7572-29-4ClC#CClZMJOVJSTYLQINE-UHFFFAOYSA-NVolatile oil with a disagreeable, sweetish odor. Mp: -68 to -65 °C; bp: 32-34 °C. Density: 1.38 g cm-3. Is not produced commercially.
7572-29-4DTXSID7020429CHEBI:4503Other Classes -> Halogenated Aliphatics, Unsaturated
Flammable agents - 3rd degree
Disagreeable, sweetish odor
Unpleasant odor
1.26 (NIOSH, 2024) - Denser than water; will sink
1.261 at 20 °C
Relative density (water = 1): 1.2
1.26
1.26 @25 °C
1.26
Colorless oil
Liquid (or colorless gas at elevated temperatures)
Insoluble in water; soluble in ethanol, diethyl ether and acetone
Solubility in water: none
90 °F at 760 mmHg (Explodes) (NIOSH, 2024)
Warning
H200: (Deleted) Unstable Explosive [Danger Explosives]
P201, P202, P203, P260, P280, P281, P318, P319, P372, P373, P380, P401, P405, and P501 (click each P-code to see the statement)
Warning
H200 (100%): (Deleted) Unstable Explosive [Danger Explosives]
P201, P202, P203, P260, P280, P281, P318, P319, P372, P373, P380, P401, P405, and P501 (click each P-code to see the statement)
Dichloroacetylene is formed from the thermal decomposition of trichloroethylene or tetrachloroethane. Dichloroacetylene poisoning causes injury to the kidneys and nervous system. Affected patients may have trigeminal nerve paralysis and reactivation of facial herpes. Most cases were reported when trichloroethylene was used as an anesthetic. [ACGIH]
Glutathione conjugation has been shown in rats following inhalation of dichloroacetylene. ...S-(1,2-dichlorovinyl)glutathione (DCVG) /was identified/ as a product of the glutathione (GSH)-dependent metabolism of /dichloroacetylene/ (DCA) in vitro and ...N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine (N-Ac-DCVC) /was identified/ as a urinary metabolite of DCA in rats. The product, DCVG, was definitively identified by H-NMR spectrometry (400 MHz), mass spectrometry and UV spectroscopy. N-Ac-DCVC was identified as a urinary metabolite from rats by GC/MS after esterification. Urine (collected for 24 hr) from male rats exposed to 36 n 5 ppm DCA (100 mmol of DCA introduced into the exposure system) for 1 hr contained 10.7 mmol of N-Ac-DCVC as determined by HPLC analysis. Formation of DCVG, renal processing to S-(1,2-dichlorovinyl)-L-cysteine, and cleavage of this cysteine S-conjugate by cysteine S-conjugate beta-lyase in the kidney and the formation of reactive and mutagenic intermediates may account for DCA nephrotoxicity and nephrocarcinogenicity. N-Ac-CDVC is the end product of DCVG processing by the enzymes of mercapturic acid formation.
Metabolites in the urine were identified as N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine, dichloroethanol, dichloroacetic acid, oxalic acid, and chloracetic acid /after inhalation exposure of rats/. Only the cysteine conjugate was found in feces. It was formed in the kidneys because only S-(1,2-dichlorovinyl) glutathione was found in the bile. Biliary cannulation did not influence renal excretion of the cysteine conjugate. /From this study, it was concluded that/ ...two metabolic pathways are operative in dichloroacetylene metabolism in vivo. Cytochrome P450-dependent oxidation represents a minor pathway accounting for the formation of 1,1-dichloro compounds after chlorine migration. The major pathway is the biosynthesis of toxic glutathione conjugates. Organ-specific toxicity and carcinogenicity of dichloroethyne (acetylene dichloride) is due most likely to the topographical distribution of gamma-glutamyl transpeptidase which is concentrated mainly in the kidney of rats.
The metabolism of inhaled 14(C)dichloroacetylene has been studied in male Wistar rats exposed to 20 or 40 ppm (78 or 156 mg/cu m) atmospheres for 1 hr. During the next 96 hr, elimination of retained (approximately 17%) 20 and 40 ppm doses, respectively, was: urine, 68% and 60%; feces, 28% and 27%. About 3.5% remained in the carcasses. Metabolites of dichloroacetylene that were identified were: N-acetyl-S-(1,2-dichlorovinyl)- L-cysteine (62%), dichloroethanol (12%), dichloroacetic acid (9%), oxalic acid (8%) and chloroacetic acid (5%) in urine; and N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine in faeces. In bile, only S-(1,2-dichlorovinyl)glutathione was identified. Biliary cannulation did not influence the renal excretion of N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine, a result that was interpreted to indicate that glutathione conjugation also occurs in the kidney. The identified metabolites are consistent with the existence of two metabolic pathways: the major pathway involves glutathione conjugation, while a minor pathway is cytochrome P450-dependent oxidation that accounts for the formation of 1,1- dichloro-compounds after chlorine migration.
