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Fluoroacetamide (CAS No. 640-19-7). Hazardous Substances Data Bank.
from Hazardous Substances Data Bank downloaded October 2003 from Toxnet FLUOROACETAMIDE CASRN: 640-19-7Human Toxicity Excerpts:
At about 1130 hr, an 18-month old girl removed a 120 ml bottle of 1% fluoroacetamide form a low drawer in the family kitchen & drank some of the contents. On the advice of a pharmacist, the child was given olive oil, the white of an egg, & milk at about noon & was made slightly sick. The child remained lively & played in the garden until her usual bedtime, 1830 hr. At about 2330 hr that evening the child vomited but was put back to bed when she appeared all right. Apparently the child was not checked until 1030 hr next morning, when she was found in a semiconscious state. On a physician's orders, she was taken to hospital, but convulsions occurred on the way & the patient arrived about 1130 hr in a shocked state. The child was given about 10 ml acetamide in water once, 3.7 ml of brandy in water each hour, & symptomatic treatment. She continued to have occasional convulsions & remained unconscious until she died almost 96 hr after ingesting the poison. Both the heart & kidney contained 6.3 mg of organic fluoride/g of dry tissue; the citrate content (108 ppm in heart & 23.9 in kidney) was not considered significantly high. From the evidence available, it was estimated that the baby had consumed about 300 mg of fluoroacetamide or 23 mg/kg.
Probable Routes of Human Exposure:
Occupational exposure to fluoroacetamide may have occurred through inhalation and dermal contact with this compound at workplaces where fluoroacetamide was produced or used. (SRC)
Emergency Medical Treatment
Emergency Medical Treatment:
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The following Overview, *** FLUOROACETAMIDE ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted. |
| Clinical Effects: |
0.2.1 SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
A. Fluoroacetamide is a fluoro ester compound used as a
rodenticide, insecticide, miticide, and aphicide. Few
specific data were available specifically about the
toxicity of fluoroacetamide in humans; its toxicity is
predicted to be similar to that of FLUOROACETATE, with
convulsions, coma, nausea, and vomiting.
1. In one experimental animal study, FLUOROACETAMIDE
caused coma and death, but NOT convulsions. In two
human poisoning cases, serious cardiac arrhythmias
were noted; grand mal seizures occurred in one case.
a. Fluoroacetamide may be absorbed and cause systemic
poisoning after ingestion or dermal contact. It is
unclear whether or not fluoroacetamide can be
absorbed by the inhalation route.
2. Fluoroacetamide is a colorless crystalline powder
solid which is freely soluble in water. It is
synthesized from fluoroacetyl chloride by a variety of
processes. The use of fluoroacetamide is restricted
to licensed pesticide applicators.
3. The following review discusses the toxicity and
treatment of poisoning with FLUOROACETATE.
B. Clinical effects are usually seen within 1/2 hour of
exposure. Nausea, vomiting, excessive salivation,
abdominal pain, numbness, a tingling sensation, and
apprehension are seen initially, and may last for up to
6 hours. Muscular twitching, blurred vision, and
hypotension may develop.
1. Coma, convulsions, and cardiac arrhythmias may be
delayed in onset for as long as 20 hours. One death
due to subacute fluoroacetate poisoning has been
reported.
2. Cardiac effects may include tachycardia, ventricular
fibrillation, and sudden onset of asystole.
3. Death may occur from respiratory depression and
hypoxia during convulsions or cardiac arrest.
4. Neurologic sequelae and acute renal failure have been
described after acute poisoning.
5. Metabolic acidosis, hyperglycemia, hyperuricemia,
elevated serum levels of hepatic transaminases, and
elevated serum creatinine levels may occur.
C. Severe poisoning with numbness and tingling of the
face, excessive salivation, blurred vision, peripheral
paresthesias, convulsions, and coma followed inhalation
and dermal contact with fluoroacetate. Fluoroacetate
can be absorbed following ingestion and inhalation, but
not through intact skin.
D. Fluoroacetate mimics acetic acid and reacts with
coenzyme A and oxaloacetic acid, forming fluorocitric
acid which enters and blocks the Kreb's cycle, allowing
accumulation of citric acid.
E. Fluoroacetamide releases toxic and irritating fumes of
fluoride and oxides of nitrogen when heated to
decomposition. Inhalation of such combustion products
would be predicted to result in respiratory tract
irritation with bronchospasm, chemical pneumonitis, or
noncardiogenic pulmonary edema.
0.2.3 VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
A. Respiratory depression, hypothermia, tachycardia, and
hypotension may occur.
0.2.4 HEENT
0.2.4.1 ACUTE EXPOSURE
A. Blurred vision, facial paresthesias, and
hypersalivation may be noted.
0.2.5 CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
A. Tachycardia, ventricular tachycardia or fibrillation,
and sudden onset of asystole may occur.
0.2.6 RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
A. Respiratory depression and cyanosis may develop. Death
may be due to hypoxia and respiratory depression during
seizures.
B. Fluoroacetamide releases toxic and irritating fumes of
fluoride and oxides of nitrogen when heated to
decomposition. Inhalation of such combustion products
would be predicted to result in respiratory tract
irritation with bronchospasm, chemical pneumonitis, or
noncardiogenic pulmonary edema.
0.2.7 NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
A. Apprehension, diaphoresis, disorientation, agitation,
paresthesias, muscle twitching, hyperactive behavior,
tingling, coma, and convulsions may develop. Status
epilepticus has been described.
B. Neurologic sequelae have been noted following acute
poisoning, including hypertonicity with arm and leg
spasms, severe mental deficits, and moderate residual
paresis. Severe cerebellar dysfunction, ataxia, and
depression were described in a 15-year-old patient who
survived acute fluoroacetate poisoning.
0.2.8 GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
A. Nausea, vomiting, hypersalivation, abdominal or
epigastric pain, and diarrhea may be seen.
0.2.9 HEPATIC
0.2.9.1 ACUTE EXPOSURE
A. Increased serum levels of hepatic transaminases may be
noted.
0.2.10 GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
A. Acute renal failure may be a sequelae of acute
poisoning. Elevated serum levels of creatinine and
uric acid may be noted.
0.2.11 ACID-BASE
0.2.11.1 ACUTE EXPOSURE
A. Metabolic acidosis may be seen.
0.2.12 FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
A. Hypocalcemia may occur.
0.2.15 MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
A. Muscle twitching may be an early effect.
0.2.17 METABOLISM
0.2.17.1 ACUTE EXPOSURE
A. Fluoroacetate mimics acetic acid and reacts with
coenzyme A and oxaloacetic acid, forming fluorocitric
acid which enters and blocks the Kreb's cycle, allowing
accumulation of citric acid.
