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
TRADE OR OTHER NAMES
Product names include Carbamine, Denapon, Dicarbam, Hexavin,
Karbaspray, Nac, Ravyon, Septene, Sevin, Tercyl, Tricarnam, and Union
Carbaryl is a wide-spectrum carbamate insecticide which controls
over 100 species of insects on citrus, fruit, cotton, forests, lawns,
nuts, ornamentals, shade trees, and other crops, as well as on poultry,
livestock and pets. It is also used as a molluscicide and an acaricide.
Carbaryl works whether it is ingested into the stomach of the pest or
absorbed through direct contact. The chemical name for carbaryl is 1-
Carbaryl is formulated as a solid which varies from colorless to
white to gray, depending on the purity of the compound. The crystals
are odorless. This chemical is stable to heat, light and acids under
storage conditions. It is non-corrosive to metals, packaging materials,
or application equipment. It is found in all types of formulations
including baits, dusts, wettable powder, granules, oil, molassas,
aqueous dispersions and suspensions (13).
Carbaryl is a general use pesticide.
Carbaryl is moderately to very toxic, and is labeled with a WARNING
signal word. It can produce adverse effects in humans by skin contact,
inhalation or ingestion. The symptoms of acute toxicity are typical of
the other carbamates. Direct contact of the skin or eyes with moderate
levels of this pesticide can cause burns. Inhalation or ingestion of
very large amounts can be toxic to the nervous and respiratory systems
resulting in nausea, stomach cramps, diarrhea and excessive salivation.
Other symptoms at high doses include sweating, blurring of vision,
incoordination, and convulsions. About fifty cases of occupational or
accidental illnesses due to exposure to carbaryl have been reported, but
no fatalities have been documented. The only documented fatality from
carbaryl was through intentional ingestion.
The oral LD50 of carbaryl ranges from 250 mg/kg to 850 mg/kg for
rats, and from 100 mg/kg to 650 mg/kg for mice (12, 13). The inhalation
LC50 for rats is 0,005 to 0.023 mg/kg (13). Low doses can cause minor
skin and eye irritation in rabbits, whose dermal LD50 has been measured
at greater than 2,000 mg/kg (12). Technical carbaryl has little
potential for skin or eye irritation.
Occupational workers have the greatest potential for exposure
through inhalation or through the skin. The general public's highest
risk of exposure is through ingestion of contaminated food (14).
Athough it may cause minor skin and eye irritation, carbaryl does
not appear to be a significant chronic health risk at or below
occupational levels. Male volunteers who consumed low doses of carbaryl
for six weeks did not show symptoms, but tests indicated slight changes
in their body chemistry (12).
Reproductive and Teratogenic Effects
No reproductive or fetal effects were observed during a long-term
study of rats which were fed high doses of carbaryl (12). The evidence
for teratogenic effects due to chronic exposure are minimal in test
amimals. Birth defects in rabbit and guinea pig offspring occurred only
at dosage levels which were highly toxic to the mother. A 1980 New
Jersey epidemiological study found no evidence of excess birth defects
in a town sprayed with carbaryl for gypsy moth control. There is only
limited evidence that carbaryl causes birth defects in humans. The EPA
has concluded that carbaryl does not pose a teratogenic risk to humans
if used properly (16).
Numerous studies indicate that carbaryl poses only a slight
mutagenic risk (8, 12). However, carbaryl can react with nitrite under
certain conditions to give rise to N-nitrosocarbaryl. Nitrosocarbaryl
has been shown to be highly mutagenic at low levels in laboratory test
systems. This may be a concern to humans because there is a possibility
that carbaryl, a pesticide, and nitrite, a substance found in food
additives and in human saliva, may react in the human stomach to form
nitrosocarbaryl (2, 8). Carbaryl has been shown to affect cell mitosis
(cell division) and chromosomes in rats (13).
Carbaryl has not caused tumors in ten longterm and lifetime studies
of mice and rats. Rats were administered high daily doses of the
pesticide for two years, and mice for eighteen months, with no signs of
carcinogenicity (3). However, N-nitrosocarbaryl, formed by the reaction
of carbaryl and nitrite, has been shown to be carcinogenic in rats at
high doses (7). Also, mice exposed to carbaryl in the product,
tricaprylin, for four weeks each, developed lung tumors (12).
Ingestion of carbaryl affects the lungs, kidneys and liver.
Inhalation will also affect the lungs (14, 17). Nerve damage can occur
after administration of high doses for 50 days in rats and pigs (12).
Several studies indicate that carbaryl can affect the immune system in
animals and insects. These effects however have not been documented in
Fate in Humans and Animals
Most animals, including humans, readily break down carbaryl and
rapidly excrete it in the urine and feces. Workers occupationally
exposed by inhalation to carbaryl dust excreted 74% of the inhaled dose
in the urine in the form of a breakdown product (13). This is
consistent with information on other species which excreted nearly three
quarters of a dose in their urine within 24 hours of administration
(14). The metabolism of up to 85% of carbaryl occurs within 24 hours
after administration (13).