Wird geladen…
33 °C
32 °C (explodes)
90 °F (explodes)
33 °C @760 [mm Hg]
90 °F (Explodes)
When dichloroacetylene was decomposed in the presence of oxygen, seven substances were found; phosgene, hexachlorobutadiene, chloroform, carbon tetrachloride, trichloroacetyl chloride, tetrachloroethylene, and trichloroacryloylchloride.
May decompose explosively on shock, friction, or concussion. May explode on heating. The substance decomposes on heating producing toxic fumes including chlorine.
-87 to -58 °F (NIOSH, 2024)
-66 to -64 °C
-66 °C
-58 to -87 °F
-65 °C
-58 to -87 °F
570.0 [mmHg]
570 mm Hg @ 25 °C /Estimated/
Fresh air, rest. Refer for medical attention.
Rinse and then wash skin with water and soap.
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Refer for medical attention . Rinse mouth.
Excerpt from NIOSH Pocket Guide for Dichloroacetylene:
(General first aid procedures)
SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. 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 soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.
SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit 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.
SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.
The worker should immediately wash the skin when it becomes contaminated.
Work clothing that becomes wet should be immediately removed due to its flammability hazard.
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 44(SRC), determined from a structure estimation method(2), indicates that dichloroacetylene is expected to have very high mobility in soil(SRC). Volatilization of dichloroacetylene from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.0X10-2 atm-cu m/mole(SRC), using a fragment constant estimation method(3). The potential for volatilization of dichloroacetylene from dry soil surfaces may exist(SRC) based upon an estimated vapor pressure of 570 mm Hg(SRC), determined from a fragment constant method(4).
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 44(SRC), determined from a structure estimation method(2), indicates that dichloroacetylene is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 2.0X10-2 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 1.0 hours and 93 hours, respectively(SRC). According to a classification scheme(5), an estimated BCF of 1.4(SRC), from an estimated log Kow of 1.1(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dichloroacetylene, which has an estimated vapor pressure of 570 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 dichloroacetylene 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 110 hours(SRC), calculated from its rate constant of 1.2X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). The rate constant for the vapor-phase reaction of dichloroacetylene with ozone has been estimated as 6.1X10-22 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). This corresponds to an atmospheric half-life of about 19,000 days at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(4).
The substance can be absorbed into the body by inhalation of its vapour.
inhalation, skin absorption, ingestion, skin and/or eye contact
Headache. Nausea. Vomiting. Sore throat. Dizziness. Facial paralysis, numbness and tremor.
Redness.
Abdominal pain. Further see Inhalation.
headache, loss of appetite, nausea, vomiting, intense jaw pain, cranial nerve palsy; In Animals: kidney, liver, brain injury; weight loss; [potential occupational carcinogen]
Using a structure estimation method based on molecular connectivity indices(1), the Koc for dichloroacetylene can be estimated to be 44(SRC). According to a classification scheme(2), this estimated Koc value suggests that dichloroacetylene is expected to have very high mobility in soil.
/SIGNS AND SYMPTOMS/ The /chronic and subchronic/ toxic effects were mainly neurological and could last from several days to years.
/SIGNS AND SYMPTOMS/ In the mid-1960s, DCA was detected in the closed system atmospheres of U.S. nuclear submarines and space craft. The crews experienced loss of appetite, extreme nausea, itchy eyes, sore gums, intense jaw pain, and welts on the face and mouth. Disabling nausea was experienced by 85% of the individuals exposed for prolonged periods at concentrations 0.5 to 1.0 ppm.
/SIGNS AND SYMPTOMS/ Dichloroacetylene can cause headaches, dizziness, nausea, vomiting, eye irritation, mucous membrane irritation, and neurological disorders such as paresis and neuralgia in several cranial nerves. Nausea has occurred at concentrations as low as 0.5 to 1.0 ppm.
/SIGNS AND SYMPTOMS/ Extreme nausea was reported by persons exposed to concentrations as low as 2-4 mg/cu m (0.5-1 ppm) dichloroacetylene.