B. Elevated blood glucose levels may be seen in
fluoroacetate poisoning.
0.2.20 REPRODUCTIVE HAZARDS
A. At the time of this review, no data were available to
assess the teratogenic potential of this agent.
B. Observed paternal toxic effects in rats following
chronic dietary administration on fluoroacetamide
included changes in the testes, epididymis, sperm duct,
and in sperm morphology and spermatid development.
0.2.21 CARCINOGENICITY
0.2.21.2 HUMAN OVERVIEW
A. At the time of this review, no data were available to
assess the carcinogenic potential of this agent.
0.2.22 GENOTOXICITY
A. Cytogenetic analysis detected chromosome aberrations in
the rat in vivo and in mammal lung cells. In Red
Muntjac in vitro, fluoroacetamide caused chromosomal
breakage, increased rate of sister chromatid exchanges,
and a lag in the cell cycle. |
| Laboratory: |
A. Fluoroacetate levels are not clinically useful.
B. Monitor serum calcium, magnesium, and potassium
concentrations.
C. Monitor EKG and vital signs frequently. |
| Treatment Overview: |
0.4.2 ORAL EXPOSURE
A. Do NOT induce emesis.
B. 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.
C. ACTIVATED CHARCOAL: Administer charcoal as a 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.
D. THERE IS NO KNOWN EFFECTIVE ANTIDOTE - for fluoroacetate
intoxication. Symptomatic and supportive care should be
provided.
1. Based on animal experiments, intravenous glyceryl
monoacetate (monoacetin) and ethanol administration
have been advocated to prevent or reverse the toxic
effects of fluoroacetate. However, it does not appear
that these treatments are effective in humans.
E. 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: 2 to 4 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.
F. REFRACTORY SEIZURES: Consider continuous infusion of
midazolam, propofol, and/or pentobarbital.
Hyperthermia, lactic acidosis and muscle destruction may
necessitate use of neuromuscular blocking agents with
continuous EEG monitoring.
G. MONITOR ECG AND VITAL SIGNS - frequently.
H. CALCIUM SALTS - Calcium gluconate or calcium chloride
should be administered parenterally in patients with
documented hypocalcemia.
I. HYPOTENSION -
1. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If
hypotension persists, administer dopamine (5 to 20
mcg/kg/min) or norepinephrine (ADULT: begin infusion
at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1
mcg/kg/min); titrate to desired response.
J. MONITORING PARAMETERS -
1. Monitor EKG and VITAL SIGNS frequently; ventricular
arrhythmias may occur suddenly. Monitor serum
electrolytes, including calcium, magnesium, and
potassium. Monitor blood sugar, liver and renal
function tests, and urinalysis.
K. OBSERVATION CRITERIA -
1. As DELAYED ONSET of SERIOUS or LIFE-THREATENING
TOXICITY may occur, all patients with possible
significant exposure should be observed for up to 24
hours in a controlled setting.
0.4.3 INHALATION EXPOSURE
A. 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
inhaled beta2 agonist and oral or parenteral
corticosteroids.
B. SYSTEMIC ABSORPTION -
1. Systemic poisoning has occurred following inhalation
exposure to fluoroacetate.
C. THERE IS NO KNOWN EFFECTIVE ANTIDOTE - for fluoroacetate
intoxication. Symptomatic and supportive care should be
provided.
1. Based on animal experiments, intravenous glyceryl
monoacetate (monoacetin) and ethanol administration
have been advocated to prevent or reverse the toxic
effects of fluoroacetate. However, it does not appear
that these treatments are effective in humans.
D. 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: 2 to 4 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.
E. REFRACTORY SEIZURES: Consider continuous infusion of
midazolam, propofol, and/or pentobarbital.
Hyperthermia, lactic acidosis and muscle destruction may
necessitate use of neuromuscular blocking agents with
continuous EEG monitoring.
F. MONITOR ECG AND VITAL SIGNS - frequently.
G. CALCIUM SALTS - Calcium gluconate or calcium chloride
should be administered parenterally in patients with
documented hypocalcemia.
H. HYPOTENSION -
1. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If
hypotension persists, administer dopamine (5 to 20
mcg/kg/min) or norepinephrine (ADULT: begin infusion
at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1
mcg/kg/min); titrate to desired response.
I. MONITORING PARAMETERS -
1. Monitor ECG and VITAL SIGNS frequently; ventricular
arrhythmias may occur suddenly. Monitor serum
electrolytes, including calcium, magnesium, and
potassium. Monitor blood sugar, liver and renal
function tests, and urinalysis.
J. COMBUSTION PRODUCTS -
1. Fluoroacetamide releases toxic and irritating fumes of
fluoride and oxides of nitrogen when heated to
decomposition. Inhalation of such combustion products
would be predicted to result in respiratory tract
irritation with bronchospasm, chemical pneumonitis, or
noncardiogenic pulmonary edema.
2. Respiratory tract irritation, if severe, can progress
to pulmonary edema which may be delayed in onset up to
24 to 72 hours after exposure in some cases.
3. If respiratory tract irritation is present, monitor
arterial blood gases and chest x-ray.
4. If bronchospasm and wheezing occur, consider treatment
with inhaled sympathomimetic agents.
5. ACUTE LUNG INJURY: Maintain ventilation and
oxygenation and evaluate with frequent arterial blood
gas or pulse oximetry monitoring. Early use of PEEP
and mechanical ventilation may be needed.
K. PATIENT DISPOSITION -
1. As DELAYED ONSET of SERIOUS or LIFE-THREATENING
TOXICITY may occur, all patients with possible
significant exposure should be observed for up to 24
hours in a controlled setting.
0.4.4 EYE EXPOSURE
A. DECONTAMINATION: Irrigate exposed eyes with copious
amounts of room temperature water for at least 15
minutes. If irritation, pain, swelling, lacrimation, or
photophobia persist, the patient should be seen in a
health care facility.
B. SYSTEMIC TOXICITY -
1. There is no evidence that fluoroacetate can be absorbed
in toxic quantities following ocular exposure. Should
systemic symptoms develop following exposure by this
route:
2. Treatment should include recommendations listed in the
INHALATION EXPOSURE section when appropriate.