Carbaryl is lethal to many nontarget insects. The pesticide is more
active in insects than in mammals. The destruction of honeybee
populations in sprayed areas is sometimes a problem. Carbaryl is
moderately toxic to aquatic organisms, such as rainbow and lake trout,
bluegill, and cutthroat. It is also moderately toxic to wild bird
species, with low toxicity to Canada geese (12).
Accumulation of carbaryl can occur in catfish, crawfish, and
snails, as well as in algae and duckweed. Residue levels in fish were
140 fold greater than the concentration of carbaryl in water. In
general, due to its rapid metabolism and rapid degradation, carbaryl
should not pose a significant bioaccumulation risk in alkaline waters.
However, under conditions below neutrality it may be significant (14).
Carbaryl has a short residual life on treated crops. The
insecticide remains at the application site, where it is slowly taken
into the plant and metabolized. Insecticidal properties are retained
for 3-10 days. Loss of carbaryl is due to evaporation and uptake into
plants. Breakdown by sunlight does not appear to be significant.
Degradation of carbaryl in the soil is mostly due to sunlight and
bacterial action. It is bound by organic matter and can be transported
in soil runoff. Carbaryl has a half-life of 7 days in aerobic soil and
28 days in anaerobic soil (9). Degradation of carbaryl in crops occurs
by hydrolysis inside the plants. It has a short residual life of less
than two weeks. The metabolites of carbaryl have lower toxicity to
humans than carbaryl itself. The breakdown of this substance is strongly
dependant on acidity and temperature.
In pond water, carbaryl is broken down by bacteria through chemical
processes. Evaporation does not occur. Carbaryl has a half-life of from
1 to 32 days in pond water. In a stream, carbaryl that had washed in
from forest spraying, decayed to 50% within a 24 hour period. It has
been shown to degrade more slowly in the presence of mud in aquatic
habitats. Carbaryl has been detected in groundwater in three separate
cases in California.
Carbaryl has a half-life in the air of one to four months. Crops,
shade trees, shrubs and other vegetation in bloom should not be sprayed
with carbaryl as bee kills are possible.
PHYSICAL PROPERTIES AND GUIDELINES
Carbaryl is a solid which varies from colorless to white or gray,
depending on the purity of the compound. The crystals are odorless.
Carbaryl is stable to heat, light and acids. It is not stable under
alkaline conditions. It is non-corrosive to metals, packaging materials
or application equipment.
|NOEL: ||0.06 mg/kg/day
|ADI: ||0.1 mg/kg/day
|STEL: ||10 mg/m3
|TLV: ||air TWA 5 mg/m3
|CL: ||625 mg/m3
|Drinking Water |
|Drinking Water Equivalent Level: (DWEL): 3.5 mg/L (13)
|CAS #: ||63-25-2
|Chemical Name: ||1-naphthyl N-methylcarbamine
|Solubility in water: ||0.005 g/100 g (20 degrees C), 0.004 g/100 g (30 degrees C)
|Solubility in solvents: ||Carbaryl is soluble in ethanol, petroleum ether, diethyl ether,and chloroform; moderately soluble in polar solvents such as acetone, dimethyl sulfoxide, mixed cresols, and cyclohexanone.
|Melting point: ||145 degrees C
|Vapor pressure: ||<0.0001 torr (20-25 degrees C)
|Log P: ||<-3.00
|Kow: ||64.6-229.1 (1, 5, 6, 10)
|Koc: ||205.0-457.1 (1, 4, 5)
|BCF: ||28.2-28.8 (1, 5)
|H: ||<9.9 x 10 to the minus 5 power torr/M
Rhone-Poulenc Ag. Co.
P.O. Box 12014
TW Alexander Dr.
Research Triangle Park, NC 27709
Review by Basic Manufacturer:
Comments solicited: October, 1992
Bracha, P. and O'Brian, R. 1966. J. Econ. Entomol. 59:1255.
Elespuru, R., Lijinski, W., and Setlow, J.K. 1974. Nature
"Evaluation of Carcinogenic, Teratogenic, and Mutagenic Activities
of Selected Pesticides and Industrial Chemicals," Volume 1:
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Farmer, W.J. 1976. "Leaching, Diffusion, and Sorption." From A
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Division of George Washington University Medical Center, pp. 185-245.
Fujita, T., et al. 1974. Agric. Biol. Chem. 38:1521.
Mount, M.E. and Oehme, F.W. 1981. Residue Rev. 80:1-64.
Regan, J.D., Setlow, R.B., Francis, A.A., and Lijinsky, W. 1976.
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and Co., Inc.: Rathway, NJ.
Vettorazzi, Gaston. 1979. International Regulatory Aspects
National Library of Medicine. Hazardous Substances Databank.
Carbaryl. February 4, 1992.
U.S. Environmental Protection Agency, Office of Drinking Water.
Carbaryl Health Advisory. Draft Report. August 1987.
Baron, Ronald L. (1991). Carbamate Insecticides. in Handbook of
Pesticide Toxocology, Volume 3, Classes of Pesticides. Wayland J.
Hayyes, Jr. and Edward R. Lawes, Jr. editors. Academic Press, Inc. NY.
Howard, Philip H. (1991). Handbook of Environmental Fate and
Exposure data for Organic Chenicals, Volume III. Lewis Publishers,
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