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Sodium Fluoroacetate. TOXNET profile from Hazardous Substances Data Bank.
See for Updates: http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB
SODIUM FLUOROACETATE
Human Health Effects:
Human Toxicity Excerpts:
... AT LEAST 16 ... FATALITIES HAVE BEEN REPORTED /FROM HIGH ACUTE EXPOSURE/.
... AFTER SUCCESSFUL RESUSCITATION FROM CARDIAC ARREST, 1 POISONED CHILD WAS
LEFT WITH SEVERE NEUROLOGIC IMPAIRMENT.
IN 1 UNUSUAL CASE OF ... /MAN/ WORKING WITH SODIUM FLUOROACETATE, GUST OF
WIND BLEW POWDER INTO HIS FACE & SOME ... WAS INHALED. THIS CAUSED ALMOST
IMMEDIATE TINGLING SENSATION AROUND CORNERS OF MOUTH & IN NASAL PASSAGES
& SOON ENTIRE FACE BECAME NUMB. THIS WAS ACCOMPANIED BY SALIVATION &
LOSS OF SPEECH. VISION WAS BLURRED FROM ONSET, WITH INABILITY TO FOCUS ON OBJECTS.
ALTHOUGH PARESTHESIAS SPREAD TO ARMS & LEGS, & VIOLENT CONVULSIONS &
COMA FOLLOWED, PATIENT ULTIMATELY RECOVERED COMPLETELY.
NATURE & BASIS OF BLURRING OF VISION ... /NOT/ ESTABLISHED ... CLINICALLY
... NO KNOWN INSTANCES OF PERMANENT VISUAL IMPAIRMENT IN PATIENT ... /WHO/ HAVE
RECOVERED FROM POISONING, BUT TRANSIENT DISTURBANCE OF VISION APPEARS DEFINITE
... /&/ FAILURE OF PUPILS TO REACT TO LIGHT APPEARS TO HAVE BEEN ASSOCIATED
ONLY WITH PERIODS OF COMA OR CONVULSIONS.
A 59-YR-OLD MALE WITH REPEATED EXPOSURE SHOWED RENAL, HEPATIC, NEUROLOGIC
& THYROID DYSFUNCTION. MOST SIGNIFICANT FINDING WAS SEVERE RENAL FAILURE,
RENAL HISTOLOGY SHOWED MEMBRANO-PROLIFERATIVE GLOMERULAR CHANGES WITH FIBRIN
ACCUM & SEVERE CHANGES IN PROXIMAL TUBULAR EPITHELIAL CELLS. TWO URINE SAMPLES
TAKEN 2 WK AFTER ADMISSION CONTAINED SODIUM MONOFLUOROACETATE AT 1.54 MG/DL
& 1.48 MG/DL.
A case report of sodium fluoroacetate ingestion in a 15 yr old female who
was attempting suicide, illustrating CNS abnormalities, is presented. Immediate
clinical features of intoxication were tachycardia, grand mal seizures, psychomotor
agitation, & deterioration of consciousness. Neurological exam 2 wk later
established severe cerebellar dysfunction. Computed tomography revealed a moderate
diffuse brain atrophy. End stage cerebellar
ataxia was evident 18 months after the acute intoxication. Mechanisms for the
brain damage are discussed.
Estimates of the mean lethal dose of fluoroacetate in humans range from 2
to 10 mg/kg, and there have been a number of human fatalities. /Fluoroacetate/
In experimental studies the lethal dose is essentially the same by all routes
of administration. Ingestion is certainly the most likely mode of poisoning,
but there is one report of a near-fatal intoxication in which the inhalation
of sodium fluoroacetate powder may have played a major role. The author of this
communication was also the victim. The compound appears to be absorbed promptly
from the alimentary tract, but initial symptoms are commonly delayed for one
or several hours. Absorption does not occur through intact skin.
In the only alleged case of chronic human poisoning, a rabbit exterminator
in New Zealand was exposed repeatedly during preparation of fluoroacetate bait
over a period of 10 years. He presented with severe and progressive lesions
of the renal tubular epithelium and with milder hepatic, neurologic and thyroid
dysfunctions.
/Sodium fluoroacetate is/ a delayed convulsant, with none of the toxic actions
of fluorides.
Oral lethal dose of sodium salt estimate to be 2-5 mg/kg body weight.
Five cases of monofluoroacetate sodium (sodium fluoroacetate) poisoning ...
led to acute renal failure ... . The subjects ingested from 8 to 40 ml of a
1% solution of the rodenticide. All 5 patients responded to treatment.
Skin, Eye and Respiratory Irritations:
Eye irritant
Medical Surveillance:
First-aid measures (consist of removal of the poison /sodium fluoroacetate/
from the stomach and the intravenous injection of 20-50 g of acetamide in 500
ml of 5% glucose solution. Definitive hospital treatment includes intravenous
injection of acetamide as above, 2-3 times a day, followed by intravenous injections
of 5-10 g of acetamide in 20-40 ml of 40-50% glucose solution, and symptomatic
therapy as required).
Probable Routes of Human Exposure:
CHRONIC INTOXICATION WITH SODIUM FLUOROACETATE IS /SRP: UNLIKELY/ ... INGESTION
IS CERTAINLY MOST LIKELY MODE OF POISONING, BUT THERE IS 1 REPORT OF NEAR-FATAL
INTOXICATION IN WHICH INHALATION ... MAY HAVE PLAYED MAJOR ROLE.
SECONDARY POISONING IN MAN CAUSED BY EATING DEER MEAT, HEARTS OR LIVER IS
REGARDED AS UNLIKELY, AS ALSO IS CHRONIC POISONING FROM DAILY INGESTION OF TISSUES
CONTAINING UP TO 9.2 PPM ... . /FLUOROACETATES/
Emergency Medical Treatment:
Emergency Medical Treatment:
| EMT Copyright Disclaimer: |
| Portions of the POISINDEX(R) database are provided here for
general 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, *** FLUOROACETATE-1080 ***, 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 Fluoroacetate is a highly toxic rodenticide that is
rapidly absorbed and may cause systemic toxicity after
oral, dermal, inhalation or ocular exposure. Clinical
effects may develop within 30 minutes of exposure but
may be delayed as long as 20 hours.
o Effects of acute exposure commonly include nausea,
vomiting and diarrhea; serious poisoning may result in
seizures, coma, respiratory depression, hypotension and
cardiac dysrhythmias including ventricular tachycardia
and fibrillation and asystole.
o Metabolic acidosis, renal insufficiency, elevated
transaminases, hypocalcemia, and hyperglycemia have
also been reported.
o Shock, metabolic acidosis renal insufficiency are
associated with an increased risk of fatal outcome
after fluoroacetate ingestion.
o The estimated lethal dose in man is 5
milligrams/kilogram; however, one milligram of the pure
compound is probably enough to cause severe toxicity.
o When sodium fluoroacetate is heated to decomposition it
emits highly toxic fumes of sodium oxide and fluorine.
VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
o Hypotension, tachycardia and irregular pulse may be
noted.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Numbness of the face and facial twitching, blurred
vision and nystagmus may occur.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Ventricular tachycardia or fibrillation, prolonged QTc,
and asystole may occur.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Respiratory depression and pulmonary edema have been
reported.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Neurologic effects may include hyperactive behavior,
auditory hallucinations, cerebellar dysfunction, loss
of speech, paresthesias, seizures, coma, carpopedal
spasm and neurologic impairment.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Nausea, vomiting, excessive salivation and diarrhea may
be noted.
HEPATIC
0.2.9.1 ACUTE EXPOSURE
o Mild hepatic dysfunction has been reported.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Degeneration of renal tubules have been reported.
0.2.10.2 CHRONIC EXPOSURE
o Renal tubular lesions and renal failure have been
reported.
ACID-BASE
0.2.11.1 ACUTE EXPOSURE
o Metabolic acidosis has been reported.
FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
o Hypocalcemia and carpopedal spasm may be noted.
ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
o Thyroid dysfunction has been reported.
o Hyperglycemia has been reported.
METABOLISM
0.2.17.1 ACUTE EXPOSURE
o Hyperuricemia has been reported
PSYCHIATRIC
0.2.18.1 ACUTE EXPOSURE
o Mental deficits, memory disturbance, and depression
have been noted.
REPRODUCTIVE HAZARDS
o At the time of this review, no data were available to
assess the teratogenic potential of this agent.
o At the time of this review, no data were available to
assess the potential effects of exposure to this agent
during pregnancy or lactation.
o Observed paternal toxic effects in male rats include
changes in the testes, epididymis, and sperm duct.
CARCINOGENICITY
0.2.21.2 HUMAN OVERVIEW
o At the time of this review, no data were available to
assess the carcinogenic potential of this agent.
GENOTOXICITY
o At the time of this review, no data were available to
assess the mutagenic or genotoxic potential of this
agent.
|
| Laboratory: |
o Fluoroacetate levels are not clinically useful.
o Monitor serum electrolytes including calcium, magnesium,
and potassium concentrations.
o Monitor liver and renal function tests after significant
intoxication
o Obtain an ECG and institute continuous cardiac monitoring
for evidence of hypocalcemia, hypokalemia, prolonged QTc
interval, ventricular dysrhythmias.
|
| Treatment Overview: |
ORAL EXPOSURE
o Do NOT induce emesis.
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 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 THERE IS NO KNOWN ANTIDOTE for fluoroacetate
intoxication. Symptomatic and supportive care should be
provided.
o DECONTAMINATION: Remove contaminated clothing and
jewelry. Wash the skin, including hair and nails,
vigorously; do repeated soap washings. Discard
contaminated clothing.
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.
o MONITOR ECG AND VITAL SIGNS frequently.
o CALCIUM SALTS - Calcium gluconate or calcium chloride
should be administered parenterally in patients with
documented hypocalcemia. Correct hypocalcemia with IV
CALCIUM GLUCONATE (ADULT AND CHILD: 0.1 to 0.2 mL/kg up
to 10 mL/dose of a 10% solution; repeat dose if
necessary) or CALCIUM CHLORIDE (ADULT: 10 to 20 mL of
10% CHILD: 10 to 20 mg/kg).
o Intravenous glyceryl monoacetate (monoacetin) and
ethanol administration have been advocated to prevent or
reverse the toxic effects of fluoroacetate. However,
their safety and efficacy have not been demonstrated in
humans.
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.
o There is no known effective specific treatment for
fluoroacetate exposure, but symptomatic supportive
therapy should be provided.
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.
o There is no known effective specific treatment for
fluoroacetate exposure, but symptomatic supportive
therapy should be provided.
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.
o There is no known effective specific treatment for
fluoroacetate exposure, but symptomatic supportive
therapy should be provided.
|
| Range of Toxicity: |
o A milligram of pure compound is probably enough to cause
severe toxicity and less may be toxic. Animal
extrapolation to man indicates a dose of 2 to 10 mg/kg may
produce death in humans.
|
Antidote and Emergency Treatment:
If sodium fluoroacetate or solutions containing sodium fluoroacetate get into
the eyes, wash eyes immediately with large amounts of water, lifting the lower
and upper lids occasionally. If irritation is present after washing, get medical
attention. Contact lens should not be worn when working with this chemical.
If sodium fluoroacetate or solutions containing sodium fluoroacetate get on
the skin, immediately flush the contaminated skin with water. If sodium fluoroacetate
or solutions containing sodium fluoroacetate penetrate through the clothing,
remove the clothing promptly and flush the skin with water. If irritation is
present after washing, get medical attention promptly.
If a person breathes in large amounts of sodium fluoroacetate, move the exposed
person to fresh air at once. If breathing has stopped, perform artificial respiration.
Keep the affected person warm and at rest. Get medical attention as soon as
possible.
When sodium fluoroacetate or solutions containing sodium fluoroacetate have
been swallowed and the person is conscious, give the person large quantities
of water immediately. After the water has been swallowed, try to get the person
to vomit by having him touch the back of his throat with his finger. Do not
make an unconscious person vomit. Get medical attention immediately.
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
FLUOROACETATE IS HIGHLY TOXIC TO ALL SPECIES ... . TOXICITY FOR RUMINANTS
... /IS CONSIDERABLY INFLUENCED BY ROUTE OF ADMIN & NATURE OF FODDER. ...
/EXPTL/ RESULTS SUGGEST THAT PROTEIN MAY EXERT PROTECTIVE EFFECT IN THESE SPECIES.
... THERE ARE 2 CLASSES OF SIGNS FOUND IN VARYING DEGREE IN DIFFERENT ANIMALS.
VENTRICULAR ARRHYTHMIAS, MARKED VENTRICULAR ALTERATION, MYOCARDIAL DEPRESSION
& VENTRICULAR FIBRILLATION ARE SEEN IN HORSES, GOATS, RABBITS & MONKEYS;
IN DOG & GUINEA PIG, CONVULSIONS OCCUR WITHOUT PARALLEL CARDIAC ABNORMALITIES;
CAT, PIG, RAT, AND HAMSTER SHOW BOTH CARDIAC AND CENTRAL NERVOUS SYSTEM RESPONSES.