0.4.5 DERMAL EXPOSURE
A. DECONTAMINATION: Remove contaminated clothing and
jewelry. Wash the skin, including hair and nails,
vigorously; do repeated soap washings. Discard
contaminated clothing.
B. SYSTEMIC ABSORPTION -
1. There is little evidence that fluoroacetate can be
absorbed systemically in toxic amounts through intact
skin; however, FLUOROACETAMIDE may be absorbed by this
route. Should systemic symptoms develop following
dermal contact with this material:
2. Treatment should include recommendations listed in the
INHALATION EXPOSURE section when appropriate. |
| Range of Toxicity: |
A. A milligram of the pure compound is probably enough to
cause severe toxicity, and less may be toxic.
Extrapolation of experimental animal toxicity data to
humans suggests that a dose of 2 to 10 mg/kg may be fatal. |
Antidote and Emergency Treatment:
REMOVAL OF THE MATERIAL FROM GI TRACT & SUPPORTIVE THERAPY ARE ONLY MEASURES THAT MIGHT BE BENEFICIAL IN CASES OF INGESTION OF SUBLETHAL DOSES IN ANIMALS.
EXPTL THERAPY (VET): THE ANTIDOTAL EFFECT OF ACETAMIDE WAS STUDIED IN CHICKENS. ADMIN ORALLY AT DOSE RATES OF 0.5 & 2.5 G/KG, ONLY AT HIGHER DOSAGE RATE DID ACETAMIDE PREVENT LETHAL ACTION OF FLUOROACETAMIDE (10 MG/KG) WHEN GIVEN 1 HR BEFORE, AT THE SAME TIME OR 10 OR 20 MIN AFTER ADMIN OF FLUOROACETAMIDE.
1. IF THIS SUBSTANCE HAS BEEN INGESTED, EMPTY THE STOMACH IMMEDIATELY BY INTUBATION, ASPIRATION, & LAVAGE, USING 5% SODIUM BICARBONATE. BEFORE WITHDRAWING THE LAVAGE TUBE, INSTILL A SLURRY OF 30-50 G ACTIVATED CHARCOAL /SRP: IN CHILDREN, 60-100 G IN ADULTS/. 2. MONITOR CARDIAC RHYTHM BY CONTINUOUS ELECTROCARDIOGRAPHY. 3. MONOACETIN (GLYCERYL MONOACETATE) HAS ANTIDOTAL PROPERTIES IN EXPERIMENTAL ANIMALS. THE LIBERATED ACETATE COMPETES SUCCESSFULLY WITH FLUOROCITRATE IN THE TRICARBOXYLIC ACID CYCLE. HOWEVER, THERE IS NO STERILE PHARMACEUTICAL PREPN OF THIS CMPD: HIGH-QUALITY, FRESH LAB GRADE MATERIAL MUST BE USED. A. IF VICTIM IS FULLY CONSCIOUS & NOT CONVULSING, ADMIN 100 ML OF MONOACETIN IN 500 ML OF WATER, BY MOUTH. REPEAT IN 1 HR. B. IF VICTIM IS OBTUNDED, UNCONSCIOUS, OR CONVULSING, GIVE 0.1-0.5 ML/KG OF UNDILUTED MONOACETIN BY DEEP IM INJECTION EVERY HALF HR FOR 4-6 HR, ROTATING THE INJECTION SITES TO MINIMIZE PAIN & SWELLING. MONOACETIN CAN ALSO BE GIVEN IV ON THE SAME SCHEDULE, USING A 1:5 DILUTION IN STERILE ISOTONIC SALINE. /SODIUM FLUOROACETATE/
4. CONTROL CONVULSIONS A. ADMIN 100% OXYGEN BY POSITIVE PRESSURE TO PROVIDE AS MUCH PULMONARY GAS EXCHANGE AS POSSIBLE, DESPITE SEIZURES. B. ANTICONVULSANT DRUGS ... (A) DIAZEPAM (VALIUM) USUALLY CONTROLS MILD CONVULSIONS. FOR ADULTS, GIVE 5-10 MG, SLOWLY, IV; FOR CHILDREN UNDER 6 YR OR 23 KG BODY WT, GIVE 0.1 MG/KG BODY WT, SLOWLY, IV. REPEAT IN 4-6 HR IF NECESSARY. (B) PENTOBARBITAL MAY BE NEEDED IN ADDN TO CONTROL SEVERE CONVULSIONS. DOSAGE: 5 MG/KG BODY WT, OR 0.20 ML/KG BODY WT, USING THE USUAL 2.5% SOLN. IF POSSIBLE, INJECT SOLN IV, AT A RATE NOT EXCEEDING 25 MG (1 ML) PER MIN UNTIL CONVULSIONS ARE CONTROLLED. IF IV ADMIN IS NOT POSSIBLE, GIVE TOTAL DOSE BY DEEP IM INJECTION, NOT EXCEEDING 5 MG/KG BODY WT (0.20 ML/KG OF 2.5% SOLN). /SODIUM FLUOROACETATE/
4. CONTROL CONVULSIONS (C) PHENYTOIN (DILANTIN) HAS PROLONGED ANTICONVULSANT ACTION. DOSAGE: LOADING DOSE 15-18 MG/KG. MAINTENANCE DOSE 4-8 MG/KG.../EVERY/ 4-24 HR AS NEEDED. IM ADMIN IS NOT RECOMMENDED. GIVE IV SLOWLY AT NO MORE THAN 20% TOTAL DOSE PER MIN. (D) THIOPENTAL (PENTOTHAL), BY CONTINUOUS IV INFUSION, MAY HELP TO CONTROL SEVERE SEIZURES. DISSOLVE 1 G IN 500 ML OF GLUCOSE SOLN, & INFUSE AT A RATE JUST SUFFICIENT TO STOP SEIZURES. ... (E) IN SOME INSTANCES, CURARIZATION WITH SUCCINYLCHOLINE OR A SIMILAR AGENT IS REQUIRED TO STOP CONVULSIONS. THIS REQUIRES TRACHEAL INTUBATION OR TRACHEOSTOMY & MECHANICAL PULMONARY VENTILATION, WITH REGULAR MONITORING OF BLOOD GASES & PH. /SODIUM FLUOROACETATE/
5. MANY OTHER AGENTS TESTED IN FLUOROACETATE POISONING ARE NOT EFFECTIVE: SODIUM ACETATE, CALCIUM CHLORIDE, ETHANOL, PROPYLENE GLYCOL, DIGITALIS GLYCOSIDES, DI- & TRI-ACETATES OF GYLCEROL. 6. ADMIN IV ELECTROLYTE SOLN CAUTIOUSLY TO AVOID FLUID OVERLOAD IN PRESENCE OF A WEAK & IRRITABLE MYOCARDIUM. /SODIUM FLUOROACETATE/
EXPTL THERAPY: CALCIUM CHLORIDE THERAPY RESTORED TO NORMAL THE MARKEDLY PROLONGED QT INTERVAL IN TWO CASES OF SEVERE ACUTE FLUOROACETAMIDE POISONING IN MAN.
