ROTENONE
Human Health Effects:
Human Toxicity Excerpts:
Local effects incl conjunctivitis, dermatitis, pharyngitis, and rhinitis. Oral
ingestion of rotenone produces GI irritation,
nausea, and vomiting. Inhalation of the dust is more hazardous; it can cause resp
stimulation followed by depression and convulsions.
No unscheduled DNA synthesis (UDS) was observed in human fibroblast cultures (VA4) in
the presence or absence of a rat S9 liver enzyme activation system when rotenone
was tested at 1, 10, and 1000 mM concn.
CHRONIC POISONING MAY PRODUCE FATTY CHANGES IN LIVER, KIDNEY.
MORE TOXIC WHEN INHALED THAN WHEN INGESTED.
ROTENONE IS RELATIVELY FREE OF HAZARDS IN
NORMAL USE, BECAUSE OF 1) THE LOW PERCENTAGE (1 TO 5%) COMMONLY USED IN FORMULATIONS; 2)
THE UNSTABLE NATURE OF ROTENONE ... 3) ITS
IRRITANT ACTIONS WHEN INGESTED ... 4) ITS LOW SOLUBILITY IN WATER. NO HUMAN FATALITIES
HAVE BEEN REPORTED. ... ALTHOUGH THE MEAN LETHAL DOSE BY MOUTH VARIES WIDELY AMONG COMMON
SPECIES OF LAB MAMMALS, A REASONABLE ESTIMATE FOR MAN IS 0.3 TO 0.5 G/KG. ... BECAUSE OF
POOR /GI/ ABSORPTION, COARSE PARTICLES OF SOLID ROTENONE
ARE MUCH LESS TOXIC THAN FINE POWDERS. FATS AND OILS PROMOTE ABSORPTION AND SO ENHANCE
TOXICITY.
In massive overdose, principal effects include protracted vomiting, respiratory
depression, and hypoglycemia and its symptoms.
When derris powder was applied to the armpits of four persons twice daily for 30 days,
one developed a mild rash at the site of application; the rash disappeared within 24 hr.
The others experienced no inconvenience, except that one person noted a very mild
smarting. When applied to the forearms as a 10% ointment in anhydrous lanolin, no local
irritation or anesthesia was observed. About 10 min after derris or a water extract of it
was taken into the mouth of volunteers, all experienced a sensation of numbness, as well
as a metallic taste; these effects lasted 3 or 4 hr ... .
A previously healthy 3.5-yr old girl died after drinking about 10 mL of an insecticidal
preparation of rotenone ... Symptoms were
initial vomiting and drowsiness leading rapidly to coma, depressed respiration, and apnea.
Despite artificial ventilation begun within 2-2.5 hr of ingestion, the girl died at 8-8.5
hr. Postmortem showed anoxic damage in the cerebrum, lungs, and heart and serohemorrhagic
pleural effusion. There was also evidence of an acute renal tubular necrosis, but the
authors suggested that this could have been due to various etherial oils present in the
insecticide. HPLC analysis of postmortem tissues showed rotenone
concentration of 6 x 10-6 to 1 x 10-5 mol/kg and the estimated oral dose was 40 mg/kg.
Ingestion of rotenone was a common means of
suicide by native of New Ireland ... When such persons were brought to medical attention
while still alive, they were found to be in a state of collapse with feeble pulse and
dilated pupils. Some, especially those suspected of having taken a very small dose,
recovered following gastric lavage and stimulants. The only finding in numerous autopsies
was that of acute congestive heart failure. The root was not generally found in the
stomach, as vomiting before death was the rule.
... mentioned the primitive industrial conditions for processing rotenone-bearing
plants in the Amazon valley. Physicians observed some cases of severe irritation of the
throat with partial destruction of the soft palate as well as of the anterior pillars and,
very frequently, an irritation of the conjunctiva followed by ulcerative keratitis.
Inflammation of the skin was notable in skin folds or where perspiration led to
accumulation of the powder.
All workers in Lyon who encountered the fine powder developed in 2 or 3 days a violent
dermatitis of the genital region. It was characterized by a red-violet color, slight
edema, and some itching. In 24 hr, if exposure was topped, the irritated skin underwent
desquamation in plaques of different sizes. If contact persisted, the dermatitis became
worse; itching, erythema, and the leatherlike texture increased. The skin became covered
with large, flat, excoriated, oozing papules in patches 0.5 cm in diameter. The dermatitis
recurred with each new exposure. Workers also experienced ulcerative rhinitis and
temporary but complete loss of the sense of smell. In some instances there was irritation
of the lips and tongue.
Derris powder or ointment produces only a mild rash or no irritation of human ... skin.
... No anesthetic effect, such as is seen in the human mouth following application of
either rotenone or derris, can be observed in
the eye. Complete recovery can be expected in several days ... .
Human Toxicity Values:
Lethal dose Human 0.3-0.5 g/kg (est)
Skin, Eye and Respiratory Irritations:
Direct contact may cause irritation of the skin or conjunctiva.
Medical Surveillance:
Consider the points of attack /CNS, eyes, respiratory system/ in preplacement and
periodic physical examinations.
Probable Routes of Human Exposure:
Inhalation, ingestion, skin and eye contact.
... Extraction of derris root, formulation or application of /rotenone/.
NIOSH (NOES Survey 1981-1983) has statistically estimated that 8,099 workers (2,470 of
these are female) are potentially exposed to rotenone
in the US(1). Occupational exposure may be through inhalation of dusts and dermal contact
with this compound at workplaces where rotenone
is produced or used(SRC). The general population may be exposed to rotenone
ingestion of food(2) and drinking water, and dermal contact with vapors, food and other
products containing rotenone(SRC). Limited
monitoring data indicate that non-occupatioal exposures can occur from the ingestion of
contaminated drinking water. The most probable human exposure would be occupational
exposure, which may occur through dermal contact or inhalation at workplaces where it is
produced or used(SRC).
Emergency Medical Treatment:
Emergency Medical Treatment:
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reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX, SHOULD BE
CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC CASES. Copyright
1974-1998 Micromedex, Inc. Denver, Colorado. All Rights Reserved. Any duplication,
replication or redistribution of all or part of the POISINDEX(R) database is a violation
of Micromedex' copyrights and is strictly prohibited. The following Overview, *** ROTENONE ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted.
|
| Clinical Effects: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o Rotenone is irritating to the eyes, skin, and mucous
membranes. It is more toxic when inhaled than when
ingested.
o Signs and symptoms may include conjunctivitis followed
by ulcerative keratitis, mydriasis, rhinitis,
pharyngitis, and numbness of the mucous membranes.
Seizures have been reported in experimental animals.
Additional signs and symptoms may include
hypersalivation, vomiting, partial destruction of the
soft palate and anterior pillars, fatty liver changes,
focal liver necrosis and neoplasms (in experimental
animals), acute tubular necrosis, acidosis, and
dermatitis.
o Acute exposure has resulted in mucous membrane
irritation, congestive heart failure, slow or irregular
pulse, incoordination, tremors, CNS depression, and
respiratory failure. Death usually occurs secondary to
respiratory depression.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Irregular pulse, decreased heart rate and strength may
occur.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o All types of irritation (pharyngitis, rhinitis, and
pulmonary) may be present. Respiratory stimulation
precedes respiratory depression.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Neurologic symptoms are unlikely, but incoordination,
seizures or CNS depression might occur.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Salivation, numbness of the mouth, vomiting, or gastric
pain could occur.
HEPATIC
0.2.9.1 ACUTE EXPOSURE
o Liver necrosis and neoplasms have been observed in
animal studies.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Acute tubular necrosis may be seen in human ingestions.
|
| Laboratory: |
o Chemical analysis or paper chromatography may
qualitatively identify rotenone, but quantitative values
are not yet correlated with symptomatology.
|
| Treatment Overview: |
SUMMARY EXPOSURE
o FIRST AID (NIOSH, 1998) -
1. EYE EXPOSURE - Immediately wash the eyes with large
amounts of water, occasionally lifting the lower and
upper lids. Get medical attention immediately.
Contact lenses should not be worn when working with
this chemical.
2. DERMAL EXPOSURE - Promptly wash the contaminated skin
with soap and water. If this chemical penetrates the
clothing, promptly remove the clothing and wash the
skin with soap and water. Get medical attention
promptly.
3. INHALATION EXPOSURE - Move the exposed person to fresh
air at once. If breathing has stopped, perform
mouth-to-mouth resuscitation. Keep the affected person
warm and at rest. Get medical attention as soon as
possible.
4. ORAL EXPOSURE - If this chemical has been swallowed,
get medical attention immediately.
5. TARGET ORGANS - Eyes, skin, respiratory system, and
CNS.
o GENERAL -
1. Move victims of inhalation exposure from the toxic
environment and administer 100% humidified supplemental
oxygen with assisted ventilation as required. Exposed
skin and eyes should be copiously flushed with water.
Because of the potential for rapid onset of CNS
depression or seizures with possible aspiration of
gastric contents, EMESIS SHOULD NOT BE INDUCED.
Cautious gastric lavage followed by administration of
activated charcoal may be of benefit if the patient is
seen soon after the exposure.
o INHALATION EXPOSURE -
1. INHALATION: Move patient to fresh air. Monitor for
respiratory distress. If cough or difficulty breathing
develops, evaluate for respiratory tract irritation,
bronchitis, or pneumonitis. Administer oxygen and
assist ventilation as required. Treat bronchospasm
with beta2 agonist and corticosteroid aerosols.
2. If bronchospasm and wheezing occur, consider treatment
with inhaled sympathomimetic agents.
3. Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
o DERMAL EXPOSURE -
1. DECONTAMINATION: Remove contaminated clothing and wash
exposed area thoroughly with soap and water. A
physician may need to examine the area if irritation
or pain persists.
2. Treat dermal irritation or burns with standard topical
therapy. Patients developing dermal hypersensitivity
reactions may require treatment with systemic or
topical corticosteroids or antihistamines.
3. Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
o EYE EXPOSURE -
1. DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
o ORAL EXPOSURE -
1. Because of the potential for gastrointestinal tract
irritation and CNS depression, DO NOT induce emesis.
2. Significant esophageal or gastrointestinal tract
irritation or burns may occur following ingestion. The
possible benefit of early removal of some ingested
material by cautious gastric lavage must be weighed
against potential complications of bleeding or
perforation.
3. GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg
and left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
a. CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation;
and trivial or non-toxic ingestion.