/FLUOROACETATES/
... DIETARY LEVEL OF 5 PPM FOR 2 YR (APPROX 0.25 MG/KG/DAY ... ) PRODUCED
TISSUE CHANGES IN RATS. ... 10 PPM ... IN DIET CAUSED ONLY TRANSIENT FLUCTUATION
IN GROWTH RATE OF RAT. ... 20 PPM (2 MG/KG IN YOUNG RATS) INHIBITED GROWTH RATE
SHARPLY DURING 1ST WK, BUT RATS SURVIVED & ... GROWTH RATE GRADUALLY BECAME
NEARLY NORMAL IN 3-4 WK. TOLERANCE FOR CHEM LASTED LESS THAN 2 WK; RATS THAT
HAD ADJUSTED TO CMPD SHOWED A SECOND RETARDATION OF GROWTH WHEN RETURNED TO
A DIETARY LEVEL OF 20 PPM AFTER 2 WK ON NORMAL DIET. RATS CONDITIONED BY DIETARY
LEVEL OF 20 PPM CAN THEN ADJUST TO LEVEL OF 40 PPM ... WITH 2ND RETARDATION
OF GROWTH.
HYPERGLYCEMIA AND GLYCOSURIA HAVE BEEN NOTED IN SOME EXPERIMENTAL STUDIES.
SIGNIFICANCE OF BLACK, TARRY BLOOD IN POISONED ANIMALS NEEDS EXPLANATION. /FLUOROACETATE/
NATURE & BASIS OF BLURRING OF VISION ... /NOT/ ESTABLISHED ... . NO KNOWN
INSTANCES OF PERMANENT VISUAL IMPAIRMENT IN ... ANIMALS THAT HAVE RECOVERED
FROM POISONING, BUT TRANSIENT DISTURBANCE OF VISION APPEARS DEFINITE ... . IN
SEVERELY POISONED CATTLE ... VISION ... SO IMPAIRED ... ANIMALS HAVE NOT AVOIDED
OBJECTS, BUT WALKED INTO THEM.
SODIUM FLUOROACETATE HAS BEEN FOUND TO INJURE SURVIVING RETINA AT CONCN OF
0.005 MOLAR OR GREATER, & AT 0.05 MOLAR CAUSES SELECTIVE DEGENERATION OF
CELLS IN CULTURED RETINA. WHETHER POISONING OF RETINA IS INVOLVED IN ILL-DEFINED
VISUAL DISTURBANCES OBSERVED IN POISONED ... ANIMALS IS NOT KNOWN.
IN OUTBREAK ... /OF POISONING/ CATTLE SHOWED LISTLESSNESS, ANOREXIA, INCOORDINATION
& ACCELERATED HEART & RESP RATES, PARTICULARLY WHEN EXERTED, BUT NO
NERVOUS SIGNS OR CONVULSIONS. SURVIVING ANIMALS REMAINED UNTHRIFTY. POST MORTEM
SHOWED ENLARGED, FLABBY HEART, FATTY LIVER & EDEMA OF BRISKET & UNDER
JAW. LAMBS EXHIBITED INCOORDINATION, GRINDING OF TEETH, DULLNESS, WEAKNESS &
RECUMBENCY ... TISSUE CITRIC ACID LEVELS WERE 3 TIMES NORMAL VALUE ... . /FLUOROACETATES/
GENETIC RESISTANCE SEEMED TO HAVE DEVELOPED AMONG SOME ANIMALS GRAZING ON
FLUOROACETATE RICH VEGETATION OF WESTERN AUSTRALIA. THE CONCN OF FLUORIDE ION
(F-) IN PLASMA OF WESTERN GRAY KANGAROO (MACROPUS FULIGINOSUS OCYDROMUS) FOLLOWING
FEEDING OF FLUOROACETATE WAS INCR SUGGESTING DETOXICATION INVOLVING SUBSTANTIAL
DEFLUORINATION OF FLUOROACETATE OR ONE OF ITS METABOLITES. ELEVATION OF PLASMA
CITRATE FOLLOWING ORAL ADMIN OF 5 MG FLUOROACETATE/KG IN GRAY KANGAROOS WERE
MUCH LESS THAN EASTERN RED KANGAROO (MEGLEIA RUFA).
The inhibitory effect of sodium fluoroacetate (0.01-100 mM) on rat embryonic
respiratory capacity (QO2) in vitro was significantly lower than on adult rat
kidney tissue slices. Admin of single dose to pregnant rats on day 9 or 10 of
pregnancy significantly decreased the respiratory capacity & dry wt of day
11 embryos, but not of day 12 embryos. The same dose was nonteratogenic, suggesting
that by end of gestation embryos can compensate for metabolic change induced.
Endogenous respiration by liver homogenates of sodium fluoroacetate (Compound
1080) intoxicated cats decreased by 40% compared to intact animals. In rats,
the hepatic respiration did not change 5 hr after introduction of sodium fluoroacetate.
Similar differences in the oxygen consumption were noticed under in vitro conditions.
Endogenous resp by skeletal muscle was 54% lower by 5 hr after ip admin than
that seen in muscle homogenates of the intact rats. In cats, no changes were
observed (6 hr) following admin. Introduction of Compound 1080 under in vitro
conditions in rat muscle homogenates reduced resp 33%. Similar effects were
noticed in cat muscle homogenates. Use of pyruvate with Compound 1080 in rat
& cat skeletal muscle homogenates prevented the inhibitory effects of compound
1080 on respiration almost totally; but only partially in cat liver homogenates.
In adult starlings (Sturnus vulgaris) fed compound 1080 at 27-432 ppm, very
high toxicity was noted. The 5 day lethal concn was 4.7 ppm. The avg testis
wt was slightly decreased.
In period since sodium fluoroacetate was banned, the number of grazing livestock
reported as lost to predation on western national forests has increased. Number
of toxic bait stations (1080) used throughout the West, from 1960 until the
1972 ban, showed a strong inverse relation with number of livestock reported
lost to predation on national forests during these same years.
Domestic animals such as cats and dogs may be poisoned by eating rodents and
birds killed by fluoroacetate poisoned bait.