EXPTL THERAPY: A 5-YR-OLD BOY POISONED BY FLUOROACETAMIDE SUBMITTED TO TESTING A FIXED-BED UNCOATED CHARCOAL DEVICE TO BE USED IN HEMOPERFUSION. CHARCOAL HEMOPERFUSION MAY BE USEFUL IN TREATING PATIENTS POISONED WITH CHEMICALS CHARACTERIZED BY AN APPARENT VOLUME OF DISTRIBUTION SMALLER THAN TOTAL BODY WATER.
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 ... . /Monofluoroacetate and related compounds/
Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or in respiratory arrest. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Treat seizures with diazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Monofluoroacetate and related compounds/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
... APPARENT SPECIES DIFFERENCES IN QUALITY OF SYMPTOMS THAT LEAD TO DEATH. DOGS DIE OF CONVULSIONS OR RESP PARALYSIS, BUT IN ... MONKEYS, HORSES, & RABBITS CNS ACTIONS ARE USUALLY INCIDENTAL, & DANGEROUS FATAL COMPLICATION IS VENTRICULAR FIBRILLATION.
... FLUOROACETAMIDE ... /IS/ HIGHLY TOXIC SUBSTANCE ... TO MOST ANIMAL SPECIES, EXCEPT FROGS & TOADS.
CATS & DOGS WERE VERY SUSCEPTIBLE TO DIRECT POISONING WITH FLUOROACETAMIDE WHILE BARN OWLS (TYTO ALBA), BUZZARDS (BUTEO BUTEO) & BLACK KITES (MILVUS MIGRANS) WERE RESISTANT. IN SECONDARY POISONING EXPT, 2 PALESTINE VIPERS (VIPERA PALESTINAE), A SYRIAN BLACK SNAKE (COLUBER JUGULARIS) & 2 MONTPELLIER SNAKES (MALPOLON MONSPESSULANUS) WERE RESISTANT. A MONGOOSE (HERPESTES ICHNEUMON) & A HYENA (HYAENA HYAENA) WERE SUSCEPTIBLE TO POISONING. APPARENTLY FLUOROACETAMIDE CONSTITUTES HEALTH HAZARD TO CARNIVORES SUCH AS DOGS, CATS & MONGOOSES BUT WOULD NOT AFFECT BIRDS OF PREY.
ANIMALS ACUTELY POISONED BY ... /FLUOROACETAMIDE/ SHOW LISTLESSNESS, IRRITABILITY, CLONIC CONVULSIONS, ABASIA, PILOERECTION, & IRREGULAR RESPIRATION. ONE CHARACTERISTIC USUALLY OBSERVED IN ANIMALS DYING FROM ACUTE POISONING WITH FLUOROACETAMIDE AS WELL AS WITH SODIUM FLUOROACETATE IS POSTMORTEM RIGIDITY. DEATH GENERALLY OCCURS IN COMA AFTER CONVULSIONS HAVE STOPPED. SUBACUTELY POISONED ANIMALS SHOW ANOREXIA, EMACIATION, ALOPECIA, & ABSCESS FORMATION.
... MALE RATS THAT RECEIVED A DIETARY LEVEL OF 50 PPM (USUALLY CALCULATED AS ABOUT 2.5 MG/KG/DAY BUT SAID TO BE ABOUT 3.4 MG/KG/DAY IN THESE RATS) SHOWED MARKED MORPHOLOGICAL CHANGES IN THE NUCLEUS OF STEP-13 SPERMATIDS WITHIN 24 HR, & EFFECTS BECAME MORE PRONOUNCED & THE ENTIRE CELL BECAME DISTORTED IN 5 DAYS. AFTER 10 DAYS OF TREATMENT, EARLIER STEP SPERMATIDS SHOWED DEGENERATIVE CHANGES & GIANT CELL FORMATION. EVENTUALLY, EVEN SPERMATOCYTES WERE AFFECTED. DIETARY LEVELS OF 20, 10, & 5 PPM, PRODUCED CHARACTERISTIC CHANGES IN LATE STAGE SPERMATIDS BUT NO EFFECT ON SPERMATOCYTES. ... SC ADMIN ... AT A RATE OF ABOUT 1.0 MG/KG/DAY PRODUCED THE CHARACTERISTIC CHANGES IN STAGE-13 SPERMATIDS WITHIN 4 DAYS & A 50% REDUCTION IN THE WT OF THE TESTES IN 28 DAYS.
SELECTIVE DESTRUCTION OF THE GERMINAL EPITHELIUM OF THE TESTES OF MALE RATS WAS REPORTED ... SINGLE DOSAGE LEVEL RESULTING FROM A DIETARY LEVEL OF 50 PPM. ON THIS DIET, THE BODY WT OF 150 TO 160 G RATS INCR BY 88% IN 90 DAYS, BUT THE TESTES WERE REDUCED TO SLIGHTLY LESS THAN 1/3 THE WT OF CONTROLS. AFTER 64 DAYS, THE TUBULES WERE ALMOST COMPLETELY LACKING IN SEMINAL CELLS ... PECULIAR GIANT CELLS WERE OBSERVED.
FLUOROACETAMIDE AT AN ORAL DOSAGE OF 15 MG/KG ... INTERFERES WITH REPRODUCTION IN FEMALE MICE, WHETHER ADMIN 2 DAYS BEFORE OR 10 DAYS AFTER FERTILIZATION; PREGNANCY WAS PROLONGED, PRENATAL MORTSEITY WAS INCR, & THE YOUNG SUFFERED FROM CYANOSIS, RESPIRATORY DISTRESS, REDUCED GROWTH, & DECR SURVIVAL.
STUDY OF CULTURED CELLS OF RED MUNTJAC IN VITRO INDICATED THAT FLUOROACETAMIDE CAN CAUSE CHROMOSOMAL BREAKAGE, INCREASE SISTER CHROMATID EXCHANGE & LAG CELL CYCLE.
