with rats over a two-year period. Unpublished study, MRID No. 00093652.
  16. International Agency for Research on Cancer. (1991). IARC Monographs on the Evaluation of the Carcinogenic Risks of Chemicals to Humans. Lyon, France. World Health Organization, 53: 309-328.