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
Trade names for products containing rotenone include Chem-Fish, Cuberol,
Fish Nox, Noxfire, Rotacide, Sinid and Tox-R. It is also marketed as Curex
Flea Duster, Derrin, Cenol Garden Dust, Chem-Mite, Cibe Extract and Green
Cross Warble Powder. The compound may be used in formulations with other
pesticides such as carbaryl, lindane, thiram, pyrethrins and quassia.
Although it is very often sold as a mixture of piperonyl butoxide or
pyrethrum, this profile applies to rotenone alone unless otherwise stated.
Rotenone is a selective, non-specific insecticide with some acaricidal
properties. Rotenone is used in home gardens for insect control, for lice and
tick control on pets and for fish eradications as part of water body
management. The use of the pesticide for control of fish and in cranberries
is restricted by the Environmental Protection Agency.
Rotenone is a rotenoid plant extract obtained from such species as
barbasco, cub, haiari, nekoe, and timbo. These plants are members of the pea
(Leguminosae) family. Rotenone containing extracts are taken from the roots,
seeds and leaves of the various plants (13). Rotenone is generally classified
as a botanical insecticide.
Rotenone is a general use pesticide.
Rotenone, when formulated as an emulsified concentrate, is highly toxic
and carries the signal word DANGER on its label. Other forms of the
insecticide are slightly toxic and require the signal word CAUTION instead.
Local effects on the body include conjunctivitis, dermatitis, sore
throat, and congestion. Ingestion produces effects ranging from mild
irritation to vomiting. Inhalation can cause increased respiration followed
by depression and convulsions. The compound is a strong eye irritant to
The oral LD50 of rotenone ranges from 132 to 1,500 mg/kg in rats (14).
Humans are believed to be fairly susceptible to the compound with an oral
lethal dose estimated from 300 to 500 mg/kg (14). No human fatalities have
been reported, perhaps because rotenone is usually sold in low concentrations
(1-5% formulation) and because its irritating action causes prompt vomiting.
Mice have a rotenone induced oral LD50 of 350 mg/kg; rabbits an LD50 of
600-2,000; and guinea pigs an LD50 of 12-200. For most laboratory animals,
rotenone is much more toxic intravenously than orally. A spray of 5% rotenone
in 80 imperial gallons of water was fatal to a 100-pound pig when exposed to
250 cucm (cubic centimeters) of the mixture.
The particle size of the powder determines the inhalation toxicity. Fine
powders are much more toxic than coarse particles. Rotenone is more toxic
when inhaled than when ingested (7).
Growth retardation and vomiting were the observable results of chronic
exposures involving rats and dogs. Rats fed diets 2.5 to 50 mg/kg for two
years developed no pathological changes that could be attributed to rotenone.
The lowest dose administered, 2.5 mg/kg, inhibited growth.
Dogs fed low to moderate doses of rotenone for 28 days experienced
vomiting and excessive salivation, but no negative weight gain. Dogs fed
rotenone for six months at low doses had reduced food consumption and
therefore reduced weight gain. At necropsy, the most frequent lesions were
bleeding patches in the small intestine.
Pregnant rats fed small amounts of the insecticide (10 mg/kg) through day
15 of gestation, experienced decreases in live births and increases in fetal
resorption. Some of the mothers died due to rotenone poisoning also. The 2.5
mg/kg dose produced no observable maternal toxicity or adverse effect on fetal
development. While low doses of the pesticide were sufficient to cause
adverse effects in the pregnant rats, there is not enough information to draw
any connection to the potential for reproductive risks to humans.
Pregnant rats fed small amounts (5 mg/kg) produced a significant number
of young with skeletal deformities. The effects was not observed at the 10
mg/kg level, so the data do not provide convincing evidence of teratogenicity
The results from a number of tests for mutagenicity make any conclusion
about mutagenic risks to humans difficult to draw. The compound was determined
to be non-mutagenic to bacteria and yeast and in treated mice and rats.
However, it was shown to cause mutations in some cultured mouse cells (13, 15).
Young mice given small amounts of rotenone (1 mg/kg) until they were four
weeks old and then fed 3 mg/kg for 18 months more months did not show a
significant increase in tumors. Rat studies which showed an increased
evidence of mammary tumor at 1.7 mg/kg for 42 days could not be duplicated in
later studies on rats and hamsters.
Male rats showed equivocal evidence of carcinogenic activity in a two-
year feeding study done by the National Cancer Institute (11). These males
had increased evidence of parathyroid gland tumors. However, female rats and
all mice showed no evidence of cancer.
Chronic poisoning may produce changes in the liver and kidneys (13).
Fate in Humans and Animals
Absorption in the stomach and intestines is relatively slow and
incomplete, although fats and oils promote its uptake. The liver breaks down
the compound fairly effectively (14). Animals have excreted about 20% of a
dose within two days.
