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Fluoroacetic Acid. TOXNET profile from Hazardous Substances Data Bank.
From: http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB
FLUOROACETIC ACID
CASRN: 144-49-0
For other data, click on the Table of Contents
Human Health Effects:
Human Toxicity Excerpts:
... ABLE TO "MIMIC" ACETIC ACID & ... REACT WITH COENZYME A & THEN
WITH OXALOACETIC ACID TO FORM FLUOROCITRIC ACID ... /WHICH/ ENTERS TRICARBOXYLIC
ACID CYCLE ... ISOMERIZATION OF CITRIC ACID TO ISOCITRIC ACID BY CATALYZING
ACTION OF ACONITASE CANNOT TAKE PLACE, CYCLE BECOMES BLOCKED, & CITRIC ACID
ACCUMULATES.
... /MAJOR EFFECTS/ INVOLVE CNS & CARDIOVASCULAR SYSTEM. SEVERE EPILEPTIFORM
CONVULSIONS ALTERNATE WITH COMA & DEPRESSION; DEATH MAY RESULT FROM ASPHYXIA
DURING CONVULSION OR FROM RESP FAILURE. MOST PROMINENT FEATURES ... ARE CARDIAC
IRREGULARITIES, NOTABLY VENTRICULAR FIBRILLATION & SUDDEN CARDIAC ARREST.
... INITIAL LATENT PERIOD ... UP TO 6 HR /IS/ CHARACTERIZED BY NAUSEA, VOMITING,
EXCESSIVE SALIVATION, NUMBNESS, TINGLING SENSATIONS, EPIGASTRIC PAIN & MENTAL
APPREHENSION; OTHER SIGNS & SYMPTOMS WHICH MAY DEVELOP SUBSEQUENTLY INCL
MUSCULAR TWITCHING, LOW BLOOD PRESSURE & BLURRED VISION.
SYMPTOMS OF POISONING IN A CHEMIST BEGAN AFTER LATENT PERIOD OF 0.5 TO SEVERAL
HR FOLLOWED RAPIDLY BY DEATH. CONVULSIONS & ARRHYTHMIA WERE COMMON TERMINAL
SIGNS. NO SPECIFIC CHANGES WERE NOTED AT POST MORTEM.
SHOULD NEVER BE USED WHERE INHALATION OR FOOD CONTAMINATION MAY OCCUR.
Skin, Eye and Respiratory Irritations:
... Irritant
Probable Routes of Human Exposure:
Occupational exposure to fluoroacetic acid can occur through dermal contact
and inhalation of dust(1).
Emergency Medical Treatment:
Emergency Medical Treatment:
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The following Overview, *** FLUOROACETIC ACID ***, 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 Fluoroacetic acid is the major metabolite of the series
of fluoro ester compounds. It is used as a
rodenticide. Little specific data were available
specifically about the toxicity of fluoroacetic acid;
its toxicity is expected to be similar to that of
FLUOROACETATE.
1. The following review discusses the toxicity and
treatment of poisoning with FLUOROACETATE.
2. Fluoroacetic acid is a colorless crystalline solid
which burns with a green flame and which is soluble in
water and alcohol. It can be irritating. It may be
absorbed following ingestion, inhalation, and dermal
contact.
o Clinical effects are usually seen within 1/2 hour of
exposure. Symptoms of 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. Severe effects such as coma, convulsions, and cardiac
arrhythmias may be delayed in onset as long as 20
hours. One death due to subacute fluoroacetate
poisoning has been reported.
2. The cardiac effects noted 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 levels of hepatic transaminases, and elevated
serum creatinine may occur in fluoroacetate poisoning.
o At least one case of severe poisoning with numbness and
tingling of the face, excessive salivation, blurred
vision, peripheral paresthesias, convulsions, and coma
has occurred from inhalation and dermal contact with
fluoroacetate. In general, fluoroacetate is absorbed
following ingestion and inhalation, but not through
intact skin.
o 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.
o Fluoroacetamide releases toxic and irritating fumes of
sodium oxide and fluoride when heated to decomposition.