RESULTS OF LAB INVESTIGATIONS ARE REPORTED IN MASS POISONING IN WHICH ABOUT 800 DOGS DIED SHORTLY AFTER CONSUMING PURCHASED POULTRY MEAT. THE TOXICOLOGICAL & PUBLIC HEALTH IMPLICATIONS OF MASS POISONING ARE DISCUSSED.
... FLUORINE DERIVATIVES WHICH ARE ONLY SLOWLY CONVERTED INTO FLUOROCITRATE & HENCE DO NOT PRODUCE THE TONIC CONVULSIONS SEEN IN FLUOROACETATE POISONING, BUT CAUSE UNCONSCIOUSNESS FOLLOWED BY DEATH IN COMA. THE ONLY DERIVATIVE OF IMPORTANCE IN THIS RESPECT IS FLUOROACETAMIDE. ... AFFECTS POISONED ANIMALS MORE SLOWLY & WITH LESS NEUROLOGICAL SYMPTOMS THAN DOES SODIUM FLUOROACETATE.
MOST POTENT RODENTICIDES KNOWN & ARE ALSO HIGHLY TOXIC TO OTHER ANIMALS.
FLUOROACETAMIDE RATED "GOOD" WHEN TESTED FOR ACCEPTABILITY BY MALE ADULT WISTAR RATS USING OSAKA UNIVERSITY TYPE SKINNER-BOX.
Non-Human Toxicity Values:
LD50 Rat oral 4 to 15 mg/kg
LD50 Mouse ip 85 mg/kg
LD50 Mouse oral 30.62 mg/kg /FROM TABLE/
LD50 Rabbit oral 1.5-2.0 mg/kg /from table/
LD50 Rabbit iv 0.25 mg/kg /from table/
LD50 Chicken oral 4.25 mg/kg /from table/
LD50 Rattus norvegicus oral 13 mg/kg
LD50 Rat skin 80 mg/kg
LD50 Rat ip 12 mg/kg
LD50 Mouse oral 25 mg/kg
LD50 Mouse skin or sc 34 mg/kg
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
INVESTIGATORS ARE AGREED THAT FLUOROACETAMIDE IS LESS TOXIC THAN FLUOROACETATE. THIS HAS BEEN ATTRIBUTED TO THE FACT THAT METABOLISM OF THE FORMER TO THE LATTER IS SLOW. ... RECOVERED, FROM THE URINE OF RATS RECEIVING FLUOROACETAMIDE AT A RATE OF 3 MG/KG/DAY, 62% OF THE TOTAL INTAKE UNMETABOLIZED ... .
2,4-Dinitrofluorobenzene reacts with glutathione to form a stable product similar to that formed with the model glutathione-S-transferase substrate, 1-chloro-2,4-dinitrobenzene. ... Fluoroacetamide, like fluoroacetate, undergoes no discernable chemical defluorinantion. Its enzymatic defluorination is approx 10% of that observed for fluoroacetate and only 0.2% of the rate for 2,4-dinitrofluorobenzene. An antibody raised to the fluoroacetate specific dehalogenase precipitated both fluoroacetate ad fluoroacetamide defluorinating activity but had no effect on either 1-chloro-2,4-dinitrobenzene or 2,4-dinitrofluorobenzene activity. ... 2,4-Dinitrofluorobenzene is metabolized by the glutathione-S-transferase while fluoroacetamide is metabolized by the fluoroacetate specific dehalogenase.
Fluoroacetate administered ip to rats and mice is defluorinated to give fluoride ion evident in urine and kidney by (19)F NMR. The use of 2-(13)C-, 1,2-(13)C-, and 1,2-(14)C-fluoroacetate, ... reveals a complex mixture of urinary metabolites including an S-(carboxymethyl) conjugate complex in rats and mice and sulfoxidation products ... in rats. ... Bile, following treatment with 2-(13)C- fluoroacetate, shows the presence of S-(carboxymethyl)glutathione or a related conjugate and an O-conjugate of fluoracetate. Incubation of (13)C-fluoroacetate with rat and mouse liver cytosol involves formation of S-((13)C-carboxymethyl) glutathione and fluoride ion. Fluorocitrate is also /detected in/ fluoracetate incubations with mouse liver cytosol. Fluoroacetamide administered ip to rats and mice yields urinary fluoride ion formed via fluoroacetate which is liberated on hydrolysis by an organophosphate-sensitive amidase. (19)F NMR ... of other metabolites of fluoroacetamide are consistent with fluoroacetohydroxamic acid in the liver of mice and fluorocitrate in the urine of rats. Fluoroethanol gives rinary fluoroacetate and fluoride ion in rats and mice and is converted to fluoroacetaldehyde by mouse and rat liver microsomes. (-)- and (+)-erythro- fluorocitrates administered ip to rats yield mostly the parent compounds in urine at 6 hr with increasing amounts of fluoride ion thereafter. ... Rat and mouse liver cytosols defluorinate (-)-erythro-fluorocitrate. Metabolic defluorination and pig heart aconitase also defluorinates (-)-erythro- fluorocitrate. Metabolic defluorination of fluoracetate and its progenitors, fluoroacetamide and fluoroethanol, is therefore attributable to both conjucation of fluoracetate with glutathione and conversion to (-)-erythro-fluorocitrate, which is both an inhibitor of and a substrate for aconitase. ... Urine of rats and mice poisoned with fluoroacetate or (-)-erythro-fluorocitrate show elevated citrate and glucose and diminished urea consistent with disruptions in the tricarboxylic acid cycle and ammonia metabolism.
Absorption, Distribution & Excretion:
THE CMPD IS ABSORBED BY THE SKIN.
Mechanism of Action:
FLUOROACETATE PRODUCES ITS TOXIC ACTION BY INHIBITING THE CITRIC ACID CYCLE. THE FLUORINE SUBSTITUTED ACETATE BECOMES INCORPORATED, AS A NORMAL ACETATE, INTO FLUOROACETYL COENZYME A, WHICH CONDENSES WITH OXALOACETATE TO FORM FLUOROCITRATE. FLUOROCITRATE INHIBITS THE ENZYME ACONITASE & THEREBY INHIBITS THE CONVERSION OF CITRATE TO ISOCITRATE. AS A RESULT THERE IS AN ACCUMULATION OF LARGE QUANTITIES OF CITRATE IN THE TISSUE, & THE CYCLE IS BLOCKED. ... THE HEART & CNS ARE THE MOST CRITICAL TISSUES INVOLVED IN POISONING BY GENERAL INHIBITION OF OXIDATIVE ENERGY METABOLISM. /FLUOROACETATE/
FLUOROACETAMIDE ... /IS/ TOXIC TO MAMMALS PRESUMABLY BECAUSE OF METABOLIC ... /HYDROLYSIS/ TO FLUOROACETATE.
