Trifluoroacetyl chloride

132.47

132.47

206-556-2

A23U71SY9G

3057

DTXSID1029176

Colorless gas|Colorless liquified gas

2915900090

17.1

1.98

Trifluoroacetyl chloride appears as a colorless gas. Shipped as a liquid under own vapor pressure. Contact with the unconfined liquid may frostbite unprotected skin. Very toxic by inhalation and may severely irritate skin, eyes, and mucous membranes. Under prolonged exposure to fire or heat the containers may rupture violently and rocket.

1.5±0.1 g/cm3

146 °C

-27 °C

-58.1±25.9℃

1.310

Exothermic reaction with water to form water soluble trifluoroacetic acid and byproduct HCl.

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Never allow product to get in contact with water during storage. Contents under pressure.

72 psia at 25 °C (3273 mm Hg)

4.6 (vs air)

Decomposes toxic hydrogen chloride and hydrogen fluoride gas in water

Pungent odor

4.50e-04 atm-m3/mole

Reacts avidly with water and with moisture in the air to give fumes of hydrogen chloride, a water-soluble toxic gas.|Incompatible with strong oxidizing agents, alcohols, amines, alkalis. Reacts vigorously with amines and alkalis. May react vigorously or explosively if mixed with diisopropyl ether or other ethers in the presence of trace amounts of metal salts.

Reacts avidly with water and with moisture in the air to give fumes of hydrogen chloride, a water-soluble toxic gas.

Halogenated Organic Compounds

Strong Reducing Agent

TRIFLUOROACETYL CHLORIDE is incompatible with strong oxidizing agents, alcohols, amines, alkalis. Reacts vigorously with amines and alkalis. May react vigorously or explosively if mixed with diisopropyl ether or other ethers in the presence of trace amounts of metal salts [J. Haz. Mat., 1981, 4, 291].

Corrosive to materials

20 kJ/mol

2.3

UN 3057 2.3

2

14-35-37

26-36/37/39-45

AO7150000

C

Storehouse ventilated at low temperature and dry; stored separately from acids, alkalis, flammables, reducing agents

Corrosive

Stable under recommended storage conditions.

P260, P261, P264, P271, P273, P280, P284, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P320, P321, P322, P363, P403+P233, P405, P501

H312

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.

Reacts violently with water.|Corrosive|Incompatible materials: Strong bases. Reacts violently with water, alcohols, metals.

Excerpt from ERG Guide 125 [Gases - Corrosive]: Some may burn but none ignite readily. Vapors from liquefied gas are initially heavier than air and spread along ground. Some of these materials may react violently with water. Cylinders exposed to fire may vent and release toxic and/or corrosive gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket. For UN1005: Anhydrous ammonia, at high concentrations in confined spaces, presents a flammability risk if a source of ignition is introduced. (ERG, 2016)

|Danger|H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]|P260, P261, P264, P271, P280, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P321, P363, P403+P233, P405, and P501

Excerpt from ERG Guide 125 [Gases - Corrosive]: As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions. SPILL: See ERG Table 1 - Initial Isolation and Protective Action Distances on the UN/NA 3057 datasheet. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, consider initial evacuation for 1600 meters (1 mile) in all directions. (ERG, 2016)

Excerpt from ERG Guide 125 [Gases - Corrosive]: Fully encapsulating, vapor-protective clothing should be worn for spills and leaks with no fire. Do not touch or walk through spilled material. Stop leak if you can do it without risk. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. Do not direct water at spill or source of leak. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Isolate area until gas has dispersed. (ERG, 2016)

Excerpt from ERG Guide 125 [Gases - Corrosive]: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. (ERG, 2016)|Eye/face protection: Tightly fitting safety goggles. Faceshield (8-inch minimum). Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Complete suit protecting against chemicals. Flame retardant protective clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type AXBEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Nonflammabale Gas

Suitable extinguishing media: Dry powder|Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

Carbon oxides, Hydrogen chloride gas, Hydrogen fluoride

ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Do not flush with water. Keep in suitable, closed containers for disposal.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.|ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Do not let product enter drains.|Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.|SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits 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.