Inhalation exposure to such fumes would be expected to
result in respiratory irritation with bronchospasm,
chemical pneumonitis, or noncardiogenic pulmonary
edema.
VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
o Respiratory depression, hypothermia, tachycardia, and
hypotension may occur.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Blurred vision, facial paresthesias, and
hypersalivation may be noted.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Tachycardia, ventricular fibrillation, and sudden onset
of asystole may occur.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Respiratory depression and cyanosis may develop. Death
may be due to hypoxia and respiratory depression during
seizures.
o Fluoroacetamide releases toxic and irritating fumes of
sodium oxide and fluoride when heated to decomposition.
Inhalation exposure to such fumes would be expected to
result in respiratory irritation with bronchospasm,
chemical pneumonitis, or noncardiogenic pulmonary
edema.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Apprehension, diaphoresis, disorientation, agitation,
paresthesias, muscle twitching, hyperactive behavior,
tingling, coma, and convulsions may develop. Status
epilepticus has been described.
o Neurologic sequelae have been noted following acute
poisoning, such as 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.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Nausea, vomiting, hypersalivation, abdominal or
epigastric pain, and diarrhea may be seen.
HEPATIC
0.2.9.1 ACUTE EXPOSURE
o Elevations of hepatic transaminases may be noted.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Acute renal failure may be a sequelae of acute
poisoning. Elevated levels of serum creatinine and
uric acid may be noted.
ACID-BASE
0.2.11.1 ACUTE EXPOSURE
o Metabolic acidosis may be seen.
FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
o Hypocalcemia may occur.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Muscle twitching may be an early effect.
METABOLISM
0.2.17.1 ACUTE EXPOSURE
o 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.
o Elevated blood glucose levels may be seen in
fluoroacetate poisoning.
REPRODUCTIVE HAZARDS
o At the time of this review, no data were available to
assess the teratogenic potential of this agent.
o In mice, oral administration of fluoroacetamide resulted
in a prolonged pregnancy and the young suffered from
cyanosis, respiratory distress, reduced growth, and
decreased survival.
o Fluoroacetamide has caused testicular degeneration in
rats.
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 calcium, magnesium, and potassium
concentrations.
o This agent may cause hepatotoxicity. Monitor liver
function tests for patients with significant exposure.
o This agent may cause nephrotoxicity. Monitor renal
function tests and urinalysis for patients with
significant exposure.
o BLOOD GASES
1. Monitor arterial blood gases for patients with
significant exposure.
o Monitor EKG and vital signs frequently.
o If respiratory tract irritation is present, monitor chest
x-ray.
|
| 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 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.
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 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.
o MONITOR ECG AND VITAL SIGNS - frequently.
o CALCIUM - Calcium gluconate or calcium chloride should
be administered parenterally in patients with documented
hypocalcemia.
o HYPOTENSION -
1. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid,
place in Trendelenburg position. If hypotension
persists, administer dopamine (5 to 20 mcg/kg/min) or
norepinephrine (0.1 to 0.2 mcg/kg/min), titrate to
desired response.
o 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.
o 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 20
hours in a controlled setting.
o See treatment of oral exposure in the main body of this
document for complete information.
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 SYSTEMIC ABSORPTION -
1. Systemic poisoning has occurred following inhalation
exposure to fluoroacetate (Ellenhorn & Barceloux,
1988).
o 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.
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 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.
o MONITOR ECG AND VITAL SIGNS - frequently.
o CALCIUM - Calcium gluconate or calcium chloride should
be administered parenterally in patients with documented
hypocalcemia.
o HYPOTENSION -
1. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid,
place in Trendelenburg position. If hypotension
persists, administer dopamine (5 to 20 mcg/kg/min) or
norepinephrine (0.1 to 0.2 mcg/kg/min), titrate to
desired response.
o 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.
o 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 20
hours in a controlled setting.
o See treatment of inhalation exposure in the main body of
this document for complete information.