Moderately fast-acting rodenticide which is less likely to lead to poison shyness because of sublethal dosing. It acts chiefly on the heart, with secondary effects on CNS.
Interactions:
TOXIC EFFECTS OF SUCROSE-CONTAINING SODIUM FLUOROSILICATE FED TO HOUSEFLIES IS DELAYED WHEN DIFLUBENZURON IS ADDED. A SIMILAR, THOUGH LESS PRONOUNCED, EFFECT IS EXERTED BY DFB IN FLUOROACETAMIDE TOXICITY.
Pharmacology:
Interactions:
TOXIC EFFECTS OF SUCROSE-CONTAINING SODIUM FLUOROSILICATE FED TO HOUSEFLIES IS DELAYED WHEN DIFLUBENZURON IS ADDED. A SIMILAR, THOUGH LESS PRONOUNCED, EFFECT IS EXERTED BY DFB IN FLUOROACETAMIDE TOXICITY.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Fluoroacetamide's production and former use as an insecticide and rodenticide may have resulted in its direct release to the environment. If released to air, an estimated vapor pressure of 0.99 mm Hg at 25 deg C indicates fluoroacetamide will exist solely as a vapor in the ambient atmosphere. Vapor-phase fluoroacetamide will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 7.8 days. If released to soil, fluoroacetamide is expected to have very high mobility based upon a Koc of 6.4. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 2.2X10-8 atm-cu m/mole. Fluoroacetamide may volatilize from dry soil surfaces based upon its vapor pressure. If released into water, fluoroacetamide is not expected to adsorb to suspended solids and sediment based upon the Koc. It has been suggested that fluoroacetamide should be degradable by biological sewage treatment provided suitable acclimatization can be achieved; field studies in soil show loss of toxicity in 3 to 11 weeks at 10 and 50 ppm, respectively. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 3 suggests the potential for bioconcentration in aquatic organisms is low. The neutral hydrolysis half-life is 2.4 yr at pH 7 which indicates that hydrolysis is slow. Occupational exposure to fluoroacetamide may have occurred through inhalation and dermal contact with this compound at workplaces where fluoroacetamide was produced or used. (SRC)
Probable Routes of Human Exposure:
Occupational exposure to fluoroacetamide may have occurred through inhalation and dermal contact with this compound at workplaces where fluoroacetamide was produced or used. (SRC)
Artificial Pollution Sources:
Fluoroacetamide's production and former use as an insecticide and rodenticide(1) may have resulted in its direct release to the environment(SRC). Fluoroacetamide effluents from a manufacturing facility in Great Britain were reportedly responsible for the poisoning of farm animals(2).
Environmental Fate:
TERRESTRIAL FATE: Based on a classification scheme(1), a Koc of 6.4(2), indicates that fluoroacetamide is expected to have very high mobility in soil(SRC). Volatilization of fluoroacetamide from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.2X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(3). The potential for volatilization of fluoroacetamide from dry soil surfaces may exist (SRC) based upon an estimated vapor pressure of 0.99 mm Hg(SRC), determined from a fragment constant method(4). The persistence of fluoroacetamide was studied in garden soil by determining its toxicity to aphids(5); at a concn of 50 ppm, toxicity had ceased after 11 weeks of incubation; at a conc of 10 ppm, toxicity lasted only 3 weeks; in a control soil that had been steam sterilized, toxicity was still evident at both concns after 17 weeks suggesting that the degradation was microbial in nature(5).
AQUATIC FATE: Based on a classification scheme(1), a Koc of 6.4(2), indicates that fluoroacetamide is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.2X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from its log Kow(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). The neutral hydrolysis rate constant for fluoroacetamide at 25 deg C was experimentally determined to be 3.3X10-5/hr which corresponds to an aqueous hydrolysis half-life of 2.4 yr at pH 7(8). This indicates that hydrolysis is slow(SRC). It has been suggested that fluoroacetamide should be degradable by biological sewage treatment provided suitable acclimatization can be achieved(9).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), fluoroacetamide, which has an estimated vapor pressure of 0.99 mm Hg at 25 deg C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere(SRC). Vapor-phase fluoroacetamide 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 7.8 days(SRC), calculated from its rate constant of 2.1X10-12 cu cm/molecule-sec at 25 deg C(SRC) determined using a structure estimation method(3).
Environmental Biodegradation:
Fluoroacetamide is reported to be a chemical that should be degradable by biological sewage treatment provided suitable acclimatization can be achieved(1). The persistence of fluoroacetamide was studied in garden soil by determining its toxicity to aphids(2). At a concn of 50 ppm, toxicity had ceased after 11 weeks of incubation and at a conc of 10 ppm, toxicity lasted only 3 weeks(2). In a control soil that had been steam sterilized, toxicity was still evident at both concs after 17 weeks suggesting that the degradation was microbial in nature(2).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction of fluoroacetamide with photochemically-produced hydroxyl radicals has been estimated as 2.1X10-12 cu cm/molecule-sec at 25 deg C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 7.8 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The neutral hydrolysis rate constant for fluoroacetamide at 25 deg C was experimentally determined to be 3.3X10-5/hr which corresponds to an aqueous hydrolysis half-life of 2.4 yr at pH 7(2). This indicates that hydrolysis is slow(SRC). Fluoroacetamide is not expected to directly photolyze due to the lack of absorption in the environmental UV spectrum (>290 nm)(SRC).
Environmental Bioconcentration:
An estimated BCF of 3 was calculated for fluoroacetamide(SRC), using a log Kow of -1.05(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).
Soil Adsorption/Mobility:
The Koc of fluoroacetamide is 6.4(1). According to a classification scheme(2), this Koc value suggests that fluoroacetamide is expected to have very high mobility in soil(SRC).
Volatilization from Water/Soil:
The Henry's Law constant for fluoroacetamide is estimated as 2.23X10-8 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that fluoroacetamide is expected to be essentially nonvolatile from water surfaces(2). The potential for volatilization of fluoroacetamide from dry soil surfaces may exist(SRC) based upon an estimated vapor pressure of 0.99 mm Hg(SRC), determined from a fragment constant method(3).