4. ACTIVATED CHARCOAL/CATHARTIC: Administer charcoal
slurry, aqueous or mixed with saline cathartic or
sorbitol. The FDA suggests 240 mL of diluent/30 g of
charcoal. Usual charcoal dose is 25 to 100 grams in
adults and adolescents, 25 to 50 grams in children (1
to 12 years old), and 1 gram/kilogram in infants less
than 1 year old.
a. Routine use of cathartics is NOT recommended. If
used, administer only ONE dose of cathartic.
Administer one dose of a cathartic, mixed with
charcoal or given separately. See "Treatment:
Prevention of Absorption" in the main document.
5. Do NOT administer oils or fats as these may enhance
absorption.
6. Administer intravenous fluids as required. Administer
supplemental oxygen with assisted ventilation if
needed.
7. SEIZURES: Administer a benzodiazepine IV; DIAZEPAM
(ADULT: 5 to 10 mg, repeat every 10 to 15 min as
needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min
as needed) or LORAZEPAM (ADULT: 4 to 8 mg; CHILD:
0.05 to 0.1 mg/kg).
a. Consider phenobarbital if seizures recur after
diazepam 30 mg (adults) or 10 mg (children > 5
years).
b. Monitor for hypotension, dysrhythmias, respiratory
depression, and need for endotracheal intubation.
Evaluate for hypoglycemia, electrolyte disturbances,
hypoxia.
8. Observe patients with ingestion carefully for the
possible development of esophageal or gastrointestinal
tract irritation or burns. If signs or symptoms of
esophageal irritation or burns are present, consider
endoscopy to determine the extent of injury.
9. Although only animal studies have suggested efficacy, a
trial of menadione sodium bisulfite or menadiol sodium
diphosphate may be warranted.
ORAL EXPOSURE
o EMESIS: Ipecac-induced emesis is not recommended
because of the potential for CNS depression.
o ACTIVATED CHARCOAL: Administer charcoal as slurry (240
mL water/30 g charcoal). Usual dose: 25 to 100 g in
adults/adolescents, 25 to 50 g in children (1 to 12
years), and 1 g/kg in infants less than 1 year old.
o GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
1. CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation; and
trivial or non-toxic ingestion.
o DO NOT administer oils or fats, for these may promote
absorption.
o SEIZURES: Administer a benzodiazepine IV; DIAZEPAM
(ADULT: 5 to 10 mg, repeat every 10 to 15 min as
needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min
as needed) or LORAZEPAM (ADULT: 4 to 8 mg; CHILD: 0.05
to 0.1 mg/kg).
1. Consider phenobarbital if seizures recur after diazepam
30 mg (adults) or 10 mg (children > 5 years).
2. Monitor for hypotension, dysrhythmias, respiratory
depression, and need for endotracheal intubation.
Evaluate for hypoglycemia, electrolyte disturbances,
hypoxia.
INHALATION EXPOSURE
o INHALATION: Move patient to fresh air. Monitor for
respiratory distress. If cough or difficulty breathing
develops, evaluate for respiratory tract irritation,
bronchitis, or pneumonitis. Administer oxygen and
assist ventilation as required. Treat bronchospasm with
beta2 agonist and corticosteroid aerosols.
EYE EXPOSURE
o DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
DERMAL EXPOSURE
o DECONTAMINATION: Remove contaminated clothing and wash
exposed area thoroughly with soap and water. A
physician may need to examine the area if irritation or
pain persists.
|
| Range of Toxicity: |
o There are few reports of human toxicity. Dermal and
ocular exposures are most common. Injection produced
greater toxicity than ingestion due to poor absorption
from the GI tract.
|
Antidote and Emergency Treatment:
In symptomatic overdose treatment is appropriate supportive therapy.
For immediate first aid: Ensure that adequate decontamination has been carried out. If
victim is not breathing, start artificial respiration, preferably with a demand-valve
resuscitator, bag-valve-mask device, or pocket mask as trained. Perform CPR if necessary.
Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If
vomiting occurs, lean patient forward or place on left side (head-down position, if
possible) to maintain an open airway and prevent aspiration. Keep victim quiet and
maintain normal body temperature. Obtain medical attention. /Rotenone
and related compounds/
For basic treatment: Establish a patent airway. Suction if necessary. Watch for signs
of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by
nonrebreather mask at 10 to 15 L/min. Anticipate seizures and treat if necessary ... For
eye contamination, flush eyes immediately with water. Irrigate each eye continuously with
normal saline during transport ... Do not use emetics. For ingestion, rinse mouth and
administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a
strong gag reflex, and does not drool. Administer activated charcoal ... /Rotenone and related compounds/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
RESP DEPRESSION & FALL IN ARTERIAL BLOOD PRESSURE IN RABBITS /IS/ PRODUCED BY IV ROTENONE ... .
GIVEN IV TO TEST ANIMALS, IT PRODUCES VOMITING, INCOORDINATION, MUSCLE TREMORS, CLONIC
CONVULSIONS & RESP FAILURE.
HIGHLY TOXIC TO FISH (LETHAL LESS THAN 50 PPB).
60 MG/KG WILL KILL GUINEA PIGS. ... POISONING RESULTS IN RESP STIMULATION &
CONVULSIONS, RESP DEPRESSION, COMA & RESP FAILURE. CHRONIC POISONING OF ANIMALS FED
DIET CONTAINING 75 PPM OF DERRIS ROOT CAUSES CENTRAL LOBULAR HEPATIC NECROSIS.
SIGNS OF INTOXICATION: ATAXIA, NUTATION/ACT OF NODDING ESPECIALLY INVOLUNTARY NODDING/,
DYSPNEA, POLYURIA, FEATHERS FLUFFED OR HELD TIGHTLY TO BODY, WING DROP, NECK PULLED IN,
IMMOBILITY. REGURGITATION OCCURRED @ LEVELS ABOVE 1500 MG/KG. SIGNS WERE OBSERVED LESS
THAN AN HOUR AFTER SINGLE ORAL ADMIN, AND MORTALITIES OCCURRED UP TO 5 DAYS AFTER
TREATMENT. REMISSION TOOK UP TO 1 WK. /MALLARDS &/OR PHEASANTS/
ROTENONE WAS ADMIN BY INJECTION TO WISTAR
RATS FOR 2-3 MO AT DOSES OF 0.1 TO 0.2 MG/RAT/DAY, 5 DAYS/WK. EARLY MAMMARY TUMORS
APPEARED 6 MO AFTER THE END OF TREATMENT AND THE NUMBER OF TUMORS INCR UP TO 24 MO.
Short term admin of rotenone in sunflower
oil, injected ip in doses of 0.1 mg/kg/day for 5 days into female rats, produced a marked
elevation in serum growth hormone concn and a decr in serum prolactin. These alterations
& transient elevations in concn of estrogens, progesterone, and corticosterone
suggested that rotenone was stimulating the
hypophysis and that the physiopathogeny of rotenone-induced
mammary tumors is indirect and hormonal.
The colony forming ability of continuously cultivated bovine cells (T4) derived from
normal ovarian tissue was reduced to 50% in the presence of 3.5X10-7 M concn of rotenone. Alkali-labile single strand DNA breakage was
observed when mouse L1210 leukemia cells were exposed to 1X10-7 M rotenone.
... No sister chromatid exchanges /were observed/ in Chinese hamster ovary cells in the
presence or absence of a rat liver S9 metabolic activation system. The max dose level used
was the dose that reduced the proportion of dividing cells to 50%. Rotenone
added to Chinese hamster cells in vitro incr the mitotic index, and mitotic cells
contained monopolar spindles with chromosomes grouped around centriole pairs near the cell
center. The cmpd was also found to arrest mitosis in cultured mammalian cells by
inhibition of the spindle microtubule assembly.
... Histological exams were conducted on 30 tissue/organ samples from approx 30 ...
/Syrian golden hamsters/ of each sex and exptl group that had received /98%/ rotenone at doses of 0, 125, 250, 500, or 1000 ppm in
the diet for as long as 18 mo. There was no evidence /of carcinogenicity/ ... in Sprague
Dawley rat study, rotenone in corn oil was admin
daily by ip injection to 25 animals of each sex at doses of 0, 1.7, or 3.0 mg/kg body wt
for 42 days. Fifteen animals of each sex were used as vehicle controls. The animals were
observed for an addnl 18 mo... In the Wistar rat study, rotenone
in corn oil was admin by gavage to 25 animals of each sex at doses of 0, 1.7, or 3.0 mg/kg
body wt for 42 days. Fifteen animals of each sex were used as vehicle controls. The Wistar
rats were observed for an addnl 12 mo... There was no evidence /of carcinogenicity in
either study/.
A 90% mortality of the 4th instar larvae of Aedes aegypti occurred after exposure for
24 hr to 1 day-aged rotenone (4 ppm) extracted
from Derris elliptica roots. The mortality percentage was dose-dependent and decreased by
aging rotenone extracts. The toxicity of rotenone to mosquitoes was completely lost within
14-15 days after extraction. The content of rotenone
in roots was higher (2.27%) in winter than in summer (1.6%).
Technical grades of rotenone at 0, 2.5, 5 or
10 mg/kg doses, suspended in corn oil, were administered orally in single doses on days
6-15 of pregnancy to Wistar rats. The dams were killed on the last day of pregnancy and
all fetuses were evaluated following routine teratologic methods. Rotenone
was associated with an increased number of non-pregnant rats and resorptions at 10 mg/kg
dose; reductions in maternal body wt gain, fetal wt and skeletal ossification; and
increased incidence of extra ribs at 5-10 mg/kg; no significant effects were noted at 2.5
mg/kg.
Applications of 2 or 5 ul/l concn of synergized rotenone
(2.5%) in the Pro-Noxfish formulation to 2
shallow, 0.05 hectare ponds caused a temporary reduction in both total number and
diversity of benthic invertebrates, a total mortality of caged Asiatic clams (Corbicula
manilensis) in both ponds, and a partial mortality of a resident population of larval
leopard frogs (Rana pipiens) in the 5 ul/l treatment. At day 7 after treatment, benthic
organisms were reduced 67% by the 2 ul/l concn and 96% by the 5 ul/l application. The
diversity index declined sharply in both ponds between days 3 and 7 after treatment, the
lowest values being recorded on day 7 and day 37 in the 2 and 5 ul/l treatments,
respectively. The equitability index declined from day 3 to day 37 in both ponds. By day
69, however, total numbers of benthic organisms had more than doubled over those
originally present in the 2 ul/l treatment, had more than tripled in the 5 ul/l treatment,
and were virtually unchanged in the control pond. Pretreatment zooplankton populations
were low; no significant deleterious effects from the treatments were observed.
