Halothan

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep drums, etc., cool by spraying with water.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Refer for medical attention .

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

(General first aid procedures)

Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Store in a tight, light resistant container.

Keep in the dark. Ventilation along the floor.

Ventilation. Collect leaking liquid in sealable containers. Absorb remaining liquid in sand or inert absorbent and remove to safe place. (Extra personal protection: self-contained breathing apparatus).

Results of personal air sampling surveys of nitrous oxide and halothane in operating theaters and recovery areas at 27 hospitals performed between 1980 and 1984 were reported. Exposures for different groups of workers during general surgical procedures with and without anesthetic gas scavenging were compared. The survey covered 40 theaters and 18 recovery areas. Geometric mean nitrous oxide exposures with consistent scavenging and without scavenging, respectively, were: anesthetists, 71 and 211 ppm; surgeons, 50 ppm and 150 ppm; other staff, 24 ppm and 70 ppm; and all staff, 32 ppm and 94 ppm. Geometric mean halothane exposures with consistent scavenging and without scavenging respectively, were: anesthesiologists, 1.1 ppm and 4.0 ppm; surgeons, 0.6 ppm and 1.3 ppm; other staff, 0.7 ppm and 1.3 ppm; and all staff, 0.7 ppm and 1.7 ppm. Geometric mean nitrous oxide and halothane exposures for recovery staff not entering the theater were 27 ppm and 0.6 ppm, respectively; no recovery areas had scavenging. Geometric mean nitrous oxide exposures for anesthetists and for other staff excluding surgeons, respectively, were: 373 ppm and 203 ppm with zero air changes per hr, 202 ppm and 64 ppm with 10 to 15 air changes/hr, 124 ppm and 45 ppm with 15 to 20 air changes per hr, and 128 ppm and 40 ppm with more than 20 air changes/hr. Mean exposures to halothane and nitrous oxide were significantly greater with passive versus active scavenging for all staff and staff other than surgeons and anesthetists. With scavenging, 40 percent of nitrous oxide results were below 25 ppm while 88% of halothane results were below 2 ppm for all staff. It was concluded that good general ventilation and effective gas scavenging systems are essential for control of exposure to inhalation anesthetics in operating theaters.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

Because of recent discovery of potential ozone decomposition in the stratosphere by fluorotrichloromethane, this material should be released to the environment only as a last resort. Waste material should be /recovered and/ returned to the vendor, or to licensed waste disposal company.

Personal protection: self-contained breathing apparatus. Ventilation. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

Sufficient exhaust and general ventilation should be provided to keep vapor concn below recommended levels. /fluorocarbons/

Inhalation of fluorocarbon vapors should be avoided. /fluorocarbons/

Forced air ventilation at the level of vapor concentration together with the use of individual breathing devices with independent air supply will minimize the risk of inhalation. Lifelines should be worn when entering tanks or other confined spaces. /Fluorocarbons/

Enclosure of process materials and isolation of reaction vessels and proper design and operation of filling heads for packaging and shipping /are administrative controls that may be instituted to limit occupational exposure to fluorocarbons during manufacture, packaging, and use/. /Fluorocarbons/

For more Preventive Measures (Complete) data for 2-BROMO-2-CHLORO-1,1,1-TRIFLUOROETHANE (17 total), please visit the HSDB record page.

In the event of overdosage, or what may appear to be overdosage, drug administration should be stopped, and assisted or controlled ventilation with pure oxygen initiated. There is no specific antidote. Treatment should be aimed at maintaining respiratory function (by moving the patient to fresh air or inserting an emergency airway with respiratory support) and cardiovascular function. Cases of internal ingestion must be treated symptomatically. (L1712)

A report of malignant hyperthermia in a 19 month old boy who was anaesthetised with halothane and then received suxamethonium.

Significantly impaired psychophysiological performance has been demonstrated in volunteers exposed for 4 hr to 120 mg/cu m (15 ppm) halothane plus 615 mg/cu m (500 ppm) nitrous oxide ... .

The effects of non-depolarizing muscle relaxants such as gallamine and tubocurare are enhanced by halothane and if required they should be given in reduced dosage. Antibiotics such as streptomycin that possess neuromuscular blocking activity should also be used with caution. Morphine increases the depressant effects of halothane on respiration and its use during anaesthesia may be followed by post-operative nausea and vomiting. Chlorpromazine also enhances depressant effect of halothane.

Halothane may prevent or reduce trimethaphan-induced tachycardia.

For more Interactions (Complete) data for 2-BROMO-2-CHLORO-1,1,1-TRIFLUOROETHANE (27 total), please visit the HSDB record page.