Environmental Standards & Regulations:
FIFRA Requirements:
In 1988, Congress amended FIFRA to strengthen and accelerate EPA's reregistration program which applies to each registered pesticide product containing an active ingredient initially registered before November 1, 1984. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for exposure and other factors, with List B being of highest concern and D of least. List: C; Case: fluoroacetic acid derivatives; Case No.: 3073; Pesticide type: insecticide, rodenticide; Case Status: RED Approved 6/95; OPP has made a decision that some/all uses of the pesticide are eligible for reregistration, as reflected in a Reregistration Eligibility Decision (RED) document. ; Active Ingredient (AI): fluoroacetamide; AI Status: The active ingredient is no longer contained in any registered products. Thus, we characterize it as "cancelled.".
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.5 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Fluoroacetamide is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 100 or 10,000 lbs. Extremely hazardous substances that are solids are subject to either of two threshold planning quantities ... The lower quantity applies only if the solid exists in powdered for and has a particle size less than 100 microns; or is handled in solution or in molten form; or meets the criteria for a National Fire Protection Association (NFPA) rating of 2, 3 or 4 for reactivity. If the solid does not meet any of these criteria, it is subject to the upper ... threshold planning quantity ... .
RCRA Requirements:
P057; As stipulated in 40 CFR 261.33, when fluoroacetamide, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).
Chemical/Physical Properties:
Molecular Formula:
C2-H4-F-N-O
Molecular Weight:
77.06
Color/Form:
Colorless crystalline powder
White...solid
Boiling Point:
Sublimes
Melting Point:
108 deg C
Octanol/Water Partition Coefficient:
log Kow= -1.05
Solubilities:
Freely sol in water, sol in acetone; sparingly sol in chloroform
Moderately sol in ethanol; sparingly sol in aliphatic and aromatic hydrocarbons
Spectral Properties:
IR: 2:389C (Aldrich Library of Infrared Spectra, Aldrich Chemical Co, Milwaukee, WI)
NMR: 3:103D (Aldrich Library of Mass Spectra, Aldrich Chemical Co, Milwaukee, WI)
IR: 3:439D (Aldrich Library of Infrared Spectra, Aldrich Chemical Co, Milwaukee, WI)
MASS: NIST 75365 (NIST/EPA/MCDC Mass Spectral Database 1990 version)
Other Chemical/Physical Properties:
Sublimes on heating
Chemical Safety & Handling:
Hazards Summary:
The major hazards encountered in the use and handling of fluoroacetamide stem from its toxicologic properties. Exposure to this colorless, crystalline powder may occur from its manufacture, formulation, and use as a rodenticide. Effects from exposure may include nausea, convulsions, cyanosis, ventricular fibrillation, and death. Effects may be delayed up to 20 hours following exposure. If contact should occur, remove clothing and vigorously wash skin, hair, and nails with soap. Fluoroacetamide should be stored in closed containers in a cool, closed area.
DOT Emergency Guidelines:
Health: Toxic; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution.
Fire or explosion: Highly flammable: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water.
Public safety: Call Emergency Response Telephone Number. ... Isolate spill or leak area immediately for at least 100 to 200 meters (330 to 660 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing which is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations.
Evacuation: ... Fire: If tank, rail car or tank truck is involved in a fire, isolate for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
Fire: CAUTION: All these products have a very low flash point. Use of water spray when fighting fire may be inefficient. Small fires: Dry chemical, CO2, water spray or alcohol-resistant foam. Large fires: Water spray, fog or alcohol-resistant foam. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material. Use water spray or fog; do not use straight streams. Fire involving tanks or car/trailer loads: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
Spill or leak: Fully encapsulating, vapor protective clothing should be worn for spills and leaks with no fire. ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor suppressing foam may be used to reduce vapors. Small spills: Absorb with earth, sand or other non-combustible material and transfer to containers for later disposal. Use clean non-sparking tools to collect absorbed material. Large spills: Dike far ahead of liquid spill for later disposal. Water spray may reduce vapor; but may not prevent ignition in closed spaces.
First aid: Move victim to fresh air. Call 911 or emergency medical service. Apply artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; induce artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves.
Toxic Combustion Products:
When heated to decomposition it emits very toxic fumes of /flourides/ and /nitrogen oxides/.
Hazardous Decomposition:
When heated to decomposition it emits very toxic fumes of /hydrogen flouride/ and /nitrogen oxides/.
Preventive Measures:
Use restricted to sewers, locked warehouses, & other areas to which the public have no access.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.
The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.
Storage Conditions:
STORE IN CLOSED CONTAINERS IN CLOSED AREA.
Disposal Methods:
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.
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P057, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 deg C and residence times of seconds for liquids and gases, and hours for solids. A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 deg C and residence times of seconds for liquids and gases, and longer for solids.
Occupational Exposure Standards:
Manufacturing/Use Information:
Major Uses:
For Fluoroacetamide (USEPA/OPP Pesticide Code: 075002) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./
Rodenticide, insecticide proposed mainly for use on fruits to combat scale insects, aphids, mites. /Former use/
Normally it is used as a bait /(20 g ai/kg)/ in areas to which the public has no access such as sewers and locked warehouses. /Former use/
Manufacturers:
Atomergic Chemetals Corp, Hq, 91 Carolyn Blvd, Farmingdale, NY 11735-1527, (516) 694-9000; ARTEL Chemical Corporaton, PO Box 550, Nitro, WV 25143; Production site: West 19th Street, Nitro, WV 25143
Methods of Manufacturing:
Fluoroacetamide is made by reacting fluoroacetyl chloride and ammonia.
Sodium fluoroacetate + ammonia (amide formation)
Made from chloroacetamide by fluorination process using KF.
General Manufacturing Information:
/FLUOROACETAMIDE/ USE IS LARGELY RESTRICTED TO LICENSED PEST CONTROL OPERATORS.
THE POISONING OF FARM ANIMALS BY EFFLUENTS FROM A FACTORY THAT MFR FLUOROACETAMIDE CAUSED THE MINISTRY OF AGRICULTURE, FISHERIES, & FOOD TO RECOMMEND THAT THE CMPD SHOULD NOT BE USED AS AN INSECTICIDE IN AGRICULTURE, HOME GARDENS, OR FOOD STORAGE IN GREAT BRITAIN, & IT WAS WITHDRAWN FROM THE MARKET.