There are apparent species differences in the quality of symptoms that lead
to death. Dogs die of convulsions or respiratory paralysis, but in ... monkeys,
horses, and rabbits central nervous system actions are usually incidental, and
the dangerous fatal complication is ventricular fibrillation. Provision of large
quantities of acetate appears to antagonize fluoroacetate poisoning in a competitive
manner in that monkeys have been successfully protected from fluoroacetate poisoning
by the administration of glycerol monoacetate. /Fluoroacetate/
Administration of 100 mg sodium fluoroacetate (compound 1080)/kg body weight
to Tiliqua rugosa resulted in a 3.4-fold increase in plasma citrate levels 48
hr after dosing while administration of 3 mg sodium fluoroacetate/kg body weight
to Rattus norvegicus produced a fivefold increase in plasma citrate levels within
4 hr. Administration of 300 mg sodium fluoroacetate/kg body weight reduced the
oxygen consumption of the skink by between 2.5 and 11% while in the rat, 2 mg
sodium fluoroacetate/kg body weight reduced oxygen consumption by between 28
and 57%. Aconitate hydratase activity in extracts of liver acetone powders from
Tiliqua rugosa was less inhibited by (-)erythrofluorocitrate (Ki; 0.065 mM)
than that in extracts derived from Rattus norvegicus (Ki; 0.026 mM). The rate
of defluorination of fluoroacetate in erythrocytes and in extracts of liver
acetone powders of Tiliqua rugosa was 8- and 4.5-fold greater, respectively,
than that found in similar preparations from Rattus norvegicus. A rapid rate
of defluorination together with a low reliance on aerobic respiration favored
detoxification of fluoroacetate in Tiliqua rugosa rather than its conversion
into fluorocitrate. Through defluorination in this species helped to minimize
the immediate effects of fluoroacetate aerobic respiration, it resulted in rapid
depletion of liver glutathione levels.
Fluoroacetic and fluorocitric acid toxicity is often characterized by seizures.
... Intrathecal injection of fluorocitrate in mice resulted in seizures after
an average latency of 15 seconds, while intracerebroventricular injection produced
seizure after 36.5 min, and required higher doses to achieve this effect. This
indicates the probable site of fluoroacetate and fluorocitrate neurotoxicity
is the spinal cord. To mimic citrate accumulation, characteristic of fluoroacetate
and fluorocitrate poisoning, citric acid was injected intrathecal and also found
to produce siezures. The structurally unrelated compounds EDTA, EGTA, glutamic
acid and lactic acid also produced seizures identical to fluorocitrate. The
ability of these compounds to chelate Ca2+ correlates well with their ability
to cause seizures when administered intrathecal and coadministration of calcium
greatly attenuated the neurotoxicity of these compounds as well as fluoroacetate
and fluorocitrate. In contrast, Ca2+ was unable to inhibit seizures elicited
by strychnine, suggesting calcium's ability to inhibit chelators of divalent
cations is not due to a general anticonvulsant effect. ... Changes in Ca2+ concentration
in the spinal cord may be responsible for some forms of seizure activity.
Birds in Australia vary greatly in their sensitivity to 1080 poison (sodium
monofluoroacetate). Median lethal doses (LD50) range from 0.63 mg/kg for red
browed firetails, Emblema temporalis, to approximately 278 mg/kg for the Emu,
Dromaius novaehollandiae. Significant differences occur between the sensitivity
of different groups of birds and may be related to differences in their metabolic
rates. A few species may also have developed a tolerance to 1080 from being
exposed to indigenous plants that contain fluoroacetate, or to insects and other
animals which have fed on such plants. The most common signs of 1080 poisoning
among birds are depression, fluffed feathers, a reluctance to move and convulsions.
Signs of poisoning first appeared among the species tested at 1 to 60 hr after
dosing, and deaths followed between 1 hr to almost 11 days after dosing. The
susceptibility of 48 /species/ /related/ of birds in Australia to 1080 pisoning
is to typical baits and poison concentrations used against vertebrate pests.
Serum citrate was studied as an indicator of toxicity for compounds which
inhibit citrate metabolism. Adult male Cr1:CD(SD)BR rats were administered 3
mg/kg, the median lethal dose of sodium monofluoroacetate. In another set of
experiments were injected with 8, 32, or 80 mg/kg of fluorocitrate. Adult beagle
dogs were administered sodium monofluoroacetate in 50, 100, or 150 ug/kg, or
fluorocitrate in doses between 2 and 32 mg/kg. ... Rats treated with 3 mg sodium
monofluoroacetate/kg were less active within 2 hours after the treatment. Convulsions
occurred in some animals between 3.5 to 4 hours after dosing. A 40% reduction
in heart adenosine triphosphate was observed 2 hours after the treatment with
sodium monofluoroacetate. The depletion of ATP was inversely correlated with
rapidly rising serum citrate level. The increases in citrate were smaller in
dogs than in rats. Elevated serum citrate was indicative of the onset of toxicity
in both species. The 60 mg/kg fluorocitrate dose produced maximum toxic effects
without excessive mortality within 4 hours postreatment. Fluorocitrate at low
doses did not cause as much depletion of heart adenosine triphosphate and accumulation
of citrate, however at doses between 8 and 32 mg/kg it produced three to eight
fold increases in serum citrate. Death followed shortly after 4 hours. In the
presence of fluorocitrate the onset of clinical signs state that the determination
of serum citrate is a readily accessible and accurate peripheral indicator of
toxicity.