Rotenone was tested for mutagenicity in the
Salmonella/microsome preincubation assay using a protocol approved by the National
Toxicology Program. Rotenone was tested over a
wide range of doses (0, 100, 333, 1000, 3333, and 10,000 ug/plate) in four Salmonella
typhimurium strains (TA98, TA100, TA1535, and TA1537) in the presence and absence of
Aroclor-induced rat or hamster liver S9. Rotenone
was negative in these tests and the highest ineffective dose level tested (not causing the
formation of a precipitate) in any Salmonella tester strain was 333 ug/plate.
Rotenone was not mutagenic when tested
according to a preincubation protocol with Salmonella typhimurium strains TA100, TA1535,
TA1537, and TA98 with or without metabolic activation by rat or hamster liver S9. Rotenone induced forward mutations in the mouse
L5178K/TK + or - lymphoma assay without activation; it was not tested in the presence of
S9. Results of tests with rotenone in Chinese
hamster oveary cells were negative for induction of sister chromatid exchanges in the
absence of exogenous metabolic activation (at concentrations at which the chemical was
very toxic), equivocal for sister chromatid exchanges in the presence of rat liver S9 (due
to a nonrepeatable positive response when tests were conducted up to toxic
concentrations), and negative for chromosomal aberratons in both the presence and absence
of metabolic activation.
It is about one half as toxic as pyrethrum. Rotenone
dust affects the nervous system and causes convulsions in animals. Animals repeatedly fed
derris powder (the botanical source containing 9.6% rotenone)
at levels from 312 to 4,000 ppm developed focal liver necrosis and mild kidney damage. Of
40 female rats given daily intraperitoneal injections of rotenone
in sunflower oil of 1.7 mg/kg for 42 days, more than 60% developed mammary tumors 6-11
months after the end of treatment; most of the tumors were mammary adenomas and one was a
differentiated adenocarcinoma; none of the control animals had tumors when examined 19
months after treatment.
Early chick embryo explants /were exposed/ for 15 minutes to 1 ug/ml and observed after
explantation various degrees of growth inhibition and neural tube defect.
Rats /were gavaged/ on days 6 through 15 with 2.5, 5 or 10 mg per kg. Maternal and
fetal weights were reduced at 5 and 10 mg. Minor skeletal defects were found in the 5 mg
group and resorptions were 46% in the 10 mg group.
Rotenone is nonphytotoxic, moderately toxic
to most animals, and very toxic to swine, but produces no harmful residues on vegetable
crops.
Signs of serious poisoning in animals include initial respiratory stimulation followed
by respiratory depression, incoordination, clonic or tonic convulsions, muscle tremors,
and death from respiratory failure ... The heart continues to beat and the blood pressure
is maintained for a relatively long time after respiration has stopped.
Dogs fed rotenone at the rate of 5 mg/kg/day
for a month appeared well but showed fatty changes of the liver and kidneys. A dosage of
10 mg/kg/day killed 3/5 dogs, and one that was killed showed severe toxic injury of the
liver, with possibly 1/3 of the bulk occupied by fat.
Dietary levels of 75 and 150 ppm of rotenone
were tolerated by pregnant guinea pigs but injured the young, which were either born dead
or failed to thrive after birth, suggesting that rotenone
or a toxic metabolite is excreted in the milk ... .
... daily oral admin of rotenone to female
rats at 5 mg/kg on days 6-15 of pregnancy resulted in reduced maternal weight gain and
that 10 mg/kg/day killed 60% of the dams. ... the high dose increased the number of
resorptions, but without producing significant fetal abnormalities. Some skeletal
malformations such as extra ribs were seen at 5 mg/kg/day although this dose rate did not
increase resorptions. Dosing at 2.5 mg/kg/day had no effects.
There is some disagreement in the literature regarding the carcinogenic potential of rotenone ... rotenone
may cause tumors only in vitamin-deficient animals. Rotenone
suppresses weight gain at or above 50 ppm in the diet of rats ... or hamsters ... and so
suppression of cell division may limit carcinogenic potential ... increased serum growth
hormone, progesterone, and estrogen levels may be involved in rotenone
carcinogenesis and showed a parallel between tumor incidence and low-level rotenone-induced obesity in rats.
Rotenone is a potential spindle poison. At
concn ranging from 1 x 10-7 to 1 x 10-5 M, the compound causes an increase in the mitotic
index of cultured hamster cells within 15 min. The index reaches a peak, the height of
which is proportional to the concn of the compound.
... Under the conditions of these 2 year feed studies ... there was no evidence of
carcinogenic activity for male or female B6C3F1 mice fed diets containing 600 or 1200 ppm rotenone for 2 years. The decreased incidence of liver
neoplasms in male mice may have been related to the administration of rotenone.
... Under the conditions of these 2 year feed studies, there was equivocal evidence of
carcinogenic activity of rotenone for male
F344/N rats, as indicated by an increased incidence of parathyroid gland adenomas
(uncommon tumors). There was no evidence of carcinogenic activity in female F344/N rats
fed diets containing 38 or 75 ppm rotenone.
Rotenone ... reduced the background incidence
of hepatocellular carcinoma in male B6C3Fl mice. In the present studies, rotenone
reduced the basal hepatic labeling index of male B6C3Fl mice in a dose dependent fashion
and inhibited hepatocellular proliferation, but not peroxisome proliferation, induced by
the peroxisome proliferator Wy-14,643. These results indicate that reduction of hepatic
tumors by rotenone may have been due to decr
liver cell replication, that peroxisome proliferation can be induced in the absence of
hepatocellular proliferation and suggest rotenone
as a potential tool in studies of relationships cell proliferation, peroxisomal
proliferation and hepatocarcinogenesis.
National Toxicology Program Studies:
Groups of 50 B6C3F1 mice of each sex were administered diets containing 0, 600, or
1,200 ppm rotenone on the same schedule. The
estimated average amount of rotenone consumed
per day was ... 115 mg/kg or 250 mg/kg for low dose and high dose mice. ... Survival of
high dose male mice was significantly greater than that of the controls (male: 29/50;
36/50; 47/50; female: 37/50; 42/50; 45/50). Final mean body weights of dosed mice were
lower than those of the controls by 8%-13% for males and 17%-24% for females. ...
Hepatocellular adenomas or carcinomas (combined) ... in the high dose group /were/ lower
than that in the controls (12/47; 12/49; 1/50). Because this low rate of combined liver
tumors is unusual, this decrease may have been related to rotenone
administration. ... Subcutaneous tissue fibromas, sarcomas, fibrosarcomas, or
neurofibrosarcomas (combined) in male mice occurred with a significant (P<0.05)
negative trend (8/49; 4/50; 2/50). The incidence in the high dose group was significantly
lower than that in the controls by the life table test (p=0.01). ... Under the conditions
of these 2 year feed studies ... there was no evidence of carcinogenic activity for male
or female B6C3F1 mice fed diets containing 600 or 1200 ppm rotenone
for 2 years. The decreased incidence of liver neoplasms in male mice may have been related
to the administration of rotenone.
Two-year studies of rotenone were conducted
by administering diets containing 0, 38, or 75 ppm rotenone
to groups of 50 F344/N rats of each sex for 103 weeks. ... The estimated average amount of
rotenone consumed per day was 1.7 mg/kg or 3.5
mg/kg for low dose or high dose rats. ... Survival of control and dosed rats was similar
(male: control, 22/50; low dose, 31/50; high dose, 30/50; female: control, 27/50; low
dose, 32/50; high dose, 31/50). Mean body weights of dosed and control male rats were
comparable. Mean body weights of high dose female rats were 5%-9% lower than those of the
controls between weeks 58 and 88. ... Parathyroid gland adenomas were observed in 1/41
control, 0/44 low dose, and 4/44 high dose male rats. The historical incidence of this
uncommon tumor in untreated control male rats in NTP studies is 4/1,314 (0.3%). Because
these tumors are rare and because the highest incidence ever seen in a control group is
1/50, the increase in these tumors may have been related to rotenone
administration. The incidence of subcutaneous tissue fibromas, fibrosarcomas, sarcomas,
myxosarcomas, or neurofibrosarcomas (combined) in low dose female rats was greater
(P<0.05) than that in the controls (0/50; 5/50; 3/50). These tumors were combined
because of their possible common histiogenic origin from fibroblasts or undifferentiated
mesenchymal cells. The incidence of those tumors in the low dose females was greater than
the historical rate at this laboratory (9/337, 3% + or - 1%) and throughout the Program
(50/2,021, 2% + or - 2%). Because of the lack of a significant dose-related trend and
because statistical significance was attained only by combining tumors of differing
morphology, the subcutaneous tissue tumors in female rats were not considered to be
chemically related. The incidences of these tumors in dosed male rats were not
significantly different from that in the controls. ... Under the conditions of these 2
year feed studies, there was equivocal evidence of carcinogenic activity of rotenone for male F344/N rats, as indicated by an
increased incidence of parathyroid gland adenomas (uncommon tumors). There was no evidence
of carcinogenic activity in female F344/N rats fed diets containing 38 or 75 ppm rotenone.