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 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.
DERMAL EXPOSURE
o DECONTAMINATION: Remove contaminated clothing and
jewelry. Wash the skin, including hair and nails,
vigorously; do repeated soap washings. Discard
contaminated clothing.
o SYSTEMIC ABSORPTION -
1. There is little evidence that fluoroacetate can be
absorbed systemically in toxic amounts through intact
skin (Ellenhorn & Barceloux, 1988). 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: |
o A milligram of pure compound is probably enough to cause
severe toxicity, and less may be toxic. Extrapolation of
experimental animal toxicity data to humans indicates that
a dose of 2 to 10 mg/kg may be fatal.
|
Antidote and Emergency Treatment:
1. Induce vomiting immediately if possible. 2. Gastric lavage with tap water
unless convulsions (or imminent convulsions) make this impractical. 3. Instill
into the stomach sodium or magnesium sulfate in water (15 to 30 g). 4. Although
the clinical efficacy of monoacetin (glyceral monoacetate) is not established,
it probably should be administered if available. The recommended dose is 0.5
ml/kg of undiluted fluid intramuscularly every half hour for several hours and
then at a reduced level for the last 12 hours. In the same dose monoacetin may
also be given intravenously after dilution with 5 parts of sterile isotonic
saline. No preparation of the pharmaceutical market. The usual commercial fluid
has large amounts of free glycerine (due to hydrolysis favored by heat and exposure
to sunlight), and the assay is seldom better than 70%. The exigency of an overt
poisoning, however, probably warrants the use of even nonsterile commercial
material. Irrespective of impurities, injections may be expected to produce
some sedation and vasodilatation. The site of intramuscular injection must be
varied because of local pain and edema. In the event that parenteral administration
is not feasible, the patient may drink a mixture of 100 ml of monoacetin in
500 ml of water. Repeat after 1 hour. /Fluoroacetate/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
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 & HAMSTER SHOW BOTH CARDIAC & CNS RESPONSES. /FLUOROACETATES/
ADMIN OF 1.0-1.5 MG/KG OF FLUOROACETATE DECR DENTIN FORMATION & ENAMEL
CALCIFICATION IN RATS. BLOOD CITRATE LEVEL INCR MORE THAN 2.4 TIME CONTROL LEVEL
AFTER 6 HR. SUCCESSIVE ADMIN INCR CITRATE CONTENT (61.5%) & PHOSPHORUS (26.6%)
IN DENTIN. /FLUOROACETATE/
HYPOTHERMIC ACTIVITY OF FLUOROACETIC ACID 1.5-60 MG/KG, IP IN RATS WAS CLOSELY
RELATED TO ITS LETHAL EFFECT. RATS WERE MORE SENSITIVE THAN MICE WITH THE LOWER
ACUTE IP LD50 VALUES OF 3-6 MG/KG.
6 MG/KG IP TO RATS PROGRESSIVELY DEPLETED ATP CONTENT, AMP & ADP LEVELS
INCR DURING INITIAL 2 HR & LATER DECLINED, INTRACELLULAR INORG PHOSPHATE
INCR CONTINUOUSLY, CITRATE LEVELS REACHED MAX AT 6 HR & REMAINED. CITRIC
ACID CYCLE NOT REACTIVATED UNDER PRESENT CONDITIONS.
ANESTHETIZED RATS UNDER MANNITOL DIURESIS WERE GIVEN IP MFA & SOME ACID-BASE
STATUS PARAMETERS WERE DETERMINED. URINARY PH & PLASMA CARBON DIOXIDE DID
NOT CHANGE AFTER ADMIN, WHEREAS URINARY FLOW RATE INCR. IT DECR H+ NET EXCRETION
& AMMONIA EXCRETION.