Non-Human Toxicity Values:
LD50 Rat oral 1.7 mg/kg
LD50 Horse oral 0.35-0.55 mg/l
LD50 Cattle oral 0.39 mg/kg
LD50 Calves oral 0.22 mg/kg
LD50 Sheep oral 0.25-0.5 mg/kg
LD50 Swine oral 0.4-1 mg/kg
LD50 Horse, male & female, oral 0.35 to 0.55 mg/kg /sample purity equal
to or greater than 90%/
Ecotoxicity Values:
LD50 Mallard, male, 3 months, oral (stomach-tube) 9.11 mg/kg (5.60 to 14.6
mg/kg, 95% confidence limit) /sample purity equal to or greater than 90%/
LD50 Mallard duckling, 7 days old + or - 1, oral 5.97 mg/kg (4.25 to 8.39
mg/kg, 95% confidence limit) /sample purity equal to or greater than 90%/
LD50 Pheasant, male, 3 to 5 months old, oral 6.46 mg/kg (3.85 to 10.8 mg/kg,
95% confidence limit) /sample purity equal to or greater than 90%/
LD50 Chukar, male & female, 3 months old, oral 3.51 mg/kg (2.58 to 4.78
mg/kg, 95% confidence limit) /sample purity equal to or greater than 90%/
LD50 Coturnix male, 3 months old, oral 17.7 mg/kg (11.0 to 28.7 mg/kg, 95%
confidence limit) /sample purity equal to or greater than 90%/
LD50 Mourning dove, male & female, oral (stomach-tube), 8.55 to 14.6 mg/kg
/sample purity equal to or greater than 90%/
LD50 House sparrow, male, oral 3.00 mg/kg (2.38 to 3.78 mg/kg, 95% confidence
limit) /sample purity equal to or greater than 90%/
LD50 Bullfrog, male, oral 54.4 mg/kg (25.6 to 115 mg/kg, 95% confidence limit)
/sample purity equal to or greater than 90%/
LD50 Redwinged blackbird, oral 4.22 mg/kg
LD50 Starling, oral 2.37 mg/kg
LD50 Pigeon acute oral 4.24 mg/kg
LD50 Mallard duck acute oral 10 mg/kg
LD50 Golden eagle acute oral 1.25-5 mg/kg
LD50 Horned owl acute oral about 10 mg/kg
LD50 RATTUS FUSCIPES (BUSH RAT FROM WESTERN AUSTRALIA) ORAL 40 MG/KG; ACQUIRED
GENETIC RESISTANCE
LD50 RATTUS FUSCIPES (BUSH RAT FROM EASTERN AUSTRALIA) ORAL 1.13 MG/KG
LD50 TRICHOSURUS VULPECULA (BRUSH-TAILED POSSUM FROM WESTERN AUSTRALIA) ORAL
ABOVE 100 MG/KG; ACQUIRED GENETIC RESISTANCE
LD50 TRICHOSURUS VULPECULA (BRUSH-TAILED POSSUM FROM EASTERN AUSTRALIA) ORAL
0.68 MG/KG
LD50 Merriam's turkey, female, oral, less than 6 months old, 4.00 mg/kg (1.20
to 13.3 mg/kg, 95% confidence limit) /sample purity equal to or greater than
90%/
LD50 Mule deer, male, 8 to 11 months old, 0.30 to 1.00 mg/kg /sample purity
equal to or greater than 90%/
LD50 Mule deer, male & female, oral 0.22 to 0.44 mg/kg /sample purity
equal to or greater than 90%/
LD50 Domestic ferret male, yearling, oral 1.41 mg/kg /sample purity equal
to or greater than 90%/
LD50 Bear acute oral 0.5-1 mg/kg
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
FOLLOWING INJECTION OF FLUOROACETATE-2-(14)C INTO RATS, ABOUT 3% OF LABEL
APPEARED IN RESP CARBON DIOXIDE & 32% IN URINE WITHIN 4 DAYS. LABELED FLUOROCITRATE
WAS RECOVERED FROM URINE. INCORPORATION OF LABEL INTO CHOLESTEROL & INTO
... LOWER & HIGHER FATTY ACID FRACTIONS WAS DEMONSTRATED. OTHER UNIDENTIFIED
LABELED MATERIALS /WERE/ ... OBSERVED.
WHEN FLUOROACETATE-2-(14)C WAS APPLIED TO PLANTS (ACACIA GEOGINAE, CASTOR
BEAN, PEANUT, PINTO BEAN), LABELED CARBON MONOXIDE WAS OBSERVED. SOME LABEL
... WAS ALSO INCORPORATED INTO WATER SOL FRACTIONS & LIPIDS. IN SOME PLANT
SEEDS ... /IT/ WAS CONVERTED INTO FLUORINE-CONTAINING LONG CHAIN FATTY ACIDS.
SODIUM FLUOROACETATE IS CONVERTED INTO FLUOROCITRIC ACID IN BODY & BLOCKS
TCA CYCLE BY INHIBITING ACONITASE ACTIVITY. POISONING CAN BE DIAGNOSED BY INCR
CITRIC ACID LEVELS IN ALL ORGANS OR BY DETERMINATION OF ACONITASE ACTIVITY.
Fluoroacetamide is metabolized to fluoroacetate, which produces its toxic
action by inhibiting the citric acid cycle. The fluorine substituted acetate
becomes incorporated, as normal acetate, into fluoroacetyl coenzyme A, which
condenses with oxaloacetate to form fluorocitrate. Fluorocitrate inhibits the
enzyme aconitase and thereby inhibits the conversion of citrate to isocitrate.
As a result there is an accumulation of large quantities of citrate in the tissue,
and the cycle is blocked. As might be expected, the heart and central nervous
system are the most critical tissues involved in poisoning by a general inhibition
of oxidative energy metabolism. Thus, the symptoms following fluoroacetate poisoning,
in addition to nonspecific signs of nausea and vomiting, include cardiac irregularities,
cyanosis, generalized convulsion, and death from ventricular fibrillation or
respiratory failure.
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 defluorination.
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-(arboxymethyl) 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:
... Rapidly absorbed by GI tract. It is not well absorbed by intact skin,
but absorption may be greater in presence of dermatitis or other skin injury.
... Samples taken at autopsy from man who survived about 17 hours after being
found unconscious ... /showed concn in/ urine, 368 ppm; liver, 58 ppm; brain,
76 ppm; & kidney, 65 ppm.
... LIVER OF PERSON WHOSE DEATH WAS SUPPOSED DUE TO SODIUM FLUOROACETATE CONTAINED
2.4 MG OF FLUORINE/100 G.
AMT OF SODIUM MONOFLUOROACETATE RECOVERED FROM BRAIN
PER UNIT WT OF TISSUE WAS ABOUT 2 TIMES THAT FROM OTHER ORGANS AFTER RABBITS
WERE KILLED WITH DOSE 10 TIMES LD50. AMT OF ORGANOFLUORINE WAS ABOUT THE SAME
24 HR AFTER DEATH AS IMMEDIATELY AFTER DEATH & DECREASED GRADUALLY, BY 10-20%
AFTER 3 DAYS & BY 50-80% WHEN CARCASS WAS KEPT AT 21-25 DEG C.
MOST OF FLUOROACETATES INGESTED IS ELIMINATED IN FECES & URINE.
Mechanism of Action:
FLUOROACETATE ... /INHIBITS/ CITRIC ACID CYCLE. FLUORINE SUBSTITUTED ACETATE
BECOMES INCORPORATED, AS NORMAL ACETATE, INTO FLUOROACETYL COENZYME A, WHICH
CONDENSES WITH OXALOACETATE TO FORM FLUOROCITRATE. FLUOROCITRATE INHIBITS ...
ACONITASE & THEREBY INHIBITS CONVERSION OF CITRATE TO ISOCITRATE. /FLUOROACETATES/
Fluoroacetate produces its toxic action by inhibiting the citric acid cycle.