Rotenone inhibits the main energy producing process in the animal cell
(the mitochondrial electron transport system). This system is one of the
essential processes which convert food into energy. One area of attack in the
body is in the cells of the central nervous system.
Rotenone is slightly toxic to wildfowl. The LD50 values for rotenone in
mallards and pheasants is (greater than) 2,000 mg/kg and 1,680 mg/kg
respectively. Some of the signs of intoxication in birds include muscle
incoordination, feathers fluffed or held tightly to the body, wings drooped
and the neck pulled in. Remission of signs of intoxication take about a week.
It appears that birds are more sensitive to ground derris root than to pure
Since rotenone is used as a fish toxin (piscicide), it follows that it is
very highly toxic to fish. Rainbow trout had a 96-hour LC50 of 23
micrograms/l (ppb) and channel catfish had 2.6 micrograms/l (ppb) (14).
Aquatic invertebrates have a wide range of sensitivity to rotenone with
96 hr LC50 values ranging from 0.002 to 100 mg/l (ppm). The compound is not
toxic to bees. However, it is toxic to bees when used in combination with
Rotenone breaks down readily by exposure to sunlight. Nearly all of the
toxicity of the compound is lost in five to six days of spring sunlight or two
to three days of summer sunlight.
Rotenone is a highly active but short-lived photosensitizer. This means
that an organism consuming the compound develops a strong sensitivity to the
sun for a short time. A number of photodecomposition products are formed when
bean leaves are exposed to light. It is also sensitive to heat with, much of
the rotenone quickly lost at high temperatures.
Rotenone is rapidly broken down in soil and in water. The half-life in
both of these environments is between one and three days (15). Because of its
short half-life and because it does not readily leach from soil, it is not
expected to be a groundwater pollutant.
PHYSICAL PROPERTIES AND GUIDELINES
|RfD: ||0.004 mg/kg/day (EPA)
|LEL: ||1.88 mg/kg/day (rat)
|CAS #: ||83-79-4
|Solubility in water: ||0.02 mg/l 20 degrees C
Fairfield American Corp
238 Wilson Ave
Newark, NJ 07105
Review by Basic Manufacturer:
Comments solicited: October, 1992
Shepard, Thomas H. 1986. Catalog of Teratogenic Agents. The John
Hopkins University Press, Baltimore, MD.
Gosselin, R.E., R.P. Smith and H.C. Hodge. 1984. Clinical Toxicology
of Commercial Products, Williams and Wilkins, Baltimore, MD.
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,
Johnson, W.W. and M.T. Finley. 1980. Handbook of Acute Toxicity of
Chemicals to Fish and Aquatic Invertebrates. U.S. Dept of the Interior, Fish
and Wildlife Service, Resource Publication 137.
Hudson, R.H., R.K. Tucker and M.A. Haegele. 1984. Handbook of
Toxicity of Pesticides to Wildlife. U.S. Dept of the Interior, Fish and
Wildlife Service, Resource Publication 153.
Negherbon, William O. 1959. Handbook of Toxicology, Volume III:
Insecticides, A Compendium. Div of Biology and Agriculture, National Academy
of Sciences, National Research Council, W. B. Saunders Company, Philadelphia,
National Library of Medicine. 1992. Hazardous Substances Databank.
TOXNET, Medlars Management Section, Bethesda, MD.
Hill, E.F. and M.B. Camardese. 1986. Lethal Dietary Toxicities of
Environmental Contaminants and Pesticides to Coturnix. U.S. Dept of the
Interior, Fish and Wildlife Service, Technical Report 2.
Menzie, Calvin M. 1969. Metabolism of Pesticides. U.S. Dept of the
Interior, Fish and Wildlife Service, Special Scientific Report, Wildlife No.
Worthing, Charles R. (ed.). 1983. The pesticide manual, a world
compendium. The British Crop Protection Council, The Ravenham Press Limited,
Ravenham, Suffolk, England.
National Toxicology Program. 1986. Toxicology and Carcinogenesis
Studies of Rotenone in F344/N Rats and B6C3F Mice. U.S. Dept of Health and
Human Services, Public Health Service, National Institute of Health, Tech
Report Series No. 320.
Briggs, Shirley A. 1992. Basic guide to pesticides: Their
characteristics and hazards. Hemisphere Publishing Corporation.
Ray, David. E. 1991. Pesticides derived from plants and other
organisms. In Handbook of Pesticide Toxicology, Volume 2, Classes of
Pesticides. Wayland J. Hayes and Edward R. Laws (eds.). Academic Press, NY.
The Agrochemicals Handbook. 1991. The Royal Society of Chemistry.
Walker, Mary M. and Lawrence H. Keith. 1992. EPA's Pesticide Fact
Sheet Database. Lewis Publishers. Chelsea, MI.
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