CITRIC ACID LEVEL IN BLOOD, MYOCARDIUM, SKELETAL MUSCLE, BRAIN
& LIVER OF RATS REACHED MAX LEVELS AT 30 MIN, 1 HR, 2 HR, 3 HR & 5 HR,
RESPECTIVELY, AFTER POISONING WITH FLUOROACETATE (5 MG/KG, IP). /FLUOROACETATE/
4.5-15 UG/KG/MIN FLUOROACETATE ADMIN INTO DOGS LEFT RENAL ARTERY FOR 90-240
MIN SHARPLY INCR UNILATERAL DIURESIS, WITH INCR EXCRETION OF SODIUM, POTASSIUM,
CALCIUM, CHLORIDES & INORG PHOSPHATES DUE TO DECR REABSORPTION. SIMILAR
CHANGES OBSERVED AFTER 37-936 UG/KG IV ADMIN. /FLUOROACETATE/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
FLUOROACETIC ACID HAS BEEN SHOWN TO BE CONVERTED
IN VIVO INTO FLUOROCITRATE.
IN RATS, MITOCHONDRIA FROM KIDNEY CORTEX ACTIVELY PRODUCED FLUOROCITRATE MORE
THAN 700% ABOVE CONTROL. 2 PATHWAYS OF FLUOROCITRATE ACTIVATION IDENTIFIED.
1 ASSOC WITH PYRUVATE METAB & NOT DEPENDENT ON OXIDATIVE PHOSPHORYLATION
ENERGY; 2ND ASSOC WITH ACETATE METAB & IS ATP DEPENDENT.
Absorption, Distribution & Excretion:
... (14)CARBON-FLUOROACETIC ACID WAS SLOWLY EXCRETED AFTER IP ADMIN TO RATS.
ONLY 1% WAS EXCRETED AS (14)CARBON-CARBON DIOXIDE AFTER 4 HR ... AT THAT TIME,
LESS THAN 1% OF (14)CARBON HAD BEEN EXCRETED IN URINE, & 60% WAS PRESENT
IN CARCASS, 12% IN LIVER, 10% IN GI TRACT, 4% IN LUNG, 3% IN KIDNEYS, &
2% IN BRAIN. AFTER 4 DAYS ... 32% ...
EXCRETED IN URINE, 3% AS (14)CARBON-CARBON DIOXIDE & MUCH OF REMAINDER HAD
PRESUMABLY BEEN RETAINED BY INCORPORATION INTO TISSUES /FROM IP ADMIN TO RATS/.
URINARY EXCRETION OF (14)CARBON ON FOURTH DAY WAS SLIGHT (0.3%).
FLUOROACETIC ACID WAS FOUND IN BRAIN
TISSUES FOR ONLY 1 MIN AFTER INJECTION EVEN THEN IT WAS LESS THAN 15% OF AMT
INJECTED.
Mechanism of Action:
... ABLE TO "MIMIC" ACETIC ACID & ... REACT WITH COENZYME A & THEN
WITH OXALOACETIC ACID TO FORM FLUOROCITRIC ACID ... /WHICH/ ENTERS TRICARBOXYLIC
ACID CYCLE ... ISOMERIZATION OF CITRIC ACID TO ISOCITRIC ACID BY CATALYZING
ACTION OF ACONITASE CANNOT TAKE PLACE, CYCLE BECOMES BLOCKED, & CITRIC ACID
ACCUMULATES.
Pharmacology:
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Fluoroacetic acid occurs naturally as a constituent of many poisonous plants.
It can be formed in nature through biochemical oxidation processes (such as
hydrolysis and beta-oxidation) from substances such as straight-chained, even-numbered
fluoro alcohols, alkanoic acids, esters and amides. If released to the atmosphere,
fluoroacetic acid is expected to exist almost entirely in the vapor-phase where
it will degrade slowly by reaction with photochemically produced hydroxyl radicals
(estimated half-life of 162 days). Physical removal from air can occur via rainfall
and other wet deposition processes. If released to soil or water, fluoroacetic
acid will probably degrade via biodegradation. Fluoroacetic acid will exist
predominantly in the ionized form in water and moist soil. The sorption characteristics
of ionized fluoroacetic acid are not known. Occupational exposure to fluoroacetic
acid can occur through dermal contact and inhalation of dust. (SRC)
Probable Routes of Human Exposure:
Occupational exposure to fluoroacetic acid can occur through dermal contact
and inhalation of dust(1).
