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
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
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).
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
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).
|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)
|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 mg.kg (ppm) (WHO)
0.001 mg.kg (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
P.O. Box 12014
2 T.W. Alexander Park, NC 27709
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received: October, 1992
Hartley, D., and H. Kidd. Editors (1986). The Agrochemicals
Handbook. The Royal Society of Chemistry, The University, Nottingham,
Kizer, Kenneth W. (1986). Memorandum to: California Department of
Food and Agriculture, from Department of Health Services, Sacramento,
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.
National Library of Medicine Hazardous Substances
databank. TOXNET, Medlars Manage-ment Section, Bethesda, MD.
U.S. Environmental Protection Agency (1987). Health Advisory,
Office of Drinking Water.
Worthing, Charles R., Editor (1983). The Pesticide Manual, A World
Compendium. The British Crop Protection Council, The Ravenham Press
Limited, Ravenham, Suffolk, England.
Food and Agriculture Organization of the United Nations (1982).
Pesticide Residues in Food - 1982. FAO Plant Production and Protection
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
Food and Drug Administration (1986). The FDA Surveillance Index.
Bureau of Foods, Department of Commerce, National Technical Information
Service, Springfield, VA.
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.
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.
Howard, Philip H. (1991). Handbook of Environmental Fate and
Exposure data for Organic Chemicals, Volume III. Lewis Publishers,
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.
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.
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.
US Environmental Protection Agency. (1989). Health advisory
Summaries. Office of Drinking Water.
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