Non-Human Toxicity Values:
LD50 Rat oral 132-1500 mg/kg
LD50 White mouse oral 350 mg/kg
LD50 Mouse ip 2.8 mg/kg
LD50 Rat oral 132 mg/kg
Iv LD50 rat = 6 mg/kg
Oral LD50 Rat oral 64 mg/kg /Calculated from original mortality fractions/
LD50 Rat oral 25 mg/kg /Calculated from original mortality fractions; oil solution/
LD50 Rat oral 60 mg/kg
LD50 rat ip 2.2 mg/kg /Calculated from original mortality fractions/
LD50 Rat ip 1.6 mg/kg
LD50 Rat iv 0.2-0.3 mg/kg
LD50 Mouse ip 5.4 mg/kg /Calculated from original mortality fractions/
LD50 Guinea pig oral 13 mg/kg /Calculated from original mortality fractions; oil
solution/
LD50 Guinea pig oral 130 mg/kg /Calculated from original mortality fractions/
LD50 Guinea pig oral 75 mg/kg /Oil solution; minimal lethal dose/
LD50 Guinea pig ip 13 mg/kg /Calculated from original mortality fractions/
LD50 Guinea pig ip 2 mg/kg /Minimal lethal dose/
LD50 Rabbit oral 1,500 mg/kg /Minimal lethal dose/
LD50 Rabbit dermal 100-200 mg/kg
LD50 Rabbit iv 0.35-0.65 mg/kg /Minimal lethal dose/
LD50 Cat iv 0.65 mg/kg /Oil solution/
Ecotoxicity Values:
LD50 ANAS PLATYRHYNCHOS (MALLARD) ORAL FEMALE GREATER THAN OR EQUAL TO 2200 MG/KG, 3 MO
OLD
LD50 PHASIANUS COLCHICUS PHEASANT) ORAL FEMALE 1680 MG/KG (95% CONFIDENCE LIMIT
1410-2000 MG/KG), 3 MO OLD
LC50 Japanese quail oral 1882 ppm (95% confidence limits 1418-2497 ppm), 14 days old
LC50 Ring-necked pheasant oral 1608 ppm (95% confidence limit 1365-1875 ppm), 10 days
old
LC50 Mallard oral approx 2600 ppm, 10 days old
EC50 Simocephalus 310 ug/l/48 hr @ 15 deg C (95% confidence interval 239-402 ug/l),
first instar. Static bioassay without aeration, pH 7.2-7.5, water hardness 40-50 mg/l as
calcium carbonate and alkalinity of 30-35 mg/l. /Technical, 44%/
EC50 Daphnia pulex 100000 ug/l/48 hr @ 15 deg C (95% confidence interval 74000-134000
ug/l), first instar. Static bioassay without aeration, pH 7.2-7.5, water hardness 40-50
mg/l as calcium carbonate and alkalinity of 30-35 mg/l. /Technical, 44%/
LC50 Gammarus fasciatus 2600 ug/l/96 hr @ 21 deg C (95% confidence interval 2100-3200
ug/l), mature. Static bioassay without aeration, pH 7.2-7.5, water hardness 40-50 mg/l as
calcium carbonate and alkalinity of 30-35 mg/l. /Technical, 44%/
LC50 Salmo gairdneri (Rainbow trout) 31 ug/l/96 hr @ 12 deg C (95% confidence interval
27-36 ug/l), wt 0.3 g. Static bioassay without aeration, pH 7.2-7.5, water hardness 40-50
mg/l as calcium carbonate and alkalinity of 30-35 mg/l. /Technical, 44%/
LC50 Ictaluras punctatus (Channel catfish) 2.6 ug/l/96 hr @ 24 deg C (95% confidence
interval 2.1-3.2 ug/l), wt 0.5 g. Static bioassay without aeration, pH 7.2-7.5, water
hardness 40-50 mg/l as calcium carbonate and alkalinity of 30-35 mg/l. /Technical, 44%/
LC50 Lepomis macrochirus (Bluegill) 23 ug/l/96 hr @ 24 deg C (95% confidence interval
20-25 ug/l), wt 0.6 g. Static bioassay without aeration, pH 7.2-7.5, water hardness 40-50
mg/l as calcium carbonate and alkalinity of 30-35 mg/l. /Technical, 44%/
LC50 Pimephales promelas (fathead minnow) 6.0 mg/l/96 hr (confidence interval not
reliable), flow-through bioassay with measured concentrations, 17.3 deg C, dissolved
oxygen 9.2 mg/l, hardness 44.7 mg/l calcium carbonate, alkalinity 42.5 mg/l calcium
carbonate, and pH 7.5. Effect: Loss of equilibrium.
LC50 Coturnix oral 5,608 ppm (95% confidence interval 4459-7053 ppm) for 5 day diet,
slope: 5.78, standard error: 1.57.
LC50 Esox lucius (Northern pike) 33.0 ug/L/96 hr, Static bioassay
LC50 Micropterus salmoides (Largemouth bass) 142 ug/L/96 hr, Static bioassay
LC50 Stizostedion vitreum (Walleye) 16 ug/L/24 hr, Static bioassay
LC50 Amia calva (bowfin) 30 ug/L/96 hr, Static bioassay
LC50 Coho salmon 62 ug/L/96 hr, Static bioassay
LC50 Chinook salmon 37 ug/L/96 hr, Static bioassay
LC50 rainbow trout 46 ug/L/96 hr, Static bioassay
LC50 Atlantic salmon 21 ug/L/96 hr, Static bioassay
LC50 brook trout 44 ug/L/96 hr, Static bioassay
LC50 lake trout 27 ug/L/96 hr, Static bioassay
LC50 goldfish 497 ug/L/96 hr, Static bioassay
LC50 carp 50 ug/L/96 hr, Static bioassay
LC50 fathead minnow 142 ug/L/96 hr, Static bioassay
LC50 Catostomus catostomus (longnose sucker) 57 ug/L/96 hr, Static bioassay
LC50 white sucker 68 ug/L/96 hr, Static bioassay
LC50 black bullhead 389 ug/L/96 hr, Static bioassay
LC50 channel catfish 164 ug/L/96 hr, Static bioassay
LC50 green sunfish 141 ug/L/96 hr, Static bioassay
LC50 bluegill sunfish 141 ug/L/96 hr, Static bioassay
LC50 smallmouth bass 142 ug/L/96 hr, Static bioassay
LC50 yellow perch 70 ug/L/96 hr, Static bioassay
32-Day LC50 Salmo gairdneri 2.1 ug/L /Conditions of bioassay not specified/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
5'BETA-(3-METHOXY-14C)ROTENONE UNDERWENT
EXTENSIVE DEMETHYLATION IN RODENTS. /5' BETA-(3-METHOXY-14C)ROTENONE/
BIOTRANSFORMATION...IN RATS LEADS TO HYDROXYLATION OF POSITION 12A AT B/C RING JUNCTION
TO GIVE ROTENOLONES...TO OXIDATION OF ISOPROPENYL SIDE-CHAIN TO AFFORD
6',7'-DIHYDRO-6',7'-DIHYDROXY-ROTENONE &
8'-HYDROXYROTENONE, & TO FORMATION OF UNIDENTIFIED WATER-SOL METABOLITES.
MICROSOME FRACTIONS FROM HOUSEFLY ABDOMENS, MOUSE LIVERS, & RAT LIVERS WERE USED TO
STUDY ROTENONE DEGRADATION. METABOLITES SO
PRODUCED WERE... /ROTENOLONE I & II, 8'-HYDROXYROTENONE, 8'-HYDROXYROTENOLONE I &
II, 6',7'-DIHYDRO-6',7'-DIHYDROXYROTENONE, 6',7'-DIHYDRO-6',7'-DIHYDROXYROTENOLONE I &
II/
In rat liver and in insects, the furan ring is enzymatically opened and cleaved,
leaving behind a methoxy group. The principal metabolite is rotenonone. An alcohol has
been found as a further metabolite, this being formed via oxidation of a methyl group of
the isopropenyl residue.
Rotenone is metabolized rather efficiently by
the liver. In order to produce the same clinical effect, the compound must be injected
into a mesenteric vein at about 10 times the dose required for injection into a femoral
vein ... .
Rat and mouse liver enzymes and intact mice hydroxylate rotenone
at carbons 7 and 24. In vitro, the change is produced by microsomes in the presence of
nicotinamide-adenine dinucleotide phosphate. The products include rotenolone I, rotenolone
II, 8'-hydroxyrotenone, 6',7'-dihydro-'6',7'-dihydroxyrotenone, two rotenolones of each of
the latter compounds, and uncharacterized polar materials.
One mechanism of detoxication of natural rotenone
... or one of its metabolites was found to be 3-O-demethylation ...
Absorption, Distribution & Excretion:
EXHALATION OF (14)CO2 WITHIN 50 HR AFTER ORAL OR IP DOSING OF 5'BETA-[3-METHOXY-(14)C]ROTENONE TO MICE & RATS RESPECTIVELY WAS 27 &
12.5%. /5'BETA-[3-METHOXY-(14)C]ROTENONE/
GI ABSORPTION IS PRESUMABLY SLOW & INCOMPLETE. ... FATS & OILS PROMOTE
ABSORPTION.
One mechanism of detoxication of natural rotenone
... or one of its metabolites was found to be 3-O-demethylation, as indicated by recovery
of 27 and 13% of the admin radiocarbon as 14C-labeled carbon dioxide within 50 hr after
admin to mice and rats, respectively. Within the same period, the animals excreted 7-17%
of the radioactivity in their urine ... In another study, 19.5 and 20.0% of the dose were
recovered in the urine of mice and rats, respectively, within 24 hr after oral admin ... .
Mechanism of Action:
Rotenone functions as an inhibitor of the
mitochondrial oxidative phosphorylation-electron transport system, but the chemical was
found to be a potent in vitro antagonist of slow-reacting substance of anaphylaxis.
Rotenone inhibits the oxidn of NADH to NAD.
Consequently, it blocks the oxidn by NAD of substrates such as glutamate,
alpha-ketoglutarate, and pyruvate.
Rotenone is a highly potent mitochondrial
poison, blocking NADH oxidation, and this property dominates its actions in animals.
Rotenone is one of the most potent known
inhibitors of the NADH dehydrogenase system. ... 20 pmol/mg protein produces 50%
inhibition of mitochondrial pyruvate oxidation. Radiolabel studies showed this to be
equivalent to 2 moles rotenone per
"mole" of NADH dehydrogenase. The site at which rotenone
acts involves Fe-S proteins and is the same as the site at which amytal produces its
inhibition, although rotenone is more selective
and shows less affinity for other proteins.
The block of NADH oxidation can lead to increased incorporation of acetate into
long-chain fatty acids by isolated mitochondria ... This may be a link with the fatty
changes seen in the liver after long-term feeding.
It is thought that rotenone acts on the
spindle by preferential binding at sulfhydryl and disulfide bonds in its protein structure
... Detailed study of cultured mammalian cells by both light and electron microscopy
confirmed that rotenone reversibly inhibits
spindle microtubule assembly ... However, rotenone
delayed cell progression in all phases of the cell cycle. This was thought to be a direct
result of respiratory inhibition, even though amytal, which blocks electron transport at
the same site as that blocked by rotenone, does
not arrest cell progression at mitosis. Thus, the total effect of rotenone
was thought to depend on inhibition of respiration and, separately and more importantly,
on inhibition of microtubule assembly ... although the relevance of the microtubule effect
in cells not unusually resistant to metabolic inhibition is unclear.
Rotenone is an inhibitor which blocks
electron transfer between NADH and coenzyme Q.