Natural Pollution Sources:
Fluoroacetic acid has been found as a toxic constituent of the poisonous South
African plant Dichapetalum cymosum, which is better known as gifblaar(1,2);
at least two dozen other poisonous plant species have also been found to contain
fluoroacetic acid(2). Fluoroacetic acid can be formed through biochemical oxidation
processes (such as hydrolysis and beta-oxidation) from substances such as straight-chained,
even-numbered fluoro alcohols, alkanoic acid, esters and amides(3,4).
Environmental Fate:
TERRESTRIAL FATE: The dominant environmental fate process for fluoroacetic
acid in soil is probably biodegradation. The results of one bioassay screening
study have shown that the toxicity of fluoroacetic acid (sodium salt) degrades
in non-sterilized garden soil, but not in sterilized control soil(1). Fluoroacetic
acid has a pKa of 2.586 at 25 deg C(2) and will therefore exist predominantly
in the ionized form in moist soil. The soil sorption properties of ionized fluoroacetic
acid can not be predicted without experimental data(SRC). Non-ionized fluoroacetic
acid can be expected to leach readily(SRC).
AQUATIC FATE: The dominant environmental fate process for fluoroacetic acid
in water is probably biodegradation. The results of one bioassay screening study
have shown that the toxicity of fluoroacetic acid (sodium salt) degrades in
non-sterilized garden soil, but not in sterilized control soil(1). Fluoroacetic
acid has a pKa of 2.586 at 25 deg C(2) and will therefore exist predominatly
in the ionized form in environmental waters. The sediment sorption properties
of ionized fluoroacetic acid can not be predicted without experimental data(SRC).
Volatilization, bioconcentration and aqueous hydrolysis are not expected to
be important environmentally(SRC).
ATMOSPHERIC FATE: Based upon an estimated vapor pressure of 1.9 mm Hg at 25
deg C(1), fluoroacetic acid is expected to exist almost entirely in the vapor-phase
in the ambient atmosphere(2,SRC). It is degraded slowly in an average ambient
atmosphere by reaction with photochemically produced hydroxyl radicals at an
estimated half-life rate of about 162 days(3,SRC). Based upon an estimated water
solubility of 1.32X10+5 mg/L at 25 deg C(1), physical removal from air via wet
deposition is likely to occur(SRC).
Environmental Biodegradation:
The toxicity of fluoroacetic acid (sodium salt) applied to a garden soil was
examined via bioassay using Aphis fabae(1); at 10 ppm, toxicity was detected
and lasted for 2 weeks; in sterilized garden soil, toxicity persisted for the
full 17 week incubation period(1); at 50 ppm, toxicity was detected for 9-11
weeks; again in sterilized soil, toxicity persisted for the full 17 week incubation
period(1).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction of fluoroacetic acid with photochemically
produced hydroxyl radicals has been estimated to be 9.91X10-14 cu cm/molecule-sec
at 25 deg C which corresponds to an atmospheric half-life of about 162 days
at an atmospheric concn of 5X10+5 hydroxyl radicals per cu cm(1,SRC). The neutral,
aqueous hydrolysis rate constant of fluoroacetic acid was experimentally determined
to be <1.7X10-6/hr at pH 7 which corresponds to a half-life of >47 years(2).
Environmental Bioconcentration:
Based upon an estimated log Koc of -0.061(1), the BCF for fluoroacetic acid
can be estimated to be 0.5 from a recommended regression-derived equation(2,SRC).
