General Description
White crystals with a mercaptan odor.
Reactivity Profile
THIOACETAMIDE(62-55-5) reacts with aqueous acid to generate hydrogen sulfide. Forms addition compounds and sulfides with salts of heavy metals. Hydrolyzed by acids or bases .
Air & Water Reactions
Slightly water soluble.
Potential Exposure
Thioacetamide is used as a replacement for hydrogen sulfide in qualitative analyses. Thioacetamide has been used as an organic solvent in the leather, textile, and paper industries; as an accelerator in the vulcanization of buna rubber; and as a stabilizer of motor fuel.
Fire Hazard
Flash point data on this compound are not available; THIOACETAMIDE is probably combustible.
First aid
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 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. Medical observation is recommended for 24-48 hours after breathing overexposure, as pulmonary edema may be delayed. As first aid for pulmonary edema, a doctor or authorized paramedic may consider administering a drug or other inhalation therapy.
Shipping
UN2811 Toxic solids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required.
Incompatibilities
Incompatible with oxidizers (chlorates, nitrates, peroxides, permanganates, perchlorates, chlorine, bromine, fluorine, etc.); contact may cause fires or explosions. Keep away from alkaline materials, strong bases, strong acids, oxoacids, epoxides.
Description
Thioacetamide (TAA) is not known to occur in nature. It is
prepared by heating ammonium acetate and aluminum sulfide.
Waste Disposal
Consult with environmental regulatory agencies for guidance on acceptable disposal practices. Generators of waste containing this contaminant (≥100 kg/mo) must conform with EPA regulations governing storage, transportation, treatment, and waste disposal. Treatment in an incinerator, boiler or cement kiln.
Definition
ChEBI: A thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur.
Hazard
Toxic by ingestion and inhalation, a possible
carcinogen.
Health Hazard
The toxicity of this compound is moderatein rats; an oral lethal dose is 200 mg/kg.Oral administration of thioacetamide causedliver cancer in rats and mice. It is, however, a weak liver carcinogen. Malvaldi and associates (1988) investigated the mechanism of its carcinogenic activity on rat liver.Whereas the initiating ability of this compound is quite low, its promoting effect isstrong. Thus thioacetamide is a very effectivepromoter of the liver carcinogenesis. A similar promoting activity of liver carcinogenesishas been observed with other thioamide substances, such as thiobenzamide (Malvaldi et al. 1986). Low et al. (2004) have proposed a modelto explain thioacetamide-induced hepatotoxicity and cirrhosis in rat livers. The pathways of thioacetamide-induced liver fibrosiswere found to be initiated by thioacetamideS-oxide derived from the biotransformationof thioacetamide by the microsomal flavinadenine nucleotide containing monooxygenase and cytochrome P450 systems andinvolve oxidative stress and depletion ofsuccinyl-CoA, thus affecting heme and ironmetabolism. Karabay et al. (2005) observedsuch hepatic damage in rats with elevationof total nitrite level in livers and decrease inarginase activity. The authors have reportedthat nitrosative stress was essentially the critical factor in thioacetamide-induced hepaticfailure in rats.Pretreatment of rats with jigrine exhibited hepatoprotective action againstthioacetamide-induced toxicity (Ahmed et al.1999). Thioacetamide decreased the concentration of glutathione in the liver of rats.Jigrine pretreatment, however, restored theglutathione levels to the near normal values.The authors claimed that the effects of jigrinewere comparable to that of silymarin. Thehepatotoxicity in rats was found to potentiatefollowing pretreatment with phenobarbital.Al-Bader et al. (2000) investigated thetoxicity of thioacetamide in the spleen inexperimental animals. The authors foundan intimate association between the levelsof trace metals and spleen pathology, asobserved in studies of other organs.
Carcinogenicity
Thioacetamide is reasonably anticipated to be a human carcinogenbased on sufficient evidence of carcinogenicity from studies in experimental animals.
Environmental Fate
TAA’s production and use as a substitute for hydrogen sulfide in
the laboratory may result in its release to the environment
through various waste streams. If released to air, TAA’s estimated
vapor pressure indicates that it will exist solely as a vapor
in the ambient atmosphere. Vapor-phase TAA will be degraded
in the atmosphere by reaction with photochemically produced
hydroxyl radicals; the half-life for this reaction in air is estimated
to be 18 h. TAA was not biodegraded by activated sludge
after 5 days, and therefore may be resistant to biodegradation
in the environment. Hydrolysis is not expected since amides
hydrolyze very slowly under environmental conditions. An
estimated bioconcentration factor for TAA suggests that the
potential for bioconcentration in aquatic organisms is low. TAA
is expected to be highly mobile in soil, and to volatilize into the
atmosphere from moist soil surfaces. In an aquatic environment,
most of the substance will leave via volatilization and is
not expected to adsorb to solids.
Purification Methods
Crystallise the amide from absolute diethyl ether or *benzene. Dry it at 70o in a vacuum and store it over P2O5 at 0o under nitrogen. (It develops an obnoxious odour on storage, and absorption at 269nm decreases, hence it should be freshly recrystallised before use). [Beilstein 2 IV 565.]
Toxicity evaluation
TAA acts as an indirect hepatotoxin and causes parenchymal
cell necrosis. It can be metabolized in vivo to acetamide, which
itself is carcinogenic. Acetamide is then hydrolyzed to acetate.
TAA-induced liver necrosis has been explained by a scheme that
includes the metabolic conversion of TAA to its S-oxide, followed
by the further metabolism of TAA-S-oxide to a reactive
intermediate that can either bind to liver macromolecules or be
further degraded to acetamide and polar products. Examples of
TAA’s biochemical effects in the liver include glucose-6-
phosphate dehydrogenase being induced within days after rats
are treated with TAA, and the level of urea product is decreased
as are the activities of hepatic carbamyl phosphate synthetase,
ornithine transcarbamylase, and arginase. Thus, TAA can
produce marked disturbances in the urea cycle in the liver.
Further, TAA administered to rats leads to functional disturbances
in mitochondria isolated from livers after 24 h, and
the maximum respiratory activity of the mitochondria is
also depressed, mitochondrial Ca2+ content is significantly
increased, and the Ca2+ transport behavior of the hepatic
mitochondria is altered. The results are indicative of structural
alterations of the inner mitochondrial membranes. The
potential role of TAA in the initiation phase of carcinogenesis
may be associated with an increase in nucleoside triphosphate
activity in cell nuclear envelopes with a corresponding increase
in RNA transport activity. Alterations in the transport
phenomenon of nuclear RNA sequences are considered an
early response to carcinogens.
