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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: 9/93


Aldicarb is an extremely toxic systemic carbamate insecticide used to control mites, nematodes, and aphids. It is applied directly to the soil and then thoroughly incorporated. It is used widely on cotton, peanut, and soybean crops. Highly publicized incidents involving contaminated cucumbers and watermelons occurred in the mid 1980s. In these cases, misapplication led to adverse effects in people. In 1990 Rhone-Poulenc Ag Company, the manufacturer of Temik, announced a voluntary halt on the sale of Temik (aldicarb) for use on potatoes because of concerns about groundwater contamination.

Aldicarb is a Restricted Use Pesticide (RUP) in the United States as determined by the US Environmental Protection Agency. Restricted Use Pesticides may be purchased and used only by certified applicators.



The primary routes of human exposure to aldicarb is consumption of contaminated food and ingestion of drinking water from contaminated wells (12). Occupational exposure to high levels of aldicarb is mostly due to product handling. Most cases of aldicarb poisoning have occurred from loading and application of the pesticide. In all cases of occupational overexposure, failure to follow the directions (product misuse) was cited as the reason (14).

Atypical of carbamates in general, aldicarb is extremely toxic through both the oral and dermal routes (17). This is one reason aldicarb is only formulated in a granular mix (10% to 15% active ingredient) rather than as an emulsified concentrate or as a liquid.

The LC50 in rats, mice, guinea pigs, and rabbits is in the range from 0.5 mg/kg to 1.5 mg/kg when administered in a liquid or oil form. The toxicities of the dry granules are distinctly lower (LC50 = 7.0 mg/kg) although this value is still well within the range of category I, "Highly Toxic" poisons. These low LC50 values make aldicarb an extremely toxic compound. Aldicarb carries the signal word DANGER-POISON on the label.

The only significant acute toxic effect of aldicarb is cholinesterase inhibition. The level of inhibition resulting from exposure to aldicarb depends on the duration of exposure and other factors. Any decrease in the enzyme's (acetylcholinesterase) activity below 70% of the baseline (or normal) value is likely to be physiologically significant. In other words, if aldicarb decreases enzyme activity by 30% chances are there will be adverse effects. Changes in the enzyme's activity of less that 10% cannot be detected due to analytical limitations, daily variations in cholinesterase levels, the influence of disease (e.g., hepatitis), pregnancy, and other factors.


There is very little evidence of chronic effects from aldicarb exposure. Rats and dogs fed low doses of aldicarb for two years showed no significant adverse effects (5).

Reproductive Effects

Aldicarb administered to pregnant rats at very low levels (0.001 to 0.1 mg/kg) depressed acetylcholinesterase activity more in the fetuses than in the mother. The aldicarb was also retained in the mother's body for longer periods than in non-pregnant rats (15). A three generation study at doses of 0.05 and 0.10 mg/kg produced no significant toxic effects (2) and another study utilizing a dose of 0.70 mg/kg/day also produced no adverse effects (9).

Teratogenic, Mutagenic and Carcinogenic Effects

No teratogenic, mutagenic or carcinogenic effects have been seen in studies conducted on rats (9, 5, 2). One epidemiological study suggested a possible link between low-level exposure and immunological abnormalities (5). The results of this study have been widely disputed.

Fate in Animals and Humans

Rats and cows eliminate 80% to 90% of a dose of aldicarb within twenty-four hours. Elimination is mainly through urine but some aldicarb leaves by way of the lungs in expired air and some through milk in cows. Absorption from the gut is rapid and almost complete. When administered in oil or other organic solvents aldicarb is absorbed rapidly through the skin. Its skin toxicity is roughly 1,000 times that of other carbamates (14). Aldicarb is absorbed more slowly from water than from organic solvents.

Aldicarb is metabolized to aldicarb sulfoxide, sulfone, oxime and nitrile that are quickly excreted. In human intoxication cases, the onset of symptoms was rapid: 15 minutes to 2 3/4 hours. Symptoms disappeared in four to twelve hours (5).


Birds are somewhat less susceptible to aldicarb than many mammals with LD50s from 1.78 mg/kg for the red-winged blackbird to 5.34 mg/kg for the ring-necked pheasant. When the latter were given diets of 300 ppm for five days no mortality was observed (8). Rainbow trout have a 96-hour LC50 of 8.8 mg/l and bluegill have a 98-hour LC50 of 1.5 mg/l. Bluegill bioaccumulate the parent compound (aldicarb) and the metabolites by a factor of less than ten (9). There is little or no hazard to bees when applied directly (1).


The potential exposure of aquatic organisms is high due to aldicarb's solubility and mobility in soil (13). Aldicarb, applied to farm fields can be transported to aquatic areas through runoff. This is most serious for sandy or sandy loam soils. The half life of aldicarb in water is from one day (4) to a few months (12). Moisture and pH have important impacts on the rate of breakdown. In a neutral solution the half life is nearly three years while in a solution 100 times more basic it is only one day. In pond water, aldicarb has a half life of five to ten days (5). Because of its rapid degradation rate, levels in surface water may be lower than those in groundwater (5).