The compound is incorporated into fluoroacetyl coenzyme A, which condenses with
oxaloacetate to form fluorocitrate. Fluorocitrate inhibits the enzyme aconitase
and thereby inhibits conversion of citrate to isocitrate. As might be expected,
the heart and CNS are the tissues most critically involved by a general inhibition
of oxidative energy metabolism. Thus, the signs and symptoms of fluoroacetate
poisoning, in addition to nonspecific signs of nausea and vomiting, include
cardiac irregularities, cyanosis, generalized convulsions, and death from ventricular
fibrillation or respiratory failure. Provision of large quantities of acetate
appears to antagonize fluoroacetate in a competitive manner; monkeys have been
successfully protected from fluoroacetate poisoning by the administration of
glycerol monoacetate.
It is not known why there is so much species variation in toxicity of fluoroacetate.
The variation is apparently not due to differences in size of animal, type of
digestive system, or basal metabolic rate. Perhaps it is related to rate of
elimination of the poison or rate of condensation of the poison with oxalacetate.
Interactions:
MALE SPRAGUE-DAWLEY RATS WERE INJECTED IP WITH 376 MG DIETHYLMALEATE 30 MIN
PRIOR TO IP ADMIN OF 1, 1.5, 2.5, 3.5, 4, 4.5, 5.5 OR 7 MG/KG SODIUM FLUOROACETATE.
REDUCTION OF LIVER GLUTATHIONE CONCN BY DIETHYLMALEATE PRE-DOSING CAUSED 35%
LOWERING IN LD50 OF SODIUM FLUOROACETATE.
SODIUM FLUOROACETATE (1 MMOLAR) INCR CITRATE CONCN OF RAT EPIDIDYMAL FAT PADS
FROM APPROX 7.0-69.8 NMOL/G IN ABSENCE OR PRESENCE OF INSULIN, BUT DID NOT ALTER
RATE OF FATTY ACID SYNTHESIS OR THE INITIAL ACTIVITIES OF PYRUVATE DEHYDROGENASE
& ACETYL-COA CARBOXYLASE. INCUBATION WITH (-)-HYDROXYCITRATE (5 MMOLAR)
INCR LEVELS OF CITRATE FROM APPROX 7.0-18.8 NMOLES/G, INHIBITED FATTY ACID SYNTH,
DECR PYRUVATE DEHYDROGENASE & INCR ACETYL-COA CARBOXYLASE ACTIVITY.
Pharmacology:
Interactions:
MALE SPRAGUE-DAWLEY RATS WERE INJECTED IP WITH 376 MG DIETHYLMALEATE 30 MIN
PRIOR TO IP ADMIN OF 1, 1.5, 2.5, 3.5, 4, 4.5, 5.5 OR 7 MG/KG SODIUM FLUOROACETATE.
REDUCTION OF LIVER GLUTATHIONE CONCN BY DIETHYLMALEATE PRE-DOSING CAUSED 35%
LOWERING IN LD50 OF SODIUM FLUOROACETATE.
SODIUM FLUOROACETATE (1 MMOLAR) INCR CITRATE CONCN OF RAT EPIDIDYMAL FAT PADS
FROM APPROX 7.0-69.8 NMOL/G IN ABSENCE OR PRESENCE OF INSULIN, BUT DID NOT ALTER
RATE OF FATTY ACID SYNTHESIS OR THE INITIAL ACTIVITIES OF PYRUVATE DEHYDROGENASE
& ACETYL-COA CARBOXYLASE. INCUBATION WITH (-)-HYDROXYCITRATE (5 MMOLAR)
INCR LEVELS OF CITRATE FROM APPROX 7.0-18.8 NMOLES/G, INHIBITED FATTY ACID SYNTH,
DECR PYRUVATE DEHYDROGENASE & INCR ACETYL-COA CARBOXYLASE ACTIVITY.
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
CHRONIC INTOXICATION WITH SODIUM FLUOROACETATE IS /SRP: UNLIKELY/ ... INGESTION
IS CERTAINLY MOST LIKELY MODE OF POISONING, BUT THERE IS 1 REPORT OF NEAR-FATAL
INTOXICATION IN WHICH INHALATION ... MAY HAVE PLAYED MAJOR ROLE.
SECONDARY POISONING IN MAN CAUSED BY EATING DEER MEAT, HEARTS OR LIVER IS
REGARDED AS UNLIKELY, AS ALSO IS CHRONIC POISONING FROM DAILY INGESTION OF TISSUES
CONTAINING UP TO 9.2 PPM ... . /FLUOROACETATES/
Environmental Biodegradation:
FLUOROACETATES ARE SLOWLY DESTROYED BY SOIL BACTERIA, & DO NOT USUALLY
PERSIST IN SOIL FOR MORE THAN 2 MO. /FLUOROACETATES/
Environmental Standards & Regulations:
FIFRA Requirements:
Classified for restricted use, limited to use by or under the direct supervision
of a certified applicator. ... Sodium fluoroacetate in all solutions & dry
baits are restricted for all uses based on acute oral toxicity, hazard to nontarget
avian species, use & accident history.
Cancelled all products except those used for livestock collars for predicide
use & control of certain rodents in CA & CO (Uses are currently under
review). Criteria of concern: Reduction in nontarget & endangered species.
Reference: PR Notice 72-2 3/9/72. 10th Circuit court's Vacation of Wyoming District
Court's Predicide Injunction, 12/2/75/ 49 FR 4830 2/5/83; 50 FR 31012 7/31/85.
TSCA Requirements:
Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety
Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers,
and processors of listed chemical substances and mixtures to submit to EPA copies
and lists of unpublished health and safety studies. Acetic acid, fluoro-, sodium
salt is included on this list.
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 10 lb or 4.54 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. Sodium Fluoroacetate is an extremely
hazardous substance (EHS) subject to reporting requirements when stored in amounts
in excess of its threshold planning quantity (TPQ) of 10/10,000 lbs.
RCRA Requirements:
P058; As stipulated in 40 CFR 261.33, when fluoroacetic acid sodium salt 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-H3-F-O2.Na
Molecular Weight:
100.02
Color/Form:
WHITE POWDER
Fluffy, colorless to white (sometimes dyed black) powder [Note: A liquid above
95 degrees F].
Odor:
ODORLESS
Odorless.
Melting Point:
200 DEG C
Solubilities:
111 G/100 CC WATER; 1.4 G/100 CC ETHANOL; 5 G/100 CC METHANOL; 40 MG/100 CC
ACETONE; 4.9 MG/100 CC CARBON TETRACHLORIDE, EACH AT 25 DEG C.
Vapor Pressure:
Approx 0.0 mm Hg at 20 deg C
Other Chemical/Physical Properties:
HYGROSCOPIC
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: Highly toxic, may be fatal if inhaled, swallowed or absorbed through
skin. Avoid any skin contact. Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire
control or dilution water may be corrosive and/or toxic and cause pollution.