If ... THERE IS NO FIRE, go directly to the Table of Initial Isolation and Protective Action Distances /(see table below)/ ... to obtain initial isolation and protective action distances. IF THERE IS A FIRE, or IF A FIRE IS INVOLVED, go directly to the appropriate guide /(see guide(s) below)/ and use the evacuation information shown under PUBLIC SAFETY.|/GUIDE 125 GASES - CORROSIVE/ Fire or Explosion: Some may burn but none ignite readily. Vapors from liquefied gas are initially heavier than air and spread along ground. Some of these materials may react violently with water. Cylinders exposed to fire may vent and release toxic and/or corrosive gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket. . For UN1005: Anhydrous ammonia, at high concentrations in confined spaces, presents a flammability risk if a source of ignition is introduced|/GUIDE 125 GASES - CORROSIVE/ Health: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Vapors are extremely irritating and corrosive. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Fire will produce irritating, corrosive and/or toxic gases. Runoff from fire control may cause pollution.|/GUIDE 125 GASES - CORROSIVE/ 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. As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions. Keep unauthorized personnel away. Stay upwind, uphill and/or upstream. Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks). Ventilate closed spaces before entering.|For more DOT Emergency Guidelines (Complete) data for Trifluoroacetyl chloride (9 total), please visit the HSDB record page.

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. Trifluoroacetyl chloride is included on the dangerous goods list.|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. Trifluoroacetyl chloride is included on the dangerous goods list.

Corrosive to skin, eyes ... .

IDENTIFICATION AND USE: Trifluororacetyl chloride (TFA) is a gas that is used in chemical synthesis. TFA is also a metabolite of halothane. HUMAN STUDIES: Anesthetics such as halothane are believed to trigger hepatitis by covalently linking a TFA hapten (metabolite of halothane) to hepatic proteins. The vast majority of patients with a clinical diagnosis of halothane hepatitis have serum antibodies, which react with one or more specific liver microsomal proteins that have been covalently altered by the TFA. The serum antibodies are specific to halothane hepatitis patients and are not seen in sera of patients with other types of liver pathology. When the purified TFA 57-kD and native 57-kD proteins from liver microsomes of halothane-treated and untreated rats respectively, were used as test antigens in an enzyme-linked immunosorbent assay, serum antibodies from halothane hepatitis patients (n = 40) reacted with both of these proteins to a significantly greater extent than did serum antibodies from control patients (n = 32). In a separate study 25 of 56 (45%) patients diagnosed with halothane hepatitis had autoantibodies that reacted with human cytochrome P450 2E1. In this case cytochrome P450 2E1 became trifluoroacetylated when it oxidatively metabolized halothane. ANIMAL STUDIES: TFA exposure by inhalation at 40 ppm and 90 ppm produced mortality and body weight loss in rats. Exposure of rats over a 90-day period to vapor of TFA at 0.1 ppm caused a predominantly lymphocytic local response in the lungs and local lymph nodes. Antibodies purified from the sera of rabbits sensitized to a TFA-protein adduct cross-reacted with a TFA-phosphatidylethanolamine adduct. These findings suggest that TFA-phosphatidylethanolamine adducts that reside in nonlamellar domains on the hepatocyte surface could be recognition sites for anti-TFA-adduct antibodies and potentially participate in immune-mediated hepatotoxicity. Furthermore, it was suggested that glutathione-S-transferase could be a target for covalent modification in the liver following an inhalation exposure to halothane.

