144-49-0O=C(O)CFQEWYKACRFQMRMB-UHFFFAOYSA-NFluoroacetic acid appears as a colorless crystalline solid. May be toxic by ingestion. Used to make other chemicals.
144-49-0DTXSID0041981CHEMBL509273CHEBI:307751.3693 at 97 °F (EPA, 1998) - Denser than water; will sink
1.3693 g/cu cm at 36 °C
Relative density (water = 1): 1.37
1.393 @ 36°C
Needles
Colorless needles
Colorless crystal
Miscible with water (1.0X10+6 mg/L) at 25 °C
Soluble in ethanol
Solubility in water: freely soluble
329 °F at 760 mmHg (EPA, 1998)
168 °C
165 °C
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Danger
H300: Fatal if swallowed [Danger Acute toxicity, oral]
P264, P270, P273, P301+P316, P321, P330, P391, P405, and P501 (click each P-code to see the statement)
Danger
H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]
P260, P264, P270, P273, P280, P301+P316, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P330, P363, P391, P405, and P501 (click each P-code to see the statement)
Chemical: Acetic acid, fluoro-
Acetic acid, fluoro-: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
When heated to decomposition, it emits highly toxic fumes of fluorine containing compounds. Some of these materials may burn but none ignite readily. These materials may ignite combustibles (wood, paper, oil, etc.). (EPA, 1998)
· Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.
Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.
This material is very toxic; ingestion of small quantities may cause death. (EPA, 1998)
· TOXIC and/or CORROSIVE; inhalation, ingestion or skin contact with material may cause severe injury or death.
The mechanism of action involves the incorporation of the fluoroacetate into fluoroacetyl-coenzyme A, which condenses with oxaloacetate to form fluorocitrate, which inhibits the enzyme aconitase and prevents the conversion of citrate to isocitrate in the tricarboxylic (Krebs) cycle. Inhibition of this system by fluorocitrate results in reduced glucose metabolism and cellular respiration and affects tissue energy stores. /Fluoroacetic acid and derivatives/
/Fluoroacetic acid is/ metabolically converted to fluorocitrate which inhibits the tricarboxylic acid cycle resulting in cellular hypoxia.
In rats, mitochondria from kidney cortex actively produced fluorocitrate more than 700% above control. Two pathways of fluorocitrate activation identified. 1 associated with pyruvate metabolism and not dependent on oxidative phosphorylation energy /and another/ associated with acetate metabolism and is ATP dependent.
Fluoroacetate administered ip to rats and mice is defluorinated to give fluoride ion evident in urine and kidney by (19)F NMR. The use of 2-(13)C-, 1,2-(13)C-, and 1,2-(14)C-fluoroacetate, ... reveals a complex mixture of urinary metabolites including an S-(carboxymethyl) conjugate complex in rats and mice and sulfoxidation products... in rats. ...Bile, following treatment with 2-(13)C- fluoroacetate, shows the presence of S-(carboxymethyl)glutathione or a related conjugate and an O-conjugate of fluoroacetate. 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/ fluoroacetate 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 urinary 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 fluoroacetate and its progenitors, fluoroacetamide and fluoroethanol, is therefore attributable to both conjugation of fluoroacetate 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.
불러오는 중…
95.4 °F (EPA, 1998)
35.2 °C
35.2 °C
35.3 °C
12.8 [mmHg]
1.27 mm Hg at 25 °C
Vapor pressure, Pa at 20 °C: 534
1.9 [mm Hg] @25 °C
Mobile liquid, fp: -32 °C. Practically odorless or faint, fruit-like odor. Specific gravity: 1.1744 at 20 dg C/4 °C; 1.1613 at 15 °C/4 °C. Index of refraction: 1.3678 at 20 °C/D. Soluble in water; slightly soluble in petroleum ether /Fluoroacetic acid, methyl ester/
A corrosive substance that can cause injury to the skin, eyes, and respiratory tract; Can be absorbed through skin; Adverse effects on the cardiovascular system, CNS, and kidneys resulting in cardiac and renal failure; [ICSC] Emergency treatment: Sodium fluoroacetate. [HSDB] See Sodium fluoroacetate.
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 Cmpds: 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.