Interactions:
WHEN APPLIED @ LOW CONCN TO PLANT FOLIAGE, ROTENONE
CATALYZES PHOTOISOMERIZATION OF DIELDRIN & OTHER CYCLODIENE INSECTICIDE RESIDUES. ...
HOWEVER PHOTODECOMPOSITION WAS PREDOMINANT EFFECT WHEN RESIDUES OF ROTENONE
WERE COMBINED WITH THOSE OF METHYLCARBAMATE & PHOSPHOTHIONATE INSECTICIDES.
Pharmacology:
Therapeutic Uses:
Vet: acaricide, ectoparasiticide
MEDICATION: ANTIPROTOZOAL; MEDICATION (VET): GRUBICIDE; HAS BEEN USED FOR DEMODECTIC
MANGE
/Former use/: Rotenone has been used
topically for treatment of head lice, scabies, and other ectoparasites, but the dust is
highly irritating to the eyes (potentially causing conjunctivitis), the skin (causing
contact dermatitis), and to the upper respiratory tract (causing rhinitis) and throat
(linked with pharyngitis).
Interactions:
WHEN APPLIED @ LOW CONCN TO PLANT FOLIAGE, ROTENONE
CATALYZES PHOTOISOMERIZATION OF DIELDRIN & OTHER CYCLODIENE INSECTICIDE RESIDUES. ...
HOWEVER PHOTODECOMPOSITION WAS PREDOMINANT EFFECT WHEN RESIDUES OF ROTENONE
WERE COMBINED WITH THOSE OF METHYLCARBAMATE & PHOSPHOTHIONATE INSECTICIDES.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Rotenone's production and use in
insecticides, flea powders, fly sprays, and moth-proofing agents will result in its
release to the environment from its use. If released into the atmosphere, rotenone will exist solely in the vapor phase in the
ambient atmosphere, based on a measured vapor pressure of 8X10-4 mm Hg at 25 deg C.
Vapor-phase rotenone is degraded in the
atmosphere by reaction with photochemically-produced hydroxyl radicals with a half-life of
about 0.05 days. An estimated Koc value of 4,000 suggests that rotenone
will have slight mobility in soil. Volatilization from moist soil is not expected based
upon an estimated Henry's Law constant of 1.12X10-13 atm-cu m/mole. Volatilization from
dry soil surfaces should not be important given the vapor pressure of this compound. The
field half-life for rotenone in anaerobic and
aerobic soils is 3 days. Rotenone is listed as
one of the organic substances which may be degraded during aerobic and anaerobic sewage
treatment if adequate acclimatization can be achieved; much depends on the concentration
to be treated and possibly on the temperature during treatment. In water, rotenone is expected to adsorb to sediment or
particulate matter based on its Koc value. This compound is not expected to volatilize
from water surfaces given its estimated Henry's Law constant. Bioconcentration in aquatic
organisms should be high based upon an estimated BCF value of 770. Given the commercial
uses of rotenone, human exposure appears to be
likely from occupational situations through dermal and inhalation routes. The general
population may be exposed to rotenone via
ingestion of food, and dermal contact with vapors, food and other products containing rotenone. (SRC)
Probable Routes of Human Exposure:
Inhalation, ingestion, skin and eye contact.
... Extraction of derris root, formulation or application of /rotenone/.
NIOSH (NOES Survey 1981-1983) has statistically estimated that 8,099 workers (2,470 of
these are female) are potentially exposed to rotenone
in the US(1). Occupational exposure may be through inhalation of dusts and dermal contact
with this compound at workplaces where rotenone
is produced or used(SRC). The general population may be exposed to rotenone
ingestion of food(2) and drinking water, and dermal contact with vapors, food and other
products containing rotenone(SRC). Limited
monitoring data indicate that non-occupatioal exposures can occur from the ingestion of
contaminated drinking water. The most probable human exposure would be occupational
exposure, which may occur through dermal contact or inhalation at workplaces where it is
produced or used(SRC).
Natural Pollution Sources:
Many plant sources of rotenone are known,
particularly Derris grown in Malaya and the East Indies, and Lonchocarpus (familiarly
known as cube) grown in Central and South America.
Artificial Pollution Sources:
Rotenone's production and use in
insecticides, flea powders, fly sprays, and moth-proofing agents(1) will result in its
release to the environment from its use(SRC).
Environmental Fate:
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of
4,000(SRC), determined from an experimental log Kow(2,SRC) and a regression-derived
equation(3), indicates that rotenone is expected
to have slight mobility in soil(SRC). Volatilization of rotenone
from moist soil surfaces is not expected(SRC) given an estimated Henry's Law constant of
1.12X10-13 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Rotenone is not expected to volatilize from dry soil
surfaces based on an estimated vapor pressure of 8X10-4 mm Hg(SRC), determined from a
fragment constant method(5). The field half-life for rotenone
in anaerobic and aerobic soils is 3 days(6).
TERRESTRIAL FATE: A cold water pond (0 to 5 deg C, November 1983) at the Geona National
Fish Hatchery, Wisconson and a warm water pond (23 to 27 deg C, July 1984) at the La
Crosse National Fisheries Research Center was treated with Noxfish
(0.25 mg/l rotenone) and analyzed. Residues of rotenone in bottom sediments in the cold water pond
peaked at 0.10 ug/g after 14 days and then declined to < 0.025 ug/g (limit of
detection) after 64 days. Accumulation and elimination were much faster in the warm water
pond: concentration in bottom sediments peaked at 0.075 ug/g after 6 hours and dropped to
<0.025 ug/g after 24 hours(1).
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of
4,000(SRC), determined from an experimental log Kow(2,SRC) and a regression-derived
equation(3), indicates that rotenone is expected
to adsorb to suspended solids and sediment in water(SRC). Rotenone
is not expected to volatilize from water surfaces(3,SRC) based on an estimated Henry's Law
constant of 1.12X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation
method(4). According to a classification scheme(5), an estimated BCF value of 770(3,SRC),
from an experimental log Kow(2,SRC), suggests that bioconcentration in aquatic organisms
is high(SRC). Decomposition of rotenone in water
followed a first-order decay curve; half-life was 10.3 days in cold water and 0.94 days in
warm water. In freshwater mussels and crayfish, rotenone
residues gradually increased for 1 week in cold water and 1 day in warm water and then
slowly decreased. Rotenone residues in fish
varied with species and water temperatures(6).
AQUATIC FATE: A cold water pond (0 to 5 deg C, November 1983) at the Geona National
Fish Hatchery, Wisconsin and a warm water pond (23 to 27 deg C, July 1984) at the La
Crosse National Fisheries Research Center was treated with Noxfish
(0.25 mg/l rotenone) and analyzed. In the cold
water pond, the mean concentration of rotenone
in samples taken 3 hours after treatment was 0.229 mg/l; concentration of rotenone declined gradually but steadily to 0.002 mg/l
(limit of detection) after 57 days. In the warm water pond the mean concentration of rotenone in samples taken after 3 hours was 0.180
mg/l; concentration of rotenone declined by more
than 50 percent in the first 12 hours and then fell to 0.002 mg/l within four days(1).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), rotenone,
which has an experimental vapor pressure of 8X10-4 mm Hg at 25 deg C(2,SRC), is expected
to exist solely as a vapor in the ambient atmosphere. Vapor-phase rotenone
is degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals(SRC); the half-life for this reaction in air is estimated to be about 0.05
days(3,SRC). Particulate-phase rotenone may be
physically removed from the air by wet and dry deposition(SRC).
Environmental Biodegradation:
ROTENONE IS BIODEGRADABLE.
Rotenone is listed as one of the organic
substances which may be degraded during aerobic and anaerobic sewage treatment if adequate
acclimatization can be achieved; much depends on the concentration to be treated and
possibly on the temperature during treatment(1).
Environmental Abiotic Degradation:
PHOTODECOMPOSITION PRODUCTS FORMED BY IRRADIATION OF ROTENONE...EXPOSED
TO LIGHT ON GLASS SURFACES OR ON BEAN LEAVES: O-DEMETHYL ROTENONE;
6ALPHABETA, 12ALPHAALPHA-ROTENOLONE; DEHYDRO-ROTENONE;
6ALPHABETA, 12ALPHABETA-ROTENOLONE; ROTENONONE; 6',7'-EPOXYROTENONE;
6',7'-EPOXY-6ALPHABETA, 12ALPHABETA-ROTENOLONE.
The material deteriorates rapidly in sun, air, and water. Formulations lose their
effectiveness within a week after application.
Rotenone is stable in the solid state but
degradation is accelerated by the presence of organic solvents. Air and light are
required. The rate of decomposition produced the yellow crystalline dehydrorotenone and
rotenonone and a complex mixture of other oxidation products of rotenone.
The rate constant for the vapor-phase reaction of rotenone
with photochemically-produced hydroxyl radicals has been estimated as 318X10-12 cu
cm/molecule-sec at 25 deg(SRC) using a structure estimation method(1,SRC). This
corresponds to an atmospheric half-life of about 0.05 days at an atmospheric concentration
of 5X10+5 hydroxyl radicals per cu cm(1,SRC). When exposed to light and air, rotenone undergoes hydroxylation at C-7, followed by
dehydration to form dehydrorotenone. These reactions inactivate rotenone
after 5 to 10 days of exposure to sunlight. In a study of photosensitizers, rotenone was found to be the most effective compound
for enhancing the photochemical alteration of dieldrin to photodieldrin when applied to
bean plants at levels as low as 0.3 ppm(4). In another study, irradiation of rotenone in oxygenated methanol solution with UV light
yielded the following crystalline products: O-demethylrotenone, 6ab,-12ab-rotenolone,
rotenonone, 4,5-dimethoxysalicylic acid, rissic acid, and tubaic acid(5).
Environmental Bioconcentration:
An estimated BCF value of 770 was calculated for rotenone(SRC),
using an experimental log Kow of 4.10(1,SRC) and a recommended regression-derived
equation(2). According to a classification scheme(3), this BCF value suggests that
bioconcentration in aquatic organisms is high(SRC). A study showed that when yearling
bluegills (L. macrohirus) were exposed to 5.2 ug/l of rotenone
for 30 days in a continuous flow system, bioconcentration factors for the head, viscera,
and carcass were 165, 3,500, and 125, respectively(4).
Soil Adsorption/Mobility:
The Koc of rotenone is estimated as
approximately 4,000(SRC), using a measured log Kow of 4.10(1) and a regression-derived
equation(2,SRC). According to a recommended classification scheme(3), this estimated Koc
value suggests that rotenone is expected to have
slight mobility in soil(SRC). The field half-life for rotenone
in anaerobic and aerobic soils is 3 days(4).