Aldicarb leaches to groundwater from soil in sufficient quantities to potentially result in human health effects (4). It has been found in wells in over twenty five counties and in twelve states at concentrations above the health advisory limit of 10 parts per billion (12).

The compound is degraded by bacteria, sunlight, and reaction with water. It is not known to bioaccumulate in aquatic organisms (12). In plants, it is rapidly converted to sulfoxide and more slowly to the sulfone compound. Citrus trees treated with 18 grams/tree had the highest residue levels in the leaves (4). Residues of aldicarb also have been reported in sugar beets and grape leaves and fruit (12). Bananas have also been shown to have elevated levels of aldicarb residue. However in early June of 1991 the manufacturer called for a halt on the use of aldicarb on bananas by growers. The time interval between pesticide application and harvest for various fruits and vegetables is generally 60-100 days because of the very toxic nature of this pesticide (7).

Physical Properties:

Common Name: aldicarb
CAS #: 116-06-2
Chemical Name: 2-methyl-2-(methylthio) propanal O-[methylamino) carbonyl]oxime
Solubility in water: 6,000 ppm at room temperatures
Solubility in solvent: acetone 35g/100g; xylene 5g/100 g; ethyl ether 20g/100 g; toluene 10 g/100 g
Melting Point: 99-100 degrees C
Vapor Pressure: 3 x 10 to the minus 5 power mm Hg at 25 degrees C
Partition Coefficient: 1.359 (octanol/ water)

Exposure guidelines:

NOEL (Rat): 0.10 mg/kg/day (ppm) cholinesterase activity, metabolites
HA: 0.001 mg/l, (ppm) lifetime
ADI: 0.003 mg/kg (ppm) (EPA)
0.005 (ppm) (WHO)
0.001 (ppm) (NAS)
RfD: 0.00125mg/kg/day (Based on an ADI of 0.003 mg/kg)
LEL: 0.025 mg/kg (human)
DWEL: 0.004 mg/l


Rhone-Poulenc, Inc.
P.O. Box 12014
2 T.W. Alexander Park, NC 27709
Telephone: 919-549-4689
Emergency: 800-334-7577

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: October, 1992


  1. Hartley, D., and H. Kidd. Editors (1986). The Agrochemicals Handbook. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Kizer, Kenneth W. (1986). Memorandum to: California Department of Food and Agriculture, from Department of Health Services, Sacramento, CA.
  3. 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 D.C.
  4. National Library of Medicine
  5. Hazardous Substances databank. TOXNET, Medlars Manage-ment Section, Bethesda, MD.
  6. U.S. Environmental Protection Agency (1987). Health Advisory, Office of Drinking Water.
  7. Worthing, Charles R., Editor (1983). The Pesticide Manual, A World Compendium. The British Crop Protection Council, The Ravenham Press Limited, Ravenham, Suffolk, England.
  8. Food and Agriculture Organization of the United Nations (1982). Pesticide Residues in Food - 1982. FAO Plant Production and Protection Paper 49.
  9. Smith, Gregory J. (1987). Pesticide Use and Toxicology in Relation to Wildlife: Organophosphates and Carbamate Compounds, United States Department of the Interior, Fish and Wildlife Service, Resource Publication 170.
  10. Food and Drug Administration (1986). The FDA Surveillance Index. Bureau of Foods, Department of Commerce, National Technical Information Service, Springfield, VA.
  11. Cornell University (1983). A Toxicological Evaluation of Aldicarb and its Metabolites in Relation to the Potential Human Health Impact of Aldicarb Residues in Long Island Ground Water, Institute for Comparative and Environmental Toxicology, Ithaca, NY.
  12. National Research Council. (1986). Drinking Water and Health, Volume 6. Board on Toxicology and Environmental Health Hazards, Commission on Life Sciences, Safe Drinking Water Committee, National Academy Press, Washington, D.C.
  13. Howard, Philip H. (1991). Handbook of Environmental Fate and Exposure data for Organic Chemicals, Volume III. Lewis Publishers, Chelsea, MI.
  14. Schlenk, Daniel, David A. Erickson, John J. Leach, and Donald R. Buhler. (1992). The Distribution, Elimination, and in vivo Biotransformation of Aldicarb in the Rainbow Trout (Oncorynchus mykiss). Fundemental and Applied Toxicology, 18, 131-136.
  15. Baron, Ronald L. (1991). Carbamate Insecticides. in Handbook of Pesticide Toxocology, Volume 3, Classes of Pesticides. Wayland J. Hayes Jr. and Edward R. Laws, Jr. editors. Academic Press, Inc. NY.
  16. Chambon, C., C. Declune, and R. Derach. (1979). Effects on the Insecticidal Carbamate Derivitives (Carbofuran, Primicarb, and Aldicarb) on the Activity of Acetylcholinesterase in Tissue From Pregnant Rats and Fetuses. Toxicology and Applied Pharmacology, 49: 203-208.
  17. US Environmental Protection Agency. (1989). Health advisory Summaries. Office of Drinking Water.
  18. Murphy, Sheldon D. (1986). Toxic Effects of Pesticides in Casarett and Doull's Toxicology, The Basic Science of Poisons, Third Edition. Curtis D. Klaassen, Mary O. Amdur, and John Doull editors. Macmillan Publishing Company, NY