Prospective, serial blood testing often demonstrates minor transient elevations in serum aminotransferase levels in the 1 to 2 weeks after major surgery and anesthesia with halothane and other halogenated anesthetics. Appearance of ALT levels above 10 times the upper limit of normal, however, is uncommon and points to significant hepatotoxicity. Clinically apparent, severe hepatic injury from halothane is rare, occurring in ~1/15,000 cases after initial exposure, but in ~1/1,000 cases after repeated exposures. The injury is marked by acute elevations in serum aminotransferase levels (5- to 50-fold) and appearance of jaundice within 2 to 14 days of surgery. There are usually minimal increases in alkaline phosphatase levels. Fever occurs before onset of jaundice in a high proportion of patients and eosinophilia in up to 30%. Rash and arthralgias can also accompany the onset of hepatic injury. The acute liver injury may be self-limited and resolve within 4 to 8 weeks, but can be severe and lead to acute liver failure. A strong risk factor is previous exposure to any of the halogenated anesthetics and particularly a history of halothane hepatitis or unexplained fever and rash after anesthesia with one of these agents. Other risk factors are hypotension, older age, obesity and concurrent use of CYP 2E1 inducers. The differential diagnosis of acute liver injury after surgery and anesthesia is sometimes difficult, and a clinical picture similar to halothane hepatitis can be caused by shock or ischemia, sepsis, other idiosyncratic forms of drug induced liver injury and acute viral or herpes hepatitis. Indeed, many cases of severe liver injury arising soon after surgery and attributed to halothane or other halogenated anesthetics in the literature probably represent liver injury from shock and ischemia. Factors favoring the diagnosis of ischemic hepatitis are rapid onset after surgery, extremely high values for ALT, AST and LDH, and subsequent rapid fall in serum enzymes.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 425(SRC), determined from a measured log Kow of 2.3(2) and a regression derived equation(3), indicates that 2-bromo-2-chloro-1,1,1-trifluoroethane is expected to have moderate mobility in soil(SRC). Volatilization of 2-bromo-2-chloro-1,1,1-trifluoroethane from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 0.0203 atm-cu m/mole(4). The potential for volatilization of 2-bromo-2-chloro-1,1,1-trifluoroethane from dry soil surfaces exists(SRC) based upon its extrapolated vapor pressure of 302 mm Hg(5). Biodegradation data were not available(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 425(SRC), determined from a measured log Kow of 2.3(2) and a regression derived equation(3), indicates that 2-bromo-2-chloro-1,1,1-trifluoroethane is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 0.0203 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 1 hour and 6 days, respectively(SRC). According to a classification scheme(5), an estimated BCF of 12(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). 2-Bromo-2-chloro-1,1,1-trifluoroethane is an alkyl halide which is susceptible to hydrolysis; however, it appears to be stable in water and hydrolysis does not appear to be environmentally relevant(7). Biodegradation data were not available(SRC, 2005).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2-bromo-2-chloro-1,1,1-trifluoroethane , which has an extrapolated vapor pressure of 302 mm Hg at 25 °C(1), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 2-bromo-2-chloro-1,1,1-trifluoroethane 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 1 year(SRC), calculated from its rate constant of 4.5X10-14 cu cm/molecule-sec at 25 °C(2). Due to its long atmospheric lifetime, some percentage of 2-bromo-2-chloro-1,1,1-trifluoroethane is expected to diffuse slowly into the stratosphere where it will undergo direct photolysis by UV-C radiation, releasing radicals that contribute to damage of the ozone layer(2).

The substance can be absorbed into the body by inhalation of its vapour and by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

inhalation

Halothane causes general anaethesia due to its actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Its immobilizing effects have been attributed to its binding to potassium channels in cholinergic neurons. Halothane's effect are also likely due to binding to NMDA and calcium channels, causing hyperpolarization. Halothane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Halothane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Halothane also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor and the glycine receptor.

Confusion. Dizziness. Drowsiness. Nausea. Unconsciousness.

Dry skin. Roughness.

Redness. Pain.

See Inhalation.

irritation eyes, skin, respiratory system; confusion, drowsiness, dizziness, nausea, analgesia, anesthesia; cardiac arrhythmias; liver, kidney damage; decreased audio-visual performance; In Animals: reproductive effects

Asymptomatic - mild liver damage, nausea, vomitting, abdominal pain, loss of appetite.

An investigation was made to determine the relationship between the halothane concn in five operating rooms in two hospitals in Italy during routine surgical operating activities and the corresponding urinary concn of halothane in 39 male and 19 female members of the operating room staffs, including anesthetists, surgeons, and nurses. Samples of urine were collected anaerobically from all subjects at the beginning and end of the 4 hr exposure period and analyzed for their halothane concn. Measurements of the time weighted average environmental halothane concn in the breathing zone were made by use of diffusive personal samplers. Breathing zone environmental halothane concn for the 58 subjects ranged from 0.35 to 74.9 mg/cu m, with a median value of 10.38 mg/cu m. Halothane was observed in the urine of all 58 subjects and ranged from 0.5 to 22.4 ug/l, with a median value of 6.55 ug/l. A significant correlation was noted between halothane urine concn and the time weighted average breathing zone concn. Calculations were made of biological exposure limits corresponding to the threshold values proposed in the literature. These limits were calculated to be 92, 6.5, and 3.9 ug/l, corresponding to environmental exposures of 50, 2, and 0.5 ppm, respectively. It was concluded that the urinary halothane concn provides an appropriate biological index of the magnitude of exposure during the production time of urine. This proposed method of measuring halothane urinary concn can be easily and rapidly performed.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed drug products, incl halothane, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act.

Used as an anesthetic; [HSDB]

Medication (vet)

Medication

Anesthetic

For the induction and maintenance of general anesthesia

Bromination of 2-chloro-1,1,2-trifluoroethylene to form 1,2-dibromo-1-chloro-1,2,2-trifluoroethane, isomerization of the product with anhydrous aluminum chloride to 1,1-dibromo-1-chloro-2,2,2-trifluoroethane, and reduction of the latter with hydrogen (catalyzed by platinum); the antimony chloride-catalysed reaction of hydrogen fluoride with 1,2-dibromo-1,1,2-trichloroethane.

Preparation from a mixture of F3CCH2Cl and FCCBrCl: Suckling, Raventos, US 2921098 (1960 to I.C.I.); by rearrangement of F2BrCCHFCl: Scherer, Kuhn, US 2959624 (1960 to Hoechst); from BrClCHCBrCl2: Chapman, McGinty, GB 805764 (1958 to I.C.I.); from Br2ClCCF3: McGinty, US 3082263 (1963 to I.C.I.)