Fire or explosion: Non-combustible, substance itself does not burn but may
decompose upon heating to produce corrosive and/or toxic fumes. Containers may
explode when heated. Runoff may pollute waterways.
Public safety: CALL Emergency Response Telephone Number on Shipping Paper.
If Shipping Paper not available or no answer, refer to appropriate telephone
number listed on the inside back cover. Isolate spill or leak area immediately
for at least 25 to 50 meters (80 to 160 feet) in all directions. Keep unauthorized
personnel away. Stay upwind. Keep out of low areas.
Protective clothing: Wear positive pressure self-contained breathing apparatus
(SCBA). Wear chemical protective clothing which is specifically recommended
by the manufacturer. Structural firefighters' protective clothing is recommended
for fire situations ONLY; it is not effective in spill situations.
Evacuation: Spill: See the Table of Initial Isolation and Protective Action
Distances for highlighted substances. For non-highlighted substances, increase,
in the downwind direction, as necessary, the isolation distance shown under
"PUBLIC SAFETY". 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: Small fires: Dry chemical, CO2 or water spray. Large fires: Water spray,
fog or regular 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.
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.
Do not get water inside containers. 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 the ends of tanks. For massive fire, use unmanned hose holders or monitor
nozzles; if this is impossible withdraw from area and let fire burn.
Spill or leak: Do not touch damaged containers or spilled material unless
wearing appropriate protective clothing. Stop leak if you can do it without
risk. Prevent entry into waterways, sewers, basements or confined areas. Cover
with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand
or other non-combustible material and transfer to containers. DO NOT GET WATER
INSIDE CONTAINERS.
First aid: Move victim to fresh air. Call emergency medical care. 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. For minor skin
contact, avoid spreading material on unaffected skin. 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.
Skin, Eye and Respiratory Irritations:
Eye irritant
Hazardous Decomposition:
DECOMP AT 200 DEG C
Immediately Dangerous to Life or Health:
2.5 mg/cu m
Protective Equipment & Clothing:
Wear appropriate personal protective clothing to prevent skin contact.
Wear appropriate eye protection to prevent eye contact.
Facilities for quickly drenching the body should be provided within the immediate
work area for emergency use where there is a possibility of exposure. [Note:
It is intended that these facilities provide a sufficient quantity or flow of
water to quickly remove the substance from any body areas likely to be exposed.
The actual determination of what constitutes an adequate quick drench facility
depends on the specific circumstances. In certain instances, a deluge shower
should be readily available, whereas in others, the availability of water from
a sink or hose could be considered adequate.]
Recommendations for respirator selection. Max concn for use: 0.25 mg/cu m.
Respirator Class(es): Any dust and mist respirator.
Recommendations for respirator selection. Max concn for use: 0.5 mg/cu m.
Respirator Class(es): Any dust and mist respirator except single-use and quarter-mask
respirators. Any supplied-air respirator.
Recommendations for respirator selection. Max concn for use: 1.25 mg/cu m.
Respirator Class(es): Any supplied-air respirator operated in a continuous flow
mode. Any powered, air-purifying respirator with a dust and mist filter.
Recommendations for respirator selection. Max concn for use: 2.5 mg/cu m.
Respirator Class(es): Any air-purifying, full-facepiece respirator 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 powered, air-purifying respirator
with a tight-fitting facepiece and a high-efficiency particulate filter. Any
self-contained breathing apparatus with a full facepiece. Any supplied-air respirator
with a full facepiece.
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 that has a full
facepiece and is operated in a 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 with a high-efficiency particulate filter. Any appropriate escape-type,
self-contained breathing apparatus.
Preventive Measures:
The AAPCO ... regulatory principle ... /states that/ "No person shall sell
or possess any sodium fluoroacetate except Federal, state, county, municipal
officers or their deputies for use in their official duties in pest control;
research or chemical laboratories in their respective fields; regularly licensed
pest control operators for use in their own service work; & wholesalers
or jobbers of economic poisons for sale to aforementioned persons, or for export".
... /Baits/ should be handled only in closed or draught-proof places ... .
All contacts by mouth should be avoided, therefore hands & exposed skin
should be carefully washed before eating, drinking & smoking ... . Bait
containers should be marked "poisons" & all rodent bodies should be burned.
... In agriculture, use is acceptable on non-edible crop & when proper precautions
are applied ... .
Contact lenses should not be worn when working with this chemical.
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.
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:
NON-VOLATILE
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.
Cleanup Methods:
1) Ventilate area of spill. 2) Collect spilled material in most convenient
& safe manner & deposit in sealed containers for reclamation or for
disposal in secured sanitary landfill. Liquid containing sodium fluoroacetate
should be absorbed in vermiculite, dry sand, earth, or similar material.
Disposal Methods:
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant,
EPA hazardous waste number P058, must conform with USEPA regulations in storage,
transportation, treatment and disposal of waste.
A poor candidate for incineration.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr Time-Weighted Avg: 0.05 mg/cu m.
Skin Designation.
Vacated 1989 OSHA PEL TWA 0.05 mg/cu m; STEL 0.15 mg/cu m, skin designation,
is still enforced in some states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 0.05 mg/cu m, skin
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.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 0.05 mg/cu m, skin.
Recommended Exposure Limit: 15 Min Short-Term Exposure Limit: 0.15 mg/cu m,
skin.
Immediately Dangerous to Life or Health:
2.5 mg/cu m
Manufacturing/Use Information:
Major Uses:
FIELD RODENTICIDE
Predator elimination (coyotes), rodenticide.
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.
Tull Chemical Co, Inc, Inc, Hq, 130 Burton St, Oxford, AL 36203, (205) 831-1154
Methods of Manufacturing:
Condensing methyl chloroacetate with potassium fluoride and then converting
the fluoroester to the sodium salt with sodium hydroxide. Reacting cobalt hydrogen
fluoride and formaldehyde at high pressures to give fluoroacetic acid which
is converted by sodium hydroxide to sodium fluoroacetate.
Ethyl chloroacetate and potassium fluoride form ethyl fluoroacetate, which
is then treated with a methanol solution of sodium hydroxide.
Formulations/Preparations:
USUALLY MARKETED AS WATER SOLN CONTAINING 0.5% NIGROSINE AS BLACK WARNING
COLOR. 90% POWDER. USUALLY IN LOCKED BAIT BOXES.
Laboratory Methods:
Clinical Laboratory Methods:
GC METHOD INVOLVES AQUEOUS EXTRACTION OF STOMACH TISSUE OR STOMACH CONTENT,
ION EXCHANGE CHROMATOGRAPHY & DISTILLATION IN PRESENCE OF SULFURIC ACID.