FLUOROACETIC ACID is a halogenated carboxylic acid derivative. Carboxylic acids donate hydrogen ions if a base is present to accept them. They react in this way with all bases, both organic (for example, the amines) and inorganic. Their reactions with bases, called "neutralizations", are accompanied by the evolution of substantial amounts of heat. Neutralization between an acid and a base produces water plus a salt. Carboxylic acids with six or fewer carbon atoms are freely or moderately soluble in water; those with more than six carbons are slightly soluble in water. Soluble carboxylic acid dissociate to an extent in water to yield hydrogen ions. The pH of solutions of carboxylic acids is therefore less than 7.0. Many insoluble carboxylic acids react rapidly with aqueous solutions containing a chemical base and dissolve as the neutralization generates a soluble salt. Carboxylic acids in aqueous solution and liquid or molten carboxylic acids can react with active metals to form gaseous hydrogen and a metal salt. Such reactions occur in principle for solid carboxylic acids as well, but are slow if the solid acid remains dry. Even "insoluble" carboxylic acids may absorb enough water from the air and dissolve sufficiently in it to corrode or dissolve iron, steel, and aluminum parts and containers. Carboxylic acids, like other acids, react with cyanide salts to generate gaseous hydrogen cyanide. The reaction is slower for dry, solid carboxylic acids. Insoluble carboxylic acids react with solutions of cyanides to cause the release of gaseous hydrogen cyanide. Flammable and/or toxic gases and heat are generated by the reaction of carboxylic acids with diazo compounds, dithiocarbamates, isocyanates, mercaptans, nitrides, and sulfides. Carboxylic acids, especially in aqueous solution, also react with sulfites, nitrites, thiosulfates (to give H2S and SO3), dithionites (SO2), to generate flammable and/or toxic gases and heat. Their reaction with carbonates and bicarbonates generates a harmless gas (carbon dioxide) but still heat. Like other organic compounds, carboxylic acids can be oxidized by strong oxidizing agents and reduced by strong reducing agents. These reactions generate heat. A wide variety of products is possible. Like other acids, carboxylic acids may initiate polymerization reactions; like other acids, they often catalyze (increase the rate of) chemical reactions.
Stay upwind; keep out of low areas. Wear self-contained, positive pressure breathing apparatus and full protective clothing. Move container from fire area. Cool containers that are exposed to flames with water from the side until well after fire is out.
In case of fire in the surroundings, use appropriate extinguishing media.
Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer immediately for medical attention.
Wear protective gloves when administering first aid. Remove contaminated clothes. Rinse skin with plenty of water or shower for at least 15 minutes. Refer immediately for medical attention.
Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer immediately for medical attention.
Rinse mouth. Do NOT induce vomiting. Refer immediately for medical attention.
· CALL 911. Then 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.
· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.
Warning: Effects usually appear within 30 minutes of exposure but may be delayed as long as 20 hours. Caution is advised. Vital signs should be monitored closely.
General First Aid:
Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.
Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.
If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use foam, dry chemical, or carbon dioxide. Keep run-off water out of sewers and water sources.
ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.
Evacuate danger area! Consult an expert! Personal protection: complete protective clothing including self-contained breathing apparatus. Do NOT wash away into sewer. Sweep spilled substance into covered sealable containers. Carefully collect remainder. Then store and dispose of according to local regulations.
SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.
Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.
Pour on sufficient sodium bicarbonate. After mixing, transfer into a drum and fill with water for drainage after 24 hours.
Evacuate danger area! Consult an expert! Personal protection: complete protective clothing including self-contained breathing apparatus. Do NOT wash away into sewer. Sweep spilled substance into covered sealable containers. Carefully collect remainder. Then store and dispose of according to local regulations.
... In cats intravenously injected with fluoroacetate at 0.03 mmol/kg the ionized calcium level in blood fell by an average of 27.2%, 40 minutes after injection. There was a corresponding prolongation of the QT interval of the electrocardiogram, and treatment with CaCl2 significantly prolonged the life of the treated animals as compared with unmedicated positive controls.
Fluoroacetic acid is corrosive to the eyes, the skin and the respiratory tract. It may cause effects on the cardiovascular system, central nervous system, kidneys, resulting in impaired functions including cardiac and renal failure. Exposure may result in death. (L1685) (L138)
EC50; Species: Chlorococcales (Green Algae Order); Conditions: freshwater, static; Concentration: 24 mg/L for 24 hr; Effect: physiology, assimilation efficiency /formulation/
LC50; Species: Daphnia magna (Water Flea) age < or =24 hr; Conditions: freshwater, static, 20-22 °C, pH 7.6-7.7; Concentration: 230 mg/L for 24 hr /formulation/
LD50; Species: Oncorhynchus mykiss (Rainbow Trout) weight 100 g; Conditions: freshwater, ip injection; Concentration: 39 mg/kg bw
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.4(SRC), determined from a structure estimation method(2), indicates that fluoroacetic acid is expected to have very high mobility in soil(SRC). A pKa of 2.59(3) indicates fluoroacetic acid will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). The potential for volatilization of fluoroacetic acid from dry soil surfaces may exist(SRC) based upon an estimated vapor pressure of 1.3 mm Hg(SRC), determined from a fragment constant method(2). Fluoracetic acid has been identified as potentially removed by biological sewage treatment provided suitable acclimatization can be achieved(5), suggesting that the compound may be subject to biodegradation in terrestrial systems(SRC).