Trifluoroacetyl chloride's production and use as an intermediate in the production of pharmaceutical chemicals, agricultural chemicals and other specialized applications(1) may result in its release to the environment through various waste streams(SRC). Gaseous trifluoroacetyl chloride provides a way to introduce trifluoromethyl groups into more complex molecules(1).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 3(SRC), determined from a structure estimation method(2), indicates that trifluoroacetyl chloride is expected to have very high mobility in soil(SRC). However, trifluoroacetyl chloride hydrolyzes rapidly when contacted with water (half-life of 0.063 seconds at 25 °C)(3); therefore, mobility in moist soil and volatilization from moist soil are not expected to be important fate processes(SRC). Trifluoroacetyl chloride is a gas at standard temperature and pressure(4) and, therefore, is expected to evaporate into the atmosphere when released as a liquid from pressurized containers(SRC).|AQUATIC FATE: Trifluoroacetyl chloride hydrolyzes rapidly when contacted with water(1). The hydrolysis half-life at 25 °C is 0.063 seconds(1). Therefore, hydrolysis is the dominant fate process in water(SRC).|ATMOSPHERIC FATE: Trifluoroacetyl chloride has a vapor pressure of 3273 mm Hg at 25 °C(1) and will exist solely as a gas in the ambient atmosphere. Results of laboratory studies have demonstrated that trifluoroacetyl chloride will react via hydrolysis with water vapor and water in the atmosphere(2,3). The tropospheric lifetime of trifluoroacetyl chloride due to hydrolysis is estimated to range from 0.04 days at 11 °C(2) to 0.2-2 days at 5 °C(3).

Based on results of laboratory studies, the tropospheric lifetime of trifluoroacetyl chloride ranges from 0.2-2 days at 5 °C(1). The degradation of trifluoroacetyl chloride in the atmosphere is the result of hydrolysis with water and water vapor. The amount of water vapor in the atmosphere (clouds, rain, etc.) and temperature affect the hydrolysis rate(1). In another laboratory study, the tropospheric lifetime of trifluoroacetyl chloride due to hydrolysis was about 0.04 days at 11 °C(2). The hydrolysis rate constant of trifluoroacetyl chloride in pure water at 25 °C is approximately 11 per second(3) which corresponds to a half-life of 0.063 seconds(SRC).

Trifluoroacetyl chloride hydrolyzes rapidly when contacted with water (half-life of 0.063 seconds at 25 °C)(1); therefore, bioconcentration in aquatic organisms is not expected to be an important fate process(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of trifluoroacetyl chloride can be estimated to be 3(SRC). According to a classification scheme(2), this estimated Koc value suggests that trifluoroacetyl chloride is expected to have very high mobility in soil. However, trifluoroacetyl chloride hydrolyzes rapidly when contacted with water (half-life of 0.063 seconds at 25 °C)(3); therefore, mobility in moist soil is not expected to be an important environmental fate process(SRC).

Trifluoroacetyl chloride is a gas at standard temperature and pressure(1) and therefore, is expected to evaporate into the atmosphere when released as a liquid from pressurized containers(SRC). Trifluoroacetyl chloride hydrolyzes rapidly when contacted with water (half-life of 0.063 seconds at 25 °C)(2); therefore, volatilization from water or moist soil may not be important fate processes(SRC).

According to the 2016 TSCA Inventory Update Reporting data, 2 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of trifluoroacetyl chloride in the United States may be as low as 50 to <100 workers and as high as 50 to < 100 workers per plant (1 plant's data was CBI); the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|Occupational exposure to trifluoroacetyl chloride may occur through inhalation and dermal contact with this compound at workplaces trifluoroacetyl chloride is produced or used. (SRC)

