Chlorethylen

Hazardous Air Pollutants (HAPs)

Urban Hazardous Air Pollutants (HAPs) - EPA specified greatest potential health threat in urban areas

Carcinogens

Volatile Organic Compound (VOC)

log Kow = 1.46

1.6

Ethereal odor

Mild, sweet odor

Pleasant odor at high concentrations

0.969 at 8.6 °F (USCG, 1999) - Less dense than water; will float

0.9106 g/cu cm at 20 °C

Density (vapour at 15 °C): 8 g/l

Relative density (water = 1): 0.9 (liquid)

0.969 at 8.6 °F

0.9106 @ 20°C

Slightly soluble (NTP, 1992)

In water, 8.8X10+3 mg/L at 25 °C

In water, 2700 mg/L

Soluble in ethanol; very soluble in ethyl ether

Soluble in carbon tetrachloride and benzene

Soluble in hydrocarbons, oil, chlorinated solvents, and most common organic solvents.

-110 °F (NTP, 1992)

-78 °C

Gas (-108.4 °F (-78 °C)) - open cup.

-78 °C (-112 °F) - closed cup

-78 °C c.c.

-110 °F

Danger

H220: Extremely flammable gas [Danger Flammable gases]

P203, P210, P222, P280, P318, P377, P381, P403, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.3% (2 of 785) of reports.

Danger

H220 (99.7%): Extremely flammable gas [Danger Flammable gases]

Chemical: Ethene, chloro-

Hazard Traits - Carcinogenicity; Neurotoxicity; Ocular Toxicity; Respiratory Toxicity

Ethene, chloro- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Ethene, chloro- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 15-05-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/16163

Restricted substance: Chloroethene

Ethene, chloro- (vinyl chloride): HSNO Approval: HSR001016 Approved with controls

Special Hazards of Combustion Products: Forms highly toxic combustion products such as hydrogen chloride, phosgene, and carbon monoxide.

· EXTREMELY FLAMMABLE.

Extremely flammable. Gives off irritating or toxic fumes (or gases) in a fire. Gas/air mixtures are explosive.

A very dangerous fire hazard when exposed to heat or flame, or oxidizers. Large fires of this material are practically inextinguishable.

Flammable gas. /Vinyl chloride, inhibited/

INHALATION: high concentrations cause dizziness, anesthesia, lung irritation. SKIN: may cause frostbite; phenol inhibitor may be absorbed through skin if large amounts of liquid evaporate. (USCG, 1999)

· Vapors may cause dizziness or asphyxiation without warning, especially when in closed or confined areas.

Vinyl chloride is a colorless gas. It burns easily and it is not stable at high temperatures. It has a mild, sweet odor. It is a manufactured substance that does not occur naturally. It can be formed when other substances such as trichloroethane, trichloroethylene, and tetrachloroethylene are broken down. Vinyl chloride is used to make polyvinyl chloride (PVC). PVC is used to make a variety of plastic products, including pipes, wire and cable coatings, and packaging materials. Vinyl chloride is also known as chloroethene, chloroethylene, and ethylene monochloride.

Increased incidence of liver cancer (angiosarcoma) was found in workers who had high exposure to vinyl chloride monomer while cleaning reaction vessels. [LaDou, p. 298-9] There is compelling evidence that exposure to vinyl chloride is associated with angiosarcoma of the liver, and strong evidence that it is associated with hepatocellular carcinoma. Together with the observation that vinyl chloride increases the risk for liver cirrhosis, which is a known risk factor for hepatocellular carcinoma, the findings from two large multicentre cohort studies provide convincing evidence that vinyl chloride causes hepatocellular carcinoma as well as angiosarcoma of the liver. [IARC Monograph 100F] There is limited evidence that vinyl chloride caused increased birth defects in exposed human populations. [ATSDR Case Studies #29] Vinyl chloride was once evaluated as an anesthetic; it can cause central nervous system depression after inhalation of high concentrations. [ATSDR Medical Management] Possible frostbite from contact with liquid; [NIOSH] Vinyl chloride, stabilized (UN1086) has warning of explosive polymerization; [ERG 2016]

1086 116P

1086 116P(inhibited)

Excerpt from ERG Guide 116 [Gases - Flammable (Unstable); polymerization hazard]:

Shut off supply; if not possible and no risk to surroundings, let the fire burn itself out. In other cases extinguish with powder, carbon dioxide, water spray. In case of fire: keep cylinder cool by spraying with water. Combat fire from a sheltered position.

Fresh air, rest. Refer immediately for medical attention.

ON FROSTBITE: rinse with plenty of water, do NOT remove clothes. Refer immediately for medical attention.

Rinse with plenty of water (remove contact lenses if easily possible). Refer 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.

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:

(General first aid procedures)

Vapors are heavier than air and may travel to a source of ignition and flash back. ... Closed containers may rupture violently when heated. /Vinyl chloride, inhibited/

Fire may restart after it has been extinguished. ... Vapors are heavier than air and will collect in low areas. Vapors may travel long distances to ignition sources and flashback. Vapors in confined areas may explode when exposed to fire. Containers may explode in fire. Storage containers and parts of containers may rocket great distances, in many directions.

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. /Vinyl chloride, stabilized/

Evacuation: If fire becomes uncontrollable or container is exposed to direct flame, consider evacuation of one-half mile radius. /Vinyl chloride, stabilized/

Use dry chemical or carbon dioxide extinguishers. ... Do not extinguish fire unless the flow of gas can be stopped and any remaining gas is out of the line. Specially trained personnel may use fog lines to cool exposures and let the fire burn itself out. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position. If cylinders are exposed to excessive heat from fire or flame contact, withdraw immediately to a secure location. ... The only respirators recommended for firefighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode.

Stop flow of gas before extinguishing fire. Fight