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.4(SRC), determined from a structure estimation method(2), indicates that fluoroacetic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 2.59(3) indicates fluoroacetic acid will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process. According to a classification scheme(4), an estimated BCF of 3(SRC), from an estimated log Kow of 0.03(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Fluoracetic acid has been identified as potentially removed by biological sewage treatment provided suitable acclimatization can be achieved(5), suggesting that the compound may be subject to biodegradation in aquatic systems(SRC).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), fluoroacetic acid, which has an estimated vapor pressure of 1.3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase fluoroacetic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 27 days(SRC), calculated from its rate constant of 5.8X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Fluoroacetic acid does not contain chromophores that absorb at wavelengths >290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).
The substance can be absorbed into the body by inhalation, through the skin and by ingestion.
Inhalation (L1685)
IDENTIFICATION AND USE: Fluoroacetic acid is a solid. It was used formerly in the production of the highly toxic rodenticide and general mammalian pest control agent sodium fluoroacetic acid. HUMAN STUDIES: Estimates of the lethal dose of fluoroacetate in humans lie in the range of 2 to 10 mg/kg. In the 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. In another case, symptoms of poisoning in a chemist began after latent period of 0.5 to several hr followed rapidly by death. Convulsions and arrhythmia were common terminal signs. No specific changes were noted at post mortem. Fluoroacetic ion alone is non-toxic but in vivo forms fluorotricarboxylic acid, which blocks cellular metabolism at the citrate stage. Symptoms occur with a delay but lethal synthesis of fluorotricarboxylic acid leads to the irreversible cellular dysfunction, especially in CNS and circulatory system. Poisoning may be treated with monoacetin and acetamide. ANIMAL STUDIES: Administration of 1.0-1.5 mg/kg of fluoroacetate decreased dentin formation and enamel calcification in rats. 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. Administration of 6 mg/kg ip to rats progressively depleted ATP content, AMP and ADP levels increased during initial 2 hr and later declined. 4.5-15 ug/kg/min fluoroacetate administration into dogs left renal artery for 90-240 min sharply increased unilateral diuresis, with increased excretion of sodium, potassium, calcium, chlorides and inorganic phosphates due to decreased reabsorption. Similar changes observed after 37-936 ug/kg iv administration. Fluoroacetic acid toxicity is often characterized by seizures. In cats intravenously injected with fluoroacetate at 0.03 mmol/kg the ionized calcium level in blood fell by an average of 27.2%, 40 minutes after injection. There was a corresponding prolongation of the QT interval of the electrocardiogram. Many plants worldwide contain monofluoroacetate and cause sudden death in livestock. These plants are primarily found in the southern continents of Africa, Australia, and South America, where they negatively affect livestock production. In goats, the main clinical signs were motor incoordination, generalized muscle tremors, broad-based posture, tachypnea, tachycardia, vocalization and respiratory distress. Two goats died 5 and 20 min after the observation of the first clinical signs. ECOTOXICITY STUDIES: In the nematode Caenorhabditis elegans, fluoroacetic acid added to the growth medium reduced reproduction in the second generation by 50% at concentrations 3,000 times lower than the concentrations that reduced 24-hour survival by 50%.