This estimated BCF indicates that bioconcentration in aquatic organisms is not
important environmentally(SRC).
Soil Adsorption/Mobility:
Based upon an pKa of 2.586 of 25 deg C(1), fluoroacetic acid will exist predominatly
in the ionized form in environmental waters(SRC); the sorption of ionized fluoroacetic
acid in soil can not be predicted without experimental data(SRC). Based upon
an estimated log Kow of -0.061(2), the Koc for non-ionized fluoroacetic acid
can be estimated to be 22 from a recommended regression-derived equation(3,SRC);
this estimated Koc suggests that fluoroacetic acid is very highly mobile in
soil(4).
Volatilization from Water/Soil:
The Henry's Law constant for fluoroacetic acid can be estimated to be 1.09X10-6
atm-cu m/mole using a structure estimation method(1,SRC). This value of Henry's
Law constant indicates slow volatilization from water(2). Based on this Henry's
Law constant, the volatilization half-life from a model river (1 m deep flowing
1 m/sec with a wind velocity of 3 m/sec) can be estimated to be about 31 days(2,SRC).
Volatilization half-life from a model environmental pond can be estimated to
be about 322 days(3,SRC).
Plant Concentrations:
Fluoroacetic acid has been found as a toxic constituent of the poisonous South
African plant Dichapetalus cymosum, which is better known as gifblaar(1,2);
at least two dozen other poisonous plant species have also been found to contain
fluoroacetic acid(2).
Environmental Standards & Regulations:
CERCLA Reportable Quantities:
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. Fluoroacetic acid 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.
Chemical/Physical Properties:
Molecular Formula:
C2-H3-F-O2
Molecular Weight:
78.04
Color/Form:
NEEDLES
COLORLESS CRYSTALS
Odor:
Odorless powder
Boiling Point:
165 DEG C AT 760 MM HG
Melting Point:
35.2 DEG C
Density/Specific Gravity:
1.3693 AT 36 DEG C
Dissociation Constants:
PKA: 2.66
Octanol/Water Partition Coefficient:
log Kow= -0.061 (est)
Solubilities:
SOL IN ... ALCOHOL
1.32X10+5 mg/l in water at 25 deg C (est)
Spectral Properties:
IR: 17442 (Sadtler Research Laboratories Prism Collection)
MASS: 98 (Atlas of Mass Spectral Data, John Wiley & Sons, New York)
Vapor Pressure:
1.9 mm Hg at 25 deg C (est)
Other Chemical/Physical Properties:
BURNS WITH A GREEN FLAME
Henry's Law constant= 1.09X10-6 (est).
Chemical Safety & Handling:
DOT Emergency Guidelines:
Fire or explosion: Combustible material: may burn but does not ignite readily.
Substance will react with water (some violently) releasing flammable, toxic
or corrosive gases and runoff. When heated, vapors may form explosive mixtures
with air: indoors, outdoors, and sewers explosion hazards. Most vapors are heavier
than air. They will spread along ground and collect in low or confined areas
(sewers, basements, tanks). Vapors may travel to source of ignition and flash
back. Contact with metals may evolve flammable hydrogen gas. Containers may
explode when heated or if contaminated with water.
Health: TOXIC; inhalation, ingestion or contact (skin, eyes) with vapors,
dusts or substance may cause severe injury, burns, or death. Reaction with water
or moist air will release toxic, corrosive or flammable gases. Reaction with
water may generate much heat which will increase the concentration of fumes
in the air. Fire will produce irritating, corrosive and/or toxic gases. Runoff
from fire control or dilution water may be corrosive and/or toxic and cause
pollution.
Public safety: CALL Emergency Response Telephone Number on Shipping Paper
first. 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 50 to 100 meters (160 to 330 feet) in all directions. Keep unauthorized
personnel away. Stay upwind. Keep out of low areas. Ventilate enclosed 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: Note: Most foams will react with the material and release corrosive/toxic
gases. Small fires: CO2, dry chemical, dry sand, alcohol-resistant foam. Large
fires: Water spray, fog or alcohol-resistant foam. FOR CHLOROSILANES, DO NOT
USE WATER; use AFFF alcohol-resistant medium expansion foam. Move containers
from fire area if you can do it without risk. 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.