FOR SAMPLES SUCH AS ANIMAL STOMACHS, THIS METHOD IS CONSIDERABLY MORE SENSITIVE,
MORE SPECIFIC, & LESS TIME-CONSUMING THAN PREVIOUSLY DESCRIBED METHODS.
A TYPICAL ANALYSIS REQUIRES 8 HR & TOXICANT LEVELS AS LOW AS 0.1-0.2 PPM
CAN BE DETECTED.
A sensitive high-pressure liq chromatographic method was developed for the
detection of sodium fluoroacetate in canine gastric content. Recovery was greater
than 95% for std sodium fluoroacetate & in the 70-90% range for spiked samples
(1-50 ppm).
ORIGINAL GLC METHOD WAS MODIFIED FOR QUANTITATIVE APPLICATION TO BIOLOGICAL
TISSUE, FOOD & BAIT SAMPLES. WITH MODIFICATIONS, RECOVERIES OF RADIOLABELED
1080 AVERAGED 85%.
Tissues of coyotes & magpies admin known dosages of 1080 were analyzed
for residues by an analytical method specifying gas chromatography & electron
capture detection. The avg coefficient of variation (CV) was 6% for quadruplicate
determinations in fresh tissues, 12-14% for samples stored at -10 deg C for
30-60 days & 24% for samples aged for 7 days at ambient temp. Residues of
1080 appeared to be relatively stable in tissues. Residue levels in muscle,
heart, kidney & intestine were comparable, slightly lower in liver &
much higher in stomach. Concn in muscle was related to admin dose.
Twenty-nine compounds (incl sodium fluoroacetate) were identified using gas
chromatography/mass spectroscopy. Most of the compounds were extracted from
biological materials. The usefulness of the method is stressed.
Analytic Laboratory Methods:
PRODUCT ANALYSIS: CONVERSION TO SODIUM FLUORIDE BY DIGESTION WITH METALLIC
SODIUM & PPTN AS LEAD CHLOROFLUORIDE; SODIUM FLUORIDE IS USUAL CONTAMINANT.
A high pressure liquid chromatography technique for the determination of sodium
fluoroacetate in poison baits for vertebrate pests is described. Recoveries
of 83 & 93% were obtained for duplicate samples of bait spiked with 100
& 1000 mg.
Hot aqueous alkaline conditions were used to defluorinate sodium fluoroacetate
with a mean efficiency of 98% & a coefficient of variation of 2%. The liberated
fluoride ion (F-) was detected by ion-selective electrode. These procedures
were used to analyze meat baits & Compound 1080 formulations.
NIOSH Method 7300: Air samples containing sodium are analyzed using Inductively
Coupled Argon Plasma - Atomic Emission Spectroscopy at a wavelength of 589.0.
An ashing step with concentrated nitric acid/concentrated perchloric acid (4:1
v/v) is necessary. This method has an instrumental detection limit of 10 ng/ml,
a sensitivity of 0.76, and a precision of 0.045 at 2.5 ug/filter. /Sodium/
Atomic absorption spectrophotometric method can be used to determine sodium
in water at wavelength of 589.0 nm. Flame gases are air-acetylene. This method
has a sensitivity of 0.005-0.2 mg/l. This method is applicable to determination
of 1-200 mg sodium/l in surface and saline waters, and domestic and industrial
wastes. /Sodium/
Method 325B. Flame Emission Photometric. Trace amounts of sodium can be determined
by flame emission photometry at a wavelengh of 589 nm. Detection limit is 100
ug/l. /Sodium/
EPA Method 200.7: An Inductively Coupled Plasma-Atomic Emission Spectrophotometric
method for the determination of dissolved, suspended or total elements in drinking
water, surface water, and domestic and industrial wastewaters, is described.
Sodium is analyzed at a wavelength of 588.995 nm and has an estimated detection
limit of 29 ug/l. /Sodium/
A gas chromatographic method was developed for the determination of sodium
fluoroacetate (Compound 1080 and 1080 poison) in baits and avian tissues. The
procedure involves extraction of 1080 with acetone/water (8:1) followed by derivatization
with pentafluorobenzyl bromide. Cleanup of the esterified extracts was carried
out using minicolumns containing Florisil and the eluates were subsequently
analyzed by electron capture gas chromatography. Bait samples were initially
screened by thin-layer chromatography and identity of derivatized extracts was
confirmed by gas chromatography/mass spectrometry.
Special References:
Special Reports:
USEPA; Chemical Profile: Sodium Fluoroacetate (1985). Aspects covered in this data sheet: chemical identity; exposure limits; physicochemical properties; fire and explosion hazards; reactivity; health hazards; uses; handling of spils or releases.
Synonyms and Identifiers:
Synonyms:
1080
**PEER REVIEWED**
ACETIC ACID, FLUORO-, SODIUM SALT
**PEER REVIEWED**
COMPD 1080
**PEER REVIEWED**
COMPOUND 1080
**PEER REVIEWED**
COMPOUND NO 1080
**PEER REVIEWED**
FLUORESSIGSAEURE (GERMAN)
**PEER REVIEWED**
FLUOROACETIC ACID, SODIUM SALT
**PEER REVIEWED**
FRATOL
**PEER REVIEWED**
FURATOL
**PEER REVIEWED**
MONOFLUORESSIGSAURES NATRIUM (GERMAN)
**PEER REVIEWED**
NATRIUMFLUORACETAAT (DUTCH)
**PEER REVIEWED**
NATRIUMFLUORACETAT (GERMAN)
**PEER REVIEWED**
RATBANE 1080
**PEER REVIEWED**
SMFA
**PEER REVIEWED**
SODIO, FLUORACETATO DI (ITALIAN)
**PEER REVIEWED**
SODIUM FLUOACETATE
**PEER REVIEWED**
SODIUM FLUOACETIC ACID
**PEER REVIEWED**
SODIUM FLUORACETATE
**PEER REVIEWED**
SODIUM FLUOROACETATE DE (FRENCH)
**PEER REVIEWED**
SODIUM MONOFLUOROACETATE
**PEER REVIEWED**
TEN-EIGHTY
**PEER REVIEWED**
TL 869
**PEER REVIEWED**
Yasoknock
**PEER REVIEWED**
Formulations/Preparations:
USUALLY MARKETED AS WATER SOLN CONTAINING 0.5% NIGROSINE AS BLACK WARNING
COLOR. 90% POWDER. USUALLY IN LOCKED BAIT BOXES.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 2629; SODIUM FLUOROACETATE
IMO 6.1; Sodium fluoroacetate
EPA Hazardous Waste Number:
P058; 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.
RTECS Number:
NIOSH/AH9100000