Volatilization from Water/Soil:
The Henry's Law constant for rotenone is
estimated as 1.12X10-13 atm-cu m/mole(SRC) from its experimental values for vapor
pressure, 8X10-4 mm Hg(1), and water solubility, 0.2 mg/l(1). This value indicates that rotenone will be essentially nonvolatile from water
surfaces(2,SRC). Rotenone's Henry's Law
constant(1,SRC) indicates that volatilization from moist soil surfaces is not
expected(SRC). Rotenone is not expected to
volatilize from dry soil surfaces based on a measured vapor pressure of 8X10-4 mm Hg(1).
Environmental Water Concentrations:
Rotenone enters surface waters through direct
application in fishery management.
GROUNDWATER: Groundwater sampling for pesticides in the United States was conducted by
the EPA from 1971 to 1991. Results showed that out of 12 wells sampled in California from
1987 to 1988, no concentration of rotenone was
detected(1).
Food Survey Values:
Pesticide residues were reported in foods for the 4-year period 1982 to 1986. Rotenone was found as a residue in FY83-86 regulatory
monitoring of approximately 11,500 samples(1).
Fish/Seafood Concentrations:
A cold water pond (0 to 5 deg C, November 1983) at the Geona National Fish Hatchery,
Wisconson and a warm water pond (23 to 27 deg C, July 1984) at the La Crosse National
Fisheries Research Center was treated with Noxfish
(0.25 mg/l rotenone) and analyzed. Channel
catfish (Ictalurus punctatus) and largemouth bass (Micropterus salmoides) were used as
representative fish for analysis in cold water; black bullheads (Ictalurus melas) and
bluegills (Lepomis macrochirus) were used as representative fish for analysis in warm
water. Concentrations of rotenone in catfish
ranged from 0.123 ug/g after 1 day to 0.178 ug/g after 20 days; no further sampling was
possible after this because all the fish had died. Concentrations of rotenone
in largemouth bass ranged from 0.082 ug/g after 1 day to 0.502 ug/g after 6 days; no
further sampling was possible after this because all the fish had died. Concentrations of rotenone in black bullheads ranged from 0.0.005 ug/g
(limit of detection) after 1 day to 0.083 ug/g after 21 days, declining to <0.005 ug/g
after 35 days. Concentrations of rotenone in
bluegills ranged from 0.064 ug/g after 1 day to <0.005 ug/g after 21 days(1).
A cold water pond (0 to 5 deg C, November 1983) at the Geona National Fish Hatchery,
Wisconsin and a warm water pond (23 to 27 deg C, July 1984) at the La Crosse National
Fisheries Research Center was treated with Noxfish
(0.25 mg/l rotenone) and analyzed. Fresh water
crayfish (Orconectes sp.) and mussels (Lampsilis sp. were used as representative
invertebrates. Crayfish in the cold water pond had rotenone
concentrations ranging from 0.0.395 ug/g after 1 day of treatment to <0.057 ug/g after
21 days; rotenone concentrations did not reach
the limit of detection because all the fish had died by day 21. Crayfish in the warm water
pond had rotenone concentrations ranging from
0.058 ug/g after 1 day of treatment to <0.005 ug/g (limit of detection) after 7 days.
Mussels in the cold water pond had rotenone
concentrations peak at 0.723 ug/g on day 7 and decline to 0.230 ug/g on day 28. In the
warm water pond, rotenone concentrations reached
1.060 ug/g after 1 day of treatment; no further sampling was possible after this because
all the mussels had died(1).
Environmental Standards & Regulations:
FIFRA Requirements:
When applied to growing crops, in accordance with good agricultural practice, the
following pesticide chemicals are exempt from the requirement of a tolerance: Rotenone or derris or cube roots.
As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of
older pesticides to consider their health and environmental effects and make decisions
about their future use. Under this pesticide reregistration program, EPA examines health
and safety data for pesticide active ingredients initially registered before November 1,
1984, and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act of 1996. Rotenone is found on List A, which contains most food
use pesticides and consists of the 194 chemical cases (or 350 individual active
ingredients) for which EPA issued registration standards prior to FIFRA, as amended in
1988. Case No: 0255; Pesticide type: Insecticide (acaricide,piscicide); Registration
Standard Date: 10/88; Case Status: OPP is reviewing data from the pesticide's producers
regarding its human health and/or environmental effects, or OPP is determining the
pesticide's eligibility for reregistration and developing the Reregistration Eligibility
Decision (RED) document.; Active ingredient (AI): Rotenone;
Data Call-in (DCI) Date(s): 10/13/95; AI Status: The producers of the pesticide has made
commitments to conduct the studies and pay the fees required for reregistration, and are
meeting those commitments in a timely manner.
State Drinking Water Guidelines:
(ME) MAINE 4 ug/l
(FL) FLORIDA 28 ug/l
Allowable Tolerances:
When applied to growing crops, in accordance with good agricultural practice, the
following pesticide chemicals are exempt from the requirement of a tolerance: Rotenone or derris or cube roots.
Chemical/Physical Properties:
Molecular Formula:
C23-H22-O6
Molecular Weight:
394.41
Color/Form:
ORTHORHOMBIC, SIX-SIDED PLATES FROM TRICHLOROETHYLENE
NEEDLES OR LEAVES (ALCOHOL, AQ ACETONE)
COLORLESS CRYSTALS
White crystals
Colorless to red, crystalline solid.
Odor:
Odorless.
Boiling Point:
210-220 DEG C @ 0.5 MM HG
Melting Point:
165-166 DEG C
Corrosivity:
Non-corrosive
Density/Specific Gravity:
1.27 @ 20 DEG C
Octanol/Water Partition Coefficient:
Log P = 4.10
Solubilities:
Sol in alcohol, acetone, carbon tetrachloride, chloroform, ether
Sol in acetic acid, acetone; sl sol in ethanol
15 PPM IN WATER AT 100 DEG C; SLIGHTLY SOL IN PETROLEUM OILS
SOL IN LIPIDS
Water solubility = 0.2 mg/l at 20 deg C
Soluble in ether, alcohol, acetone, and other organic solvents
Spectral Properties:
MAX ABSORPTION (ALCOHOL): 237 NM (LOG E= 4.15), 293.5 NM (LOG E= 4.25), 330.5 NM (LOG
E= 3.80); SADTLER REFERENCE NUMBER: 373 (IR, PRISM)
Specific optical rotation: -228 deg at 20 deg C/D (concn by vol= 2.22 g in 100 ml
benzene)
Specific optical rotation: -225.2 deg at 29.5 deg C/D (benzene)
Intense mass spectral peaks: 192 m/z (100%), 191 m/z (31%), 394 m/z (20%), 177 m/z
(18%)
IR: 21008 (Sadtler Research Laboratories IR Grating Collection)
UV: 149 (Sadtler Research Laboratories Spectral Collection)
NMR: 16340 (Sadtler Research Laboratories Spectral Collection)
MASS: 5060 (National Bureau of Standards EPA-NIH Mass Spectra Data Base, NSRDS-NBS-63)
Strongly levorotatory in solution; specific rotation for D line 230 deg in benzene, 62
deg in ethylene dichloride.
Vapor Pressure:
8X10-4 mm Hg at 20 deg C
Other Chemical/Physical Properties:
MP: 185-186 DEG C /DIMORPHIC ROTENONE/
SHOWS RAPID RACEMIZATION ON ALKALI TREATMENT; CRYSTALLIZES WITH SOLVENT OF
CRYSTALLIZATION; CIS CONFIGURATION IS GENERALLY ACCEPTED
Dec upon exposure to light and air; colorless solns in organic solvents oxidize upon
exposure and become yellow, orange, and then deep red and may deposit crystals of
dehydrorotenone and rotenone.
Chemical Safety & Handling:
Skin, Eye and Respiratory Irritations:
Direct contact may cause irritation of the skin or conjunctiva.
Fire Potential:
Flammable if preheated.
Hazardous Reactivities & Incompatibilities:
Strong oxidizers, alkalis.
Hazardous Decomposition:
When heated to decomposition it emits acrid smoke and irritating fumes.
Decomposes on exposure to light and air.
Immediately Dangerous to Life or Health:
2500 mg/cu m
Protective Equipment & Clothing:
Wear appropriate personal protective clothing to prevent skin contact.
Wear appropriate eye protection to prevent eye contact.
Recommendations for respirator selection. Max concn for use: 50 mg/cu m. Respirator
Class(es): Any chemical cartridge respirator with organic vapor cartridge(s) in
combination with a dust, mist, and fume filter. Any supplied-air respirator.
Recommendations for respirator selection. Max concn for use: 125 mg/cu m. Respirator
Class(es): Any supplied-air respirator operated in a continuous flow mode. Any powered,
air-purifying respirator with organic vapor cartridge(s) in combination with a dust, mist,
and fume filter.
Recommendations for respirator selection. Max concn for use: 250 mg/cu m. Respirator
Class(es): Any chemical cartridge respirator with a full facepiece and organic vapor
cartridge(s) in combination with a high-efficiency particulate filter. Any air-purifying,
full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted organic
vapor canister having a high-efficiency particulate filter. Any powered, air-purifying
respirator with a tight-fitting facepiece and organic vapor cartridge(s) in combination
with a high-efficiency particulate filter. Any supplied-air respirator that has a
tight-fitting facepiece and is operated in a continuous-flow mode. Any self-contained
breathing apparatus with a full facepiece. Any supplied-air respirator with a full
facepiece.
Recommendations for respirator selection. Max concn for use: 2500 mg/cu m. Respirator
Class(es): Any supplied-air respirator operated in a pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection. Condition: Emergency or planned entry into
unknown concn or IDLH conditions: Respirator Class(es): Any self-contained breathing
apparatus that has a full facepiece and is operated in a pressure-demand or other positive
pressure mode. Any supplied-air respirator with a full facepiece and operated in
pressure-demand or other positive pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other positive pressure
mode.
Recommendations for respirator selection. Condition: Escape from suddenly occurring
respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator
(gas mask) with a chin-style, front- or back-mounted organic vapor canister having a
high-efficiency particulate filter. Any appropriate escape-type, self-contained breathing
apparatus.
Wear rubber gloves for all handling ... Wear canister-type mask /if combustion occurs/.
... Self-contained breathing apparatus, rubber gloves, hats, suits, and boots must be worn
/if extinguishing/.