Spill or leak: 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 damaged containers or spilled material unless wearing
appropriate protective clothing. Stop leak if you can do it without risk. A
vapor suppressing foam may be used to reduce vapors. FOR CHLOROSILANES, use
AFFF alcohol-resistant medium expansion foam to reduce vapors. DO NOT GET WATER
on spilled substance or inside containers. Use water spray to reduce vapors
or divert vapor cloud drift. Prevent entry into waterways, sewers, basements
or confined areas. Small spills: Cover with DRY earth, DRY sand, or other non-combustible
material followed with plastic sheet to minimize spreading or contact with rain.
Use clean non-sparking tools to collect material and place it into loosely covered
plastic containers for later disposal.
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:
... Irritant
Hazardous Decomposition:
WHEN HEATED TO DECOMP, IT EMITS HIGHLY TOXIC FUMES OF /HYDROGEN FLUORIDE/.
Preventive Measures:
ITS MFR & USE REQUIRE EXTREME PRECAUTION & SPECIAL TRAINING.
Stability/Shelf Life:
STABLE
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:
Do not handle in areas where risk of inhalation and/or food contamination
may be possible. Adequate ventilation. Wear rubber gloves, full protective shield,
and all-purpose canister mask. Avoid contact with alkaline metals.
Disposal Methods:
Pour on sufficient sodium bicarbonate. After mixing, transfer into a drum
and fill with water for drainage after 24 hours.
Occupational Exposure Standards:
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 2.5 mg/cu m /Fluorides, as F/
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. /Fluorides, as F/
BEI (Biological Exposure Index): Fluoride in urine prior to shift is 3 mg/g
creatinine. Fluoride in urine at the end of the shift is 10 mg/g creatinine.
The determinant is usually present in a significant amt in biological specimens
collected from subjects who have not been occupationally exposed. Such background
levels are incl in the BEI value. The determinant is nonspecific, since it is
observed after exposure to some other chemicals. These nonspecific tests are
preferred because they are easy to use and usually offer a better correlation
with exposure than specific tests. In such instances, a BEI for a specific,
less quantitative biological determinant is recommended as a confirmatory test.
(1990 adoption) /Fluorides/
A4. A4= Not classifiable as a human carcinogen. /Fluorides, as F/
Manufacturing/Use Information:
Major Uses:
Rodenticide /Fluoroacetic acid, sodium salt/
Methods of Manufacturing:
...FROM METHYL IODOACETATE BY HEATING WITH SILVER FLUORIDE OR MERCUROUS FLUORIDE
OR FROM METHYL CHLOROACETATE BY HEATING WITH POTASSIUM FLUORIDE, FOLLOWED BY
SAPONIFICATION OF METHYL ESTER WITH BARYTA.
Laboratory Methods:
Clinical Laboratory Methods:
AN ANALYTICAL METHOD IS DESCRIBED FOR DETECTION OF SODIUM FLUOROACETATE RESIDUE
IN 1-10 G TISSUE & MEASURED BY ELECTRON CAPTURE GLC.
Analytic Laboratory Methods:
QUALITATIVE TEST FOR MONOFLUOROACETIC ACID AS PESTICIDE RESIDUE BY TITRATION
METHOD.
DETERMINATION OF SODIUM FLUOROACETATE (CMPD 1080) IN POISON BAITS BY HIGH
PERFORMANCE LIQUID CHROMATOGRAPHY.
NIOSH Method: S301. Analyte: Fluoroacetate ion. Matrix: Air . Procedure: Ion
chromatography/electrolytic conductivity detection. This method has a detection
limit of 20 ng and sensitivity of 6 umho/cm/ug. The working range for a precision
better than 0.02-0.13 mg/cu m RSD/CV is 0.060. Interference: No specific interferences.