We recently showed that when rats were administered the inhalation anesthetic halothane, a 58 kDa liver endoplasmic reticulum protein became covalently trifluoroacetylated by the trifluoroacetyl chloride metabolite of halothane. Although the 58 kDa protein showed 99% identity to that of the deduced amino acid sequence of a cDNA reported to correspond to phosphatidylinositol-specific phospholipase C-alpha, it did not have phosphatidylinositol-specific phospholipase C activity. It was concluded that the reported cDNA of phosphatidylinositol-specific phospholipase C-alpha actually encoded for the 58 kDa endoplasmic reticulum protein of unknown function. Other researchers have come to the same conclusion and have shown that the 58 kDa protein has protein disulfide-isomerase and protease activities. We now report that patients with halothane hepatitis have serum antibodies that react with both purified trifluoroacetylated and native rat liver 58 kDa proteins. These results suggest that when patients are exposed to halothane a human liver orthologue of the rat liver trifluoroacetylated-58 kDa protein is formed. In certain patients, this protein may become immunogenic and lead to the formation of specific antibodies and or specific T-cells, which may react with both trifluoroacetylated and native 58 kDa proteins, and ultimately be responsible, at least in part, for the hepatitis caused by halothane.|The anesthetic halothane is bioactivated by the liver cytochrome P450 system to the reactive intermediate, trifluoroacetyl chloride, which can acylate liver protein. Cytosolic glutathione-S-transferase (GST) was identified as a major target for protein adduct formation in guinea pig liver slices exposed to halothane. To determine if GST is also a target in vivo, male Hartley guinea pigs were exposed to 1% halothane in 40% O2 for 4 hr. At 10 hr post exposure, livers were removed and microsomal and cytosolic fractions prepared. Past studies have shown these conditions resulted in maximal covalent binding of halothane intermediates to hepatic protein. Protein was isolated by ethanol precipitation and washed with trichloroacetic acid to remove unbound metabolites. Cytosolic GST was isolated by gel filtration and S-hexyl-glutathione affinity chromatography to electrophoretic purity. Protein adducts were quantified using a covalently bound fluorine assay. Covalent binding of a halothane intermediate to cytosolic and microsomal protein was determined as 2.0 +/- 0.4 and 13.2 +/- 2.3 nmol F/mg protein, respectively. Liver glutathione depletion by buthionine sulfoximine pretreatment produced an increase in covalent binding only to cytosolic proteins (3.3 +/- 0.4 nmol F/mg protein). Adduct formation to cytosolic GST was determined to be 4.7 +/- 1.6 nmol F/mg protein. Glutathione-S-transferase is a target for covalent modification in the liver following an inhalation exposure to halothane.|Autoantibodies against specific human cytochrome P450s have been found in the sera of patients suffering from a variety of diseases, including those caused by drugs. In the cases of tienilic acid- and dihydralazine-induced hepatitis, patients have serum autoantibodies directed against cytochromes P450 2C9 and P450 1A2, respectively. In the present study, we have found that 25 of 56 (45%) patients diagnosed with halothane hepatitis have autoantibodies that react with human cytochrome P450 2E1 that was purified from a baculovirus expression system. The autoantibodies inhibited the activity of cytochrome P450 2E1 and appeared to be directed against mainly conformational epitopes. In addition, because cytochrome P450 2E1 became trifluoroacetylated when it oxidatively metabolized halothane, it is possible that the covalently altered form of cytochrome P450 2E1 may be able to bypass the immunologic tolerance that normally exists against cytochrome P450 2E1. A similar mechanism may explain the formation of autoantibodies that have been found against other cellular targets of the reactive trifluoroacetyl chloride metabolite of halothane.|Halothane causes an idiosyncratic hepatitis that is thought to result, in part, from immune reactions against one or more lumenal endoplasmic reticulum (ER) proteins that have been covalently modified by the trifluoroacetyl chloride metabolite of halothane. In this study, we have identified a 170 kDa protein target of halothane in the liver of rats. The 170 kDa protein was first detected when proteins in lysates of hepatocytes from halothane-treated rats were immunoprecipitated with antisera against several resident ER proteins. This 170 kDa protein was found to be associated with other protein targets of halothane, including protein disulfide isomerase, a protein disulfide isomerase isoform, a 59 kDa carboxylesterase, and 78 kDa glucose-regulated protein. Immunoblotting with antiserum directed against the trifluoroacetylated hapten indicated that the 170 kDa protein was trifluoroacetylated. Based upon its subcellular localization, molecular mass, N-terminal amino acid sequence, and antigenicity, the trifluoroacetylated 170 kDa protein was identified as UDP-glucose:glycoprotein glucosyltransferase (UGGT), a lumenal ER protein that is thought to have a role in the folding of N-linked glycoproteins. Moreover, treatment of rats with halothane caused a 44% decrease in the activity of liver microsomal UGGT, and at least 36% of the change in the activity of the enzyme could be due to a decrease in the level of the protein. The results suggest that the function of UGGT in folding of N-linked glycoproteins may be affected by other resident ER proteins or xenobiotics such as halothane.|For more Metabolism/Metabolites (Complete) data for Trifluoroacetyl chloride (10 total), please visit the HSDB record page.|Trifluoroacetyl chloride is a known human metabolite of Halothane.