Preventive Measures:
DO NOT REUSE EMPTY CONTAINER. DESTROY IT BY PERFORATING & CRUSHING. BURY OR DISCARD
IN SAFE PLACE AWAY FROM WATER SUPPLIES.
Wear appropriate clothing to prevent repeated or prolonged skin contact. Wear eye
protection to prevent any reasonable probability of eye contact. Employees should wash
promptly when skin is wet or contaminated. Work clothing should be changed daily if it is
possible that clothing is contaminated. Remove nonimpervious clothing promptly if wet or
contaminated.
SRP: The scientific literature for the use of contact lenses in industry is
conflicting. The benefit or detrimental effects of wearing contact lenses depend not only
upon the substance, but also on factors including the form of the substance,
characteristics and duration of the exposure, the uses of other eye protection equipment,
and the hygiene of the lenses. However, there may be individual substances whose
irritating or corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn. In any
event, the usual eye protection equipment should be worn even when contact lenses are in
place.
Contact lenses should not be worn when working with this chemical.
The worker should immediately wash the skin when it becomes contaminated.
Work clothing that becomes wet or significantly contaminated should be removed and
replaced.
Workers whose clothing may have become contaminated should change into uncontaminated
clothing before leaving the work premises.
Stability/Shelf Life:
DECOMP UPON EXPOSURE TO LIGHT & AIR; COLORLESS SOLN IN ORG SOLVENTS OXIDIZE UPON
EXPOSURE & BECOME YELLOW, ORANGE & THEN DEEP RED
DRY CRYSTALLINE POWDER IS RELATIVELY STABLE.
DUSTS PREPARED FROM EXTRACTS DETERIORATE RAPIDLY, ESP IN PRESENCE OF SMALL AMT OF ANY
VOLATILE INERT SOLVENT, BUT ARE STABILIZED BY INCORPORATION OF SMALL AMT OF STRONG ACID
... .
The dusts /of rotenone/ are stabilized with
phosphoric acid to reduce oxidation.
... Detoxified by heating; 2 hr at 100 deg C results in 76% decomposition.
Racemized by alkalis to less insecticidal compounds, more rapidly in certain solvents.
Storage Conditions:
Containers: Fiber drums; tins; multiwall paper sacks; keep in well-ventilated area.
Cleanup Methods:
AQ SOLN OF ROTENONE WERE PERCOLATED THROUGH
GLASS COLUMNS CONTAINING GRANULAR ACTIVATED CARBON. THE ABSORPTIVE CAPACITY OF THE
ACTIVATED CARBON WAS 0.1 MG/G FOR ROTENONE.
1. Ventilate area of spill. 2. For small quantities, sweep onto paper or other suitable
material, place in an appropriate container and burn in a safe place (such as a fume
hood). Large quantities can be reclaimed; however, if this is not practical, dissolve in a
flammable solvent (such as alc) and atomize in a suitable combustion chamber.
Disposal Methods:
1. By making packages of rotenone in paper or
other flammable material and burning in a suitable combustion chamber. 2. By dissolving rotenone in a flammable solvent (such as alcohol) and
atomizing in a suitable combustion chamber.
SRP: At the time of review, criteria for land treatment or burial (sanitary landfill)
disposal practices are subject to significant revision. Prior to implementing land
disposal of waste residue (including waste sludge), consult with environmental regulatory
agencies for guidance on acceptable disposal practices.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 5 mg/cu m.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 5 mg/cu m /Rotenone
(commercial)/
Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three
times the TLV-TWA for no more than a total of 30 min during a work day, and under no
circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not
exceeded. /Rotenone (commercial)/
A4. A4= Not classifiable as a human carcinogen. /Rotenone
(commercial)/
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 5 mg/cu m.
Immediately Dangerous to Life or Health:
2500 mg/cu m
Manufacturing/Use Information:
Major Uses:
Control of aphids, thrips, psyllids, moths, beetles, spider mites, etc in fruit and
vegetable cultivation. Insecticidal control of premises. Control of fire ants. Control of
lice, ticks, and warble flies on animals. Also used to control fish populations in fish
management.
Flea powders, fly sprays, moth-proofing agents; insecticide.
In the form of ground derris root, rotenone
has been used as a nonpersistent insecticide to control pests on plants and animals and as
a fish poison to manage or to eliminate undesirable species in reservoirs, lakes, and
streams.
Acaricide; insecticide
MEDICATION
MEDICATION (VET)
Rotenone is very toxic to fish, and one of
its main uses by native people over the centuries was to paralyze fish for capture and
consumption.
Manufacturers:
Prentiss Inc, CB 2000, Floral Park, NY 11002-2000 (516) 326-2312
Roussel Uclaf Corp, 95 Chestnit Ridge Rd, Montvale, NJ 07645 (201) 307-3281
Tifa Ltd, 50 Division Ave, Millington, NJ 07946 (908) 647-4570
Methods of Manufacturing:
The current methods of extraction of rotenone
and other natural insecticides from their plant sources are enhanced by mixing the known
solvents such as dialkyl phthalates, dichloromethane, or trichlormethane at 10-70% with
30-90% of (C)8-20 aliphatic acid esters with (C)1-16 alkyls or alkenyls. Thus, agitation
of 100 g dichloromethane at 45 deg for 0.5 hr, followed by removal of dichloromethane by
distillation gave an extraction containing 14% rotenone
plus 64% octyl stearate. The extraction was diluted to 7% rotenone
and emulsified by a surfactant for spraying plants.
Pure crystalline rotenone is prepared by
extracting powdered rotenone containing roots
with a solvent, eg ether or carbon tetrachloride, and concentrating the solution to
produce crystallization.
Produced in Malaysia from Derris elipitica roots and in South America from Lonchocarpus
roots; white crystalline solid separated from the root by solvent extraction followed by
crystallization.
General Manufacturing Information:
USEFUL...TO ELIMINATE UNDESIRABLE FISH SPECIES WHICH MAY DOMINATE FARM PONDS, ENABLING
DESIRABLE SPECIES TO BE REESTABLISHED.
IT HAS...BEEN EMPLOYED CLINICALLY FOR EXTERNAL TREATMENT OF CHIGGERS (2% LOTION) &
SCABIES (10% EMULSION).
ITS USE FOR LOUSE CONTROL ON HUMANS IS NOT RECOMMENDED SINCE IRRITATION IS OFTEN
PRODUCED, ESP IN GROIN REGION. ...WIDELY USED TO CONTROL PESTS SUCH AS MEXICAN BEAN
BEETLE, CABBAGE WORMS, LEAF HOPPERS & OTHER INSECTS...IT IS ESP USEFUL FOR APPLICATION
TO VEGETABLES NEAR TIME FOR HARVEST WHEN CERTAIN...EFFECTIVE NEWER INSECTICIDES CANNOT BE
USED BECAUSE OF POTENTIALLY EXCESSIVE RESIDUES. ...USED FOR CONTROLLING INSECT PARASITES
OF ANIMALS. IT IS EFFECTIVE FOR CONTROLLING CATTLE GRUBS, & IS EMPLOYED ALSO FOR LICE,
FLEAS, & TICKS ON PETS & LIVESTOCK.
SELECTIVE CONTACT INSECTICIDE WITH SOME ACARICIDAL PROPERTIES. CUBE (GENUS
LONCHOCARPUS) IS NOW THE ONLY COMMERCIAL SOURCE IN USA OF ROTENONE
FOR INSECTICIDE PRODUCTION... PERU IS MAJOR SOURCE OF ROOT OF PLANT... ROOTS ARE PREPARED
FOR USE IN INSECTICIDES BY...EXTRACTING INSECTICIDAL PRINCIPLES WITH ACETONE, CARBON
TETRACHLORIDE, BENZENE, OR OTHER SOLVENTS... FORMULATIONS LOSE THEIR EFFECTIVENESS WITHIN
A WK AFTER APPLICATION.
/Rotenone/ is of low persistence in spray or
dust residues.
The (13)C NMR spectra of epimers of rotenone
and 4 12a-hydroxy-analogs were examined to determine the stereochemical effect of B/C ring
fusion involving the 6a- and 12a-C centers. Chemical shift differences between the
epimeric carbon resonances of cis- and trans-6a, 12a-cmpd were notably larger than those
of diastereoisomers derived from the same B/C ring junction stereochemically. Results of
the spectral analysis are useful for the quantification of mixtures of epimers and for the
measurement of rates of epimerization and oxygenation.
Formulations/Preparations:
Prentox Prenfish toxicant (5% rotenone); Prentox Synpren-Fish toxicant (2.5% rotenone and 2.5% piperonyl butoxide technical);
Prentox, Rotenone Powder and Resins. Chem-Fish
Synergized is 2.5% rotenone and 2.5% piperonyl
butoxide; Chem-Fish Regular is 5%; Rotenone
Resin (Blue Spruce) 45%; Rotenone Powder (Blue
Spruce) at 5 to 7.5% pure. Rotenone Soln FK-11
(piperonyl butoxide 2.5% and rotenone 1.5%)
(Fairfield American).
Formulations incl dusts of 0.75 to 1.5% concn, emulsifiable concentrates of 2 to 3%
concn, wettable powder of 5% concn, soln of up to 5% concn, and resins of 30% concn
intended for manufacture.
Grades: CP crystals; technical; also as extracts of derris and cube root.
Formulations include dusts of 0.75-5% concentration, crystalline preparations of 97%
purity, and emulsified solution of up to 50% and resins of 42-45% concentration intended
for manufacture.
... Noxfire (5% rotenone) tank mixed with
Roussel Bio Corp piperonyl butoxide EC92% for insects which have become resistant to
pyrethroid-based insecticides. Nusyn-Noxfish
(2.5% rotenone/2.5% piperonyl butoxide
technical). Foliafume E.C. (pyrethrins) ... PB-Nox (4.3% rotenone/8.6%
piperonyl butoxide).
Dust, emulsifiable concentrate, wettable powder
Consumption Patterns:
21% USED ON CROPS; 78% USED ON LIVESTOCK; 1% FOR OTHER APPLICATIONS (1975)
U. S. Production:
(1971) 1.4X10+7 GRAMS (CONSUMPTION)
(1974) 2.27X10+7 GRAMS (CONSUMPTION)
Laboratory Methods:
Analytic Laboratory Methods:
A rapid, specific, and sensitive HPLC procedure (limit of detection less than 0.005
mg/l) was developed for monitoring application and degradation rates of rotenone.