A rebuttable presumption against registration was issued by EPA on November 22, 1976 on the basis of toxicity to nontarget species ... . The RPAR was terminated on February 28, 1980
Formulations/Preparations:
USEPA/OPP Pesticide Code 075002; Trade Names: Fluorkill, compound 1081, 1081.
BAIT, DYED CEREAL BASE (30 G AI/KG) WHICH IS MIXED WITH WATER FOR USE.
Poisoned grains; bait pellets
Usually packed in 8 oz (227 g) or 5 kg cans
Impurities:
Sometimes colored with black dye, nigrosine.
Consumption Patterns:
ESSENTIALLY 100% AS A RODENTICIDE.
Laboratory Methods:
Clinical Laboratory Methods:
THE RECOVERY OF FLUOROACETAMIDE FROM ANIMAL & HUMAN TISSUE BY GAS CHROMATOGRAPHY USING MASS SPECTROMETER IN MULTIPLE ION MONITORING MODE WAS 30-35% & THE MIN DETECTABLE LEVELS IN TISSUE WAS APPROX 0.7 UG/G.
Analytic Laboratory Methods:
PRODUCT ANALYSIS: ... IS BY REACTION WITH SODIUM & PRECIPITATION AS LEAD CHLORIDE FLUORIDE.
Special References:
Special Reports:
USEPA; FLUOROACETAMIDE (COMPOUND 1080): POSITION DOCUMENT 2; US NTIS PB REP PB80-216831: 23 (1980). EPA POSITION DOCUMENT ON REGISTRATION IS PRESENTED. REGULATORY HISTORY & BASIS OF REBUTTABLE PRESUMPTION, INCL LACK OF EMERGENCY TREATMENT, ACUTE TOXICITY TO MAMMALIAN & AVIAN SPECIES, & SIGNIFICANT REDUCTION OF POPULATIONS OF NONTARGET ORGANISMS & ENDANGERED SPECIES ARE CONSIDERED.
HALL RJ; EFFECTS OF ENVIRONMENTAL CONTAMINANTS ON REPTILES: A REVIEW; US FISH WILDL SERV SPEC SCI REP WILDL 228: 12 (1980). LITERATURE ON EFFECTS OF ENVIRONMENTAL CONTAMINANTS (INCL FLUOROACETAMIDE) ON REPTILES IS REVIEWED. SUGGESTIONS FOR FUTURE RESEARCH INCL BEHAVIORAL & REPRODUCTION STUDIES, DETERMINATION OF SUBLETHAL EFFECTS WHICH MAY HAVE GREAT CONSEQUENCES IN NATURE, & EXAM OF POSSIBLE CONTRIBUTION OF POLLUTANTS TO STATUS OF ENDANGERED SPECIES.
USEPA; Chemical Profile: Fluoroacetamide (1985). A chemical safety information sheet.
Synonyms and Identifiers:
Synonyms:
1081
**PEER REVIEWED**
ACETAMIDE, 2-FLUORO-
**PEER REVIEWED**
AFL 1081
**PEER REVIEWED**
Baran
**PEER REVIEWED**
COMPOUND 1081
**PEER REVIEWED**
Pesticide Code: 075002
**PEER REVIEWED**
FAA
**PEER REVIEWED**
FLUORAKIL 100
**PEER REVIEWED**
2-FLUOROACETAMIDE
**PEER REVIEWED**
FLUOROACETIC ACID AMIDE
**PEER REVIEWED**
FUSSOL
**PEER REVIEWED**
MEGATOX
**PEER REVIEWED**
MONOFLUOROACETAMIDE
**PEER REVIEWED**
NAVRON
**PEER REVIEWED**
RODEX
**PEER REVIEWED**
YANOCK
**PEER REVIEWED**
Formulations/Preparations:
USEPA/OPP Pesticide Code 075002; Trade Names: Fluorkill, compound 1081, 1081.
BAIT, DYED CEREAL BASE (30 G AI/KG) WHICH IS MIXED WITH WATER FOR USE.
Poisoned grains; bait pellets
Usually packed in 8 oz (227 g) or 5 kg cans
Shipping Name/ Number DOT/UN/NA/IMO:
UN 3021; Pesticide, liquid, flammable, toxic, nos, flash point less than 23 deg C.
UN 2902; Pesticide, liquid, toxic, nos.
UN 2903; Pesticide, liquid, flammable, toxic, nos, flash point between 23 deg C and 61 deg C.
UN 2588; Pesticide, solid, toxic, nos.
IMO 3.2; Pesticide, liquid, flammable, toxic, nos, flash point less than 23 deg C.
IMO 6.1; Pesticide, liquid or solid, toxic, nos; Pesticide, liquid, flammable, toxic, nos, flash point between 23 deg C and 61 deg C.
EPA Hazardous Waste Number:
P057; An acute hazardous waste when a discarded commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate.
Administrative Information:
Hazardous Substances Databank Number: 2880
Last Revision Date: 20030124
Last Review Date: Reviewed by SRP on 9/15/2001
Update History:
Complete Update on 01/24/2003, 2 fields added/edited/deleted.
Field Update on 11/08/2002, 1 field added/edited/deleted.
Complete Update on 04/19/2002, 43 fields added/edited/deleted.
Field Update on 01/14/2002, 1 field added/edited/deleted.
Field Update on 08/08/2001, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 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 10/20/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 02/27/1998, 1 field added/edited/deleted.
Complete Update on 10/26/1997, 1 field added/edited/deleted.
Complete Update on 05/08/1997, 1 field added/edited/deleted.
Complete Update on 04/23/1997, 1 field added/edited/deleted.
Complete Update on 10/15/1996, 1 field added/edited/deleted.
Complete Update on 07/11/1996, 1 field added/edited/deleted.
Complete Update on 05/11/1996, 1 field added/edited/deleted.
Complete Update on 01/26/1996, 1 field added/edited/deleted.
Complete Update on 12/30/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 02/28/1993, 2 fields added/edited/deleted.
Field update on 12/27/1992, 1 field added/edited/deleted.
Complete Update on 09/10/1991, 43 fields added/edited/deleted.
Complete Update on 04/16/1990, 1 field added/edited/deleted.
Field update on 12/29/1989, 1 field added/edited/deleted.
Complete Update on 12/19/1989, 1 field added/edited/deleted.
Complete Update on 10/14/1986
Record Length: 84366