Fluoroacetate is similar to acetate, which has a pivotal role in cellular metabolism. Fluoroacetate disrupts the citric acid cycle by combining with coenzyme A to form fluoroacetyl CoA. Fluoroacetyl CoA then reacts with citrate synthase to produce fluorocitrate. A metabolite of fluorocitrate binds very tightly to aconitase, thereby halting the citric acid cycle. This inhibition results in an accumulation of citrate in the blood which deprives cells of energy. (L1713) (A2849) (A2850)
/OTHER TERRESTRIAL SPECIES/ Fluoroacetic acid is known to lead to inhibition of aconitase and block both the Krebs and glyoxylate cycles. In this study, /investigators/ discovered it to be a potent and specific inhibitor of reproduction in a bioassay using the nematode Caenorhabditis elegans. Fluoroacetic acid added to the growth medium reduced reproduction in the second generation by 50% at concentrations 3,000 times lower than the concentrations that reduced 24-hour survival by 50%. Four concentrations (2, 4, 8, and 17 mM) of fluoroacetic acid were tested thoroughly. At the two lower concentrations, the survival rates were unaffected, and first-generation reproduction was greatly reduced but not completely eliminated. Survival was reduced at the higher concentrations. Malonate, which inhibits the Krebs cycle, and itaconate, which inhibits the glyoxylate cycle, were tested individually and in combination. The combination did not specifically inhibit reproduction, suggesting another mode of action for fluoroacetic acid. ...
Fluoroacetic acid is reported present at a maximum concentration of 9.5 ppm in gum of Cluster-Bean (Cyamopsis tetragonoloba; Fabaceae)(1). Fluoroacetic acid has been found as a toxic constituent of gifblaar (Dichapetalum cymosum; Dichapetalaceae), a poisonous South African plant(2,3); at least two dozen other poisonous plant species have also been found to contain fluoroacetic acid(3).
Cough. Sore throat. Shortness of breath. Laboured breathing. Muscle cramps. Confusion. Irregular heartbeat. Symptoms may be delayed.
MAY BE ABSORBED! Redness. Serious skin burns. Pain.
Blurred vision. Severe deep burns.
Burns in mouth and throat. Abdominal pain. Convulsions. Shock or collapse. Further see Inhalation.
Cough, laboured breathing, nausea, sore throat, vomiting, excessive salivation, numbness and tingling sensation, arrhythmia are observed after fluoroacetic acid inhalation; redness, serious skin burns, pain occur after skin contact; abdominal pain and convulsions in case of ingestion; blurred vision and severe deep burns if eye contact. These symptoms may be delayed. (L1685)
EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of February 4, 2019: http://actor.epa.gov/dashboard/]
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 or 10,000 lbs. Extremely hazardous substances that are solids are subject to either of two threshold planning quantities ... The lower quantity applies only if the solid exists in powdered form and has a particle size less than 100 microns; or is handled in solution or in molten form; or meets the criteria for a National Fire Protection Association (NFPA) rating of 2, 3 or 4 for reactivity. If the solid does not meet any of these criteria, it is subject to the upper ... threshold planning quantity ... .
...Fluoroacetic ion alone is non-toxic but in vivo forms fluorotricarboxylic acid, which blocks cellular metabolism at the citrate stage. Symptoms occur with a delay but lethal synthesis of fluorotricarboxylic acid leads to the irreversible cellular dysfunction, especially in CNS and circulatory system. Poisoning may be treated with monoacetin and acetamide.
A rapid method is described for the extraction and identification of fluoroacetamide and fluoroacetic acid from tissues, by gas chromatography, using a mass spectrometer in the multiple ion monitoring mode as the detector. Recoveries from animal and human tissue macerates, after the addition of each compound, were approximately 30-35% for fluoroacetamide and 50-55% for fluoroacetic acid. Minimum detectable levels in tissues were found to be circa 0.7 ug/g for the amide and 0.1 mug/g for the acid. Visceral tissue levels were found to be approximately 3 ug/g for fluoroacetamide, and 2.5-10 ug/g fluoroacetic acid in guinea pigs and rabbits which had been fatally poisoned with these compounds.
... (14)-carbon-fluoroacetic acid was slowly excreted after ip administration to rats. Only 1% was excreted as (14)-carbon dioxide after 4 hr. ... At that time, less than 1% of (14)-carbon had been excreted in urine, and 60% was present in carcass, 12% in liver, 10% in GI tract, 4% in lung, 3% in kidneys, and 2% in brain. After 4 days ... 32% ... excreted in urine, 3% as (14)-carbon dioxide and much of remainder had presumably been retained by incorporation into tissues /from ip administration 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 amount injected.
Most of fluoroacetates ingested is eliminated in feces and urine. /Fluoroacetates/
Toxic component of poisonous South African gifblaar and other plants; [Merck Index] Used to make other chemicals; [CAMEO]
For fluoroacetic acid (USEPA/OPP Pesticide Code: 075001) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./
/Former/ use in the production of the highly toxic rodenticide and general mammalian pest control agent sodium fluoroacetic acid
This is a man-made compound that is used as a pesticide.