Excerpt from ERG Guide 125 [Gases - Corrosive]: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Vapors are extremely irritating and corrosive. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Fire will produce irritating, corrosive and/or toxic gases. Runoff from fire control may cause pollution. (ERG, 2016)

Excerpt from ERG Guide 125 [Gases - Corrosive]: Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves. Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give 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 liquefied gas, thaw frosted parts with lukewarm water. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. In case of contact with Hydrogen fluoride, anhydrous (UN1052), flush with large amounts of water. For skin contact, if calcium gluconate gel is available, rinse 5 minutes, then apply gel. Otherwise, continue rinsing until medical treatment is available. For eyes, flush with water or a saline solution for 15 minutes. Keep victim calm and warm. Keep victim under observation. Effects of contact or inhalation may be delayed. (ERG, 2016)

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Inorganic acids and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. Activated charcoal is not effective. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Inorganic acids and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's(LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Inorganic acids and related compounds/

/CASE REPORTS/ Three cases of drug-induced liver injury (DILI) have been reported after desflurane anesthesia. However, no previous reports have detected serum autoantibodies such as that reported with DILI from halothane or isoflurane. We describe the first documentation of cytochrome P450 2E1 IgG4 autoantibodies, as well as 58 kDa endoplasmic reticulum protein and trifluoroacetyl chloride hapten-specific IgG4 antibodies, in a patient who developed DILI after desflurane anesthesia. These findings suggest that allergic and autoimmune mechanisms have critical roles in the development of desflurane DILI.|/ALTERNATIVE and IN VITRO TESTS/ Clinical and laboratory evidence suggests that the fulminant liver failure sometimes associated with the inhalation anesthetic halothane may be an immune-mediated toxicity. Most importantly, the vast majority of patients with a clinical diagnosis of halothane hepatitis have serum antibodies, which react with one or more specific liver microsomal proteins that have been covalently altered by the trifluoroacetyl chloride metabolite of halothane. The serum antibodies are specific to halothane hepatitis patients and are not seen in sera of patients with other types of liver pathology. In this study, a 57-kD trifluoroacetylated liver microsomal neoantigen associated with halothane hepatitis and native 57-kD protein were purified from liver microsomes of halothane-treated and -untreated rats, respectively. When the purified trifluoroacetylated 57-kD and native 57-kD proteins were used as test antigens in an enzyme-linked immunosorbent assay, serum antibodies from halothane hepatitis patients (n = 40) reacted with both of these proteins to a significantly greater extent than did serum antibodies from control patients (n = 32). On the basis of its apparent monomeric molecular mass, isoelectric point and NH2-terminal amino acid and tryptic peptide sequences, the 57-kD protein has been identified as rat liver protein disulfide isomerase. Antibodies raised against rat liver protein disulfide isomerase also reacted with a protein of approximately 58-kD in human liver microsomes. The results of this investigation suggest that trifluoroacetylated protein disulfide isomerase is one of the immunogens associated with halothane hepatitis. In certain patients it might lead either to specific antibodies or, possibly, to specific T cells, which could be responsible for halothane hepatitis.|/OTHER TOXICITY INFORMATION/ Anesthetics are believed to trigger hepatitis by covalently linking a trifluoroacetyl (TFA) chloride hapten to hepatic proteins, forming haptenated self-proteins

TFA chloride

Agriculture, forestry, fishing and hunting|Acetyl chloride, 2,2,2-trifluoro-: ACTIVE|Exothermic reaction with water to form water soluble trifluoroacetic acid and byproduct HCl.