For analysis, a water sample is buffered to pH 5 and injected through a Sep Pak (C)18
disposable cartridge. The cartridge adsorbs and retains the rotenone
which then can be eluted quantitatively from the cartridge with a small volume of
methanol. This step effectively concentrates the sample and provides sample cleanup. The
methanol extraction is analyzed directly by HPLC on an MCH 10 reverse-phase column.
Methanol:water (75:25, vol:vol) is the mobile phase and flow rate is 1.5 ml/min. Rotenone is detected by UV spectrophotometry at a
wavelength of 295 nm.
Determination of rotenone in Derris and Cube
powder using crystalization method; an infrared spectroscopic method (not applicable to
derris products).
Rotenone in pesticide formulations is
determined by reverse phase liquid chromatographic method with UV detection at 280 nm.
Analysis of products: by infrared spectrophotometry; by HPLC. Analysis of residues: by
GLC and TLC; by HPLC.
NIOSH Method: 5007. Analyte: Rotenone.
Matrix: Air. Procedure: HPLC, UV detection For rotenone
this method has an estimated detection limit of 4 ug/sample. The precision/RSD is 0.024
and the recovery is not determined. Applicability: The working range is 0.4 to 10 mg/cu m
for a 100 liter air sample and the method is applicable to commercial formulations.
Interferences: None known.
EPA Method 635. Determination of rotenone in
industrial and municipal wastewaters by high performance liquid chromatography coupled
with ultra violet detector. Approximately 1 liter is solvent extracted with methylene
chloride using a separately funnel. The method detection limit is 1.60 ug/l as defined by
EPA.
Sampling Procedures:
NIOSH Method 5007. Analyte: Rotenone. Matrix:
Air. Sampler: Filter (1 um polytetrafluoroethylene membrane). Flow Rate: 1 to 3
liters/min. Sample Size: 100 liters. Shipment: Routine. Sample Stability: At least 7 days
at 25 deg C in dark.
Special References:
Special Reports:
DHHS/NTP; Toxicology & Carcinogenesis Studies of Rotenone
in F344/N Rats and B6C3F1 Mice (Feed Studies) Technical Report Series No. 320 (1988) NIH
Publication No. 88-2576
Synonyms and Identifiers:
Synonyms:
BARBASCO
**PEER REVIEWED**
(1)BENZOPYRANO(3,4-B)FURO(2,3-H)(1)BENZOPYRAN-6(6AH)-ONE,
1,2,12,12A-TETRAHYDRO-8,9-DIMETHOXY-2-(1-METHYLETHENYL)-, (2R-(2ALPHA,6AALPHA, 12AALPHA))-
**PEER REVIEWED**
(1)BENZOPYRANO(3,4-B)FURO(2,3-H)(1)BENZOPYRAN-6(6AH)-ONE,
1,2,12,12A-TETRAHYDRO-2-ALPHA-ISOPROPENYL-8,9-DIMETHOXY-
**PEER REVIEWED**
(1)BENZOPYRANO(3,4-B)FURO(2,3-H)(1)BENZOPYRAN-6(6ALPHAH)-ONE,
1,2,12,12AALPHA-TETRAHYDRO-2ALPHA-ISOPROPENYL-8,9-DIMETHOXY-
**PEER REVIEWED**
CENOL GARDEN DUST
**PEER REVIEWED**
Chem-Fish Synergized
**PEER REVIEWED**
CHEM-MITE
**PEER REVIEWED**
Cube
**PEER REVIEWED**
CUBE EXTRACT
**PEER REVIEWED**
CUBE-PULVER
**PEER REVIEWED**
CUBE ROOT
**PEER REVIEWED**
CUBOR
**PEER REVIEWED**
CUREX FLEA DUSTER
**PEER REVIEWED**
DACTINOL
**PEER REVIEWED**
DERIL
**PEER REVIEWED**
DERRIN
**PEER REVIEWED**
DERRIS
**PEER REVIEWED**
Dri-kil
**PEER REVIEWED**
ENT 133
**PEER REVIEWED**
EXTRAX
**PEER REVIEWED**
FISH-TOX
**PEER REVIEWED**
Foliafume E.C.
**PEER REVIEWED**
GREEN CROSS WARBLE POWDER
**PEER REVIEWED**
HAIARI
**PEER REVIEWED**
LIQUID DERRIS
**PEER REVIEWED**
MEXIDE
**PEER REVIEWED**
NCI-C55210
**PEER REVIEWED**
NICOULINE
**PEER REVIEWED**
Noxfire
**PEER REVIEWED**
NOXFISH
**PEER REVIEWED**
Nusyn-Noxfish
**PEER REVIEWED**
Paraderil
**PEER REVIEWED**
PB-Nox
**PEER REVIEWED**
POWDER AND ROOT
**PEER REVIEWED**
Prenfish
**PEER REVIEWED**
PRENTOX
**PEER REVIEWED**
Prentox Synpren-Fish
**PEER REVIEWED**
PRO-NOX FISH
**PEER REVIEWED**
RO-KO
**PEER REVIEWED**
RONONE
**PEER REVIEWED**
Rotacide E.C.
**PEER REVIEWED**
ROTEFIVE
**PEER REVIEWED**
ROTEFOUR
**PEER REVIEWED**
ROTENON
**PEER REVIEWED**
Rotenona [Spanish]
**PEER REVIEWED**
(-)-ROTENONE
**PEER REVIEWED**
5'BETA-ROTENONE
**PEER REVIEWED**
ROTESSENOL
**PEER REVIEWED**
ROTOCIDE
**PEER REVIEWED**
1,2,12,12a-Tetrahydro-8,9-dimethoxy-2-(1-methylethenyl)-[1]benzopyrano[3,4-b]
furo[2,3-h][1]benzopyran-6(6aH)-one
**PEER REVIEWED**
[2R-(2ALPHA,6AALPHA,12AALPHA)]-1,2,12,12A-TETRAHYDRO-8,9-DIMETHOXY-
2-(1-METHYLETHENYL)[1]BENZOPYRANO[3,4-B]FURO[2,3-H]BENZOPYRAN-6(6AH)-ONE
**PEER REVIEWED**
1,2,12,12AALPHA-TETRAHYDRO-2A-ISOPROPENYL-8,9-DIMETHOXY[1]
BENZOPYRANO[3,4-B]FURO[2,3-H][1]BENZOPYRAN-6(6AH)-ONE
**PEER REVIEWED**
TUBATOXIN
**PEER REVIEWED**
TUBOTOXINE
**PEER REVIEWED**
Formulations/Preparations:
Prentox Prenfish toxicant (5% rotenone); Prentox Synpren-Fish toxicant (2.5% rotenone and 2.5% piperonyl butoxide technical);
Prentox, Rotenone Powder and Resins. Chem-Fish
Synergized is 2.5% rotenone and 2.5% piperonyl
butoxide; Chem-Fish Regular is 5%; Rotenone
Resin (Blue Spruce) 45%; Rotenone Powder (Blue
Spruce) at 5 to 7.5% pure. Rotenone Soln FK-11
(piperonyl butoxide 2.5% and rotenone 1.5%)
(Fairfield American).
Formulations incl dusts of 0.75 to 1.5% concn, emulsifiable concentrates of 2 to 3%
concn, wettable powder of 5% concn, soln of up to 5% concn, and resins of 30% concn
intended for manufacture.
Grades: CP crystals; technical; also as extracts of derris and cube root.
Formulations include dusts of 0.75-5% concentration, crystalline preparations of 97%
purity, and emulsified solution of up to 50% and resins of 42-45% concentration intended
for manufacture.
... Noxfire (5% rotenone) tank mixed with
Roussel Bio Corp piperonyl butoxide EC92% for insects which have become resistant to
pyrethroid-based insecticides. Nusyn-Noxfish
(2.5% rotenone/2.5% piperonyl butoxide
technical). Foliafume E.C. (pyrethrins) ... PB-Nox (4.3% rotenone/8.6%
piperonyl butoxide).
Dust, emulsifiable concentrate, wettable powder
RTECS Number:
NIOSH/DJ2800000
Administrative Information:
Hazardous Substances Databank Number: 1762
Last Revision Date: 20011010
Last Review Date: Reviewed by SRP on 9/18/1997
Update History:
Complete Update on 10/10/2001, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 03/09/2000, 1 field added/edited/deleted.
Complete Update on 03/03/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 08/24/1999, 5 fields added/edited/deleted.
Complete Update on 03/23/1999, 1 field added/edited/deleted.
Complete Update on 01/27/1999, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 09/02/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 12/08/1997, 60 fields added/edited/deleted.
Field Update on 09/08/1997, 5 fields added/edited/deleted.
Field Update on 05/08/1997, 1 field added/edited/deleted.
Field Update on 03/06/1997, 1 field added/edited/deleted.
Field Update on 02/13/1997, 1 field added/edited/deleted.
Complete Update on 10/15/1996, 1 field added/edited/deleted.
Complete Update on 06/24/1996, 8 fields added/edited/deleted.
Field Update on 06/06/1996, 1 field added/edited/deleted.
Complete Update on 01/21/1996, 1 field added/edited/deleted.
Complete Update on 08/21/1995, 1 field added/edited/deleted.
Complete Update on 01/24/1995, 1 field added/edited/deleted.
Complete Update on 12/28/1994, 1 field added/edited/deleted.
Complete Update on 08/02/1994, 1 field added/edited/deleted.
Complete Update on 04/26/1994, 57 fields added/edited/deleted.
Field Update on 03/21/1994, 1 field added/edited/deleted.
Field Update on 09/15/1993, 1 field added/edited/deleted.
Field Update on 08/03/1993, 1 field added/edited/deleted.
Field update on 12/22/1992, 1 field added/edited/deleted.
Complete Update on 09/03/1992, 1 field added/edited/deleted.
Complete Update on 04/27/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 09/26/1991, 1 field added/edited/deleted.
Complete Update on 10/15/1990, 6 fields added/edited/deleted.
Field Update on 05/14/1990, 1 field added/edited/deleted.
Field Update on 03/06/1990, 1 field added/edited/deleted.
Field Update on 01/15/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 5 fields added/edited/deleted.
Express Update on 01/26/1989, 2 fields added/edited/deleted.
Complete Update on 12/09/1988, 2 fields added/edited/deleted.
Complete Update on 09/30/1988, 1 field added/edited/deleted.
Complete Update on 07/12/1988, 2 fields added/edited/deleted.
Complete Update on 04/30/1986
Record Length: 138119