Sampling Procedures:
NIOSH Method: S301. Analyte: Fluoroacetate ion. Matrix: Air. Procedure: Filter
collection, deionized water extraction. Flow Rate: 1.5-2.0 l/min. Sample Size:
480 liters.
Special References:
Special Reports:
BUFFA P ET AL; FLUORIDE 6 (4): 224 (1973). REVIEW OF THE METABOLIC EFFECTS
OF FLUOROACETATE POISONING IN ANIMALS. (53 REFERENCES).
EGYED MN; FLUORIDE 6 (4): 215 (1973). A REVIEW OF THE CLINICAL, PATHOLOGICAL,
DIAGNOSTIC & THERAPEUTIC ASPECTS OF FLUOROACETATE RESEARCH IN ANIMALS. (37
REFERENCES).
PETERS R; METABOLIC ASPECTS OF FLUOROACETATE ESP RELATED TO FLUOROCITRATE;
CARBON-FLUORINE CMPD: CHEM, BIOCHEM BIOL ACTIV, SYMP 55 (1972). A REVIEW WITH
46 REFERENCES. TOXICITY & BEHAVIOR IN ANIMALS, PLANTS & FORMATION &
METAB OF FLUOROACETATE, FLUOROCITRATE & FLUOROACETONE ARE DISCUSSED.
GRIBBLE GW; J CHEM EDUC 50 (7): 460 (1973). A REVIEW WITH 25 REFERENCES ON PREPN, TOXICITY & MECHANISM OF ACTION OF FLUOROACETIC ACID.
Synonyms and Identifiers:
Related HSDB Records:
Synonyms:
ACETIC ACID, FLUORO-
**PEER REVIEWED**
ACIDE-MONOFLUORACETIQUE (FRENCH)
**PEER REVIEWED**
ACIDO MONOFLUORACETIO (ITALIAN)
**PEER REVIEWED**
CYMONIC ACID
**PEER REVIEWED**
FAA
**PEER REVIEWED**
ALPHA-FLUOROACETIC ACID
**PEER REVIEWED**
2-FLUOROACETIC ACID
**PEER REVIEWED**
FLUOROETHANOIC ACID
**PEER REVIEWED**
GIFBLAAR POISON
**PEER REVIEWED**
HFA
**PEER REVIEWED**
MFA
**PEER REVIEWED**
MONOFLUORAZIJNZUUR (DUTCH)
**PEER REVIEWED**
MONOFLUORESSIGSAURE (GERMAN)
**PEER REVIEWED**
MONOFLUOROACETATE
**PEER REVIEWED**
MONOFLUOROACETIC ACID
**PEER REVIEWED**
Shipping Name/ Number DOT/UN/NA/IMO:
UN 2642; Fluoroacetic acid
IMO 6.1; Fluoroacetic acid
RTECS Number:
NIOSH/AH5950000
Administrative Information:
Hazardous Substances Databank Number: 2082
Last Revision Date: 20010809
Last Review Date: Reviewed by SRP on 08/07/1991
Update History:
Complete Update on 08/09/2001, 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 11/12/1998, 1 field added/edited/deleted.
Complete Update on 10/20/1998, 1 field added/edited/deleted.
Complete Update on 09/11/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 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, 2 fields added/edited/deleted.
Complete Update on 12/03/1996, 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 05/10/1996, 1 field added/edited/deleted.
Complete Update on 01/23/1996, 1 field added/edited/deleted.
Complete Update on 06/12/1995, 1 field added/edited/deleted.
Complete Update on 12/28/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Field update on 12/24/1992, 1 field added/edited/deleted.
Complete Update on 02/24/1992, 50 fields added/edited/deleted.
Field Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 10/04/1990, 3 fields added/edited/deleted.
Field Update on 05/05/1989, 1 field added/edited/deleted.
Complete Update on 10/03/1986