/SIGNS AND SYMPTOMS/ Toxic effects have been reported after accidental exposure to dichloroacetylene in various settings: its generation during use of trichloroethylene as an anesthetic, after use of a solvent mixture containing trichloroethylene as a cleaning agent either domestically or in enclosed work spaces, and during the cleaning of tank cars containing vinylidene chloride copolymers where dichloroacetylene was present. The signs and symptoms observed in each of these reports included headache, dizziness, nausea, vomiting, irritation of the mucous membranes of the mouth and throat as well as eye irritation, facial and oral herpes and neurological disorders. The latter were manifested in paresis and neuralgia in several cranial and cervical nerves. In some cases, the signs and symptoms of cranial-nerve involvement persisted for periods ranging from several days to years. These effects were closely related to findings in dichloroacetylene-exposed animals.
Dichloroacetylene's release as a byproduct in the production of vinylidine chloride or in the dehydrochlorination of trichloroethylene, from exposure of trichloroethylene vapor to Hopcalite in a closed environmental system (submarine) or soda lime in close circuit (rebreathing) anesthesia machines, and from exposure of trichloroethylene liquid in degreaser tanks(1) may result in its release to the environment through various waste streams(SRC).
Dichloroacetylene
Group 3: Not classifiable as to its carcinogenicity to humans
Volume 39: (1986) Some Chemicals Used in Plastics and Elastomers
1999
1998
In vitro studies have demonstrated that glutathione conjugation of dichloroacetylene is predominantly enzymatic and the rate of reaction resulting in the formation of S-(1,2- dichlorovinyl)glutathione is similar for microsomes from rat kidney and liver. However, under different reaction conditions (20-500-fold higher protein concentrations), the rate was highest for microsomes from liver, followed by lung, brain and kidney. The further handling of this metabolite in kidney is not clearly defined, but it is known that gamma-glutamyltranspeptidase and dipeptidases (e.g., in biliary epithelium) can transform S-(1,2-dichlorovinyl)glutathione to S-(1,2-dichlorovinyl)- L-cysteine, which can then be acetylated in tissues or by intestinal bacteria . An alternative to acetylation is beta-lyase-mediated metabolism to form chlorothioketene as an intermediate, which can react with tissue nucleophiles or with water, when it forms chloroacetic acid. Cysteine conjugate beta-lyase activity has also been shown in rat cerebellar tissue.
The glutathione (GSH) dependent metabolism of dichloroacetylene (DCA) was investigated in rat liver and kidney subcellular fractions. The study also included the metabolism of DCA in rats to identify and quantify any metabolites formed by GSH conjugation. S-(1,2-dichlorovinyl)glutathione (DCVG) was identified as a product of the in-vitro metabolism and N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine (N-Ac-DCVC) was identified as a urinary metabolite of DCA in rats. ...N-Ac-DCVC was identified as a urinary metabolite from rats by gas chromatography/mass spectrometry after esterification. Male rats exposed to 36 ppm DCA for 1 hr produced urine which contained 10.7 micromoles of N-Ca-DCVC as determined by high pressure liquid chromatographic analysis. .../It was suggested/ that the formation of DCVG, renal processing to cysteine S-conjugate beta-lyase in the kidney with formation of reactive and mutagenic intermediates may account for DCA nephrotoxicity and nephrocarcinogenicity.
The metabolism of inhaled 14(C)dichloroacetylene has been studied in male Wistar rats exposed to 20 or 40 ppm (78 or 156 mg/cu m) atmospheres for 1 hr. During the next 96 hr, elimination of retained (approximately 17%) 20 and 40 ppm doses, respectively, was: urine, 68% and 60%; feces, 28% and 27%. About 3.5% remained in the carcasses.
Using a nose-only dynamic system, ...rats /were given 14C-dichloroacetylene/ for 1 hr at concentrations of 20 or 40 ppm. Retention rates of 17.6 and 15.6% of the radioactivity were reported for 20 and 40 ppm, respectively. Elimination of radioactivity was almost quantitative in 96 hr. Elimination of radioactivity in urine was 67.8% at 20 ppm and 60% at 40 ppm. Elimination in feces was 27.5% at 20 ppm and 27% at 40 ppm. Only 3.4 to 3.5% remained in the carcass.
A by-product of vinylidene chloride production and trichloroethylene thermal decomposition; Not produced commercially; [ACGIH]
Transport forbidden; [HMT]
Dichloroacetylene is not commercially available in large quantities. It is reportedly a byproduct of the synthesis of vinylidene chloride and is not known to be used commercially.
Dichloroacetylene is an... undesired, and non-commercial product of the dehydrochlorination of trichloroethylene. It has resulted form exposure of trichloroethylene vapor to Hopcalite in a closed environmental system (submarine) and soda lime in a closed circuit (rebreathing) anesthesia machines and from exposure of trichloroethylene liquid to caustic in degreaser tanks.
VerwendenDCA is not commercially available in large quantities. It is reportedly a by-product of the synthesis of vinylidene chloride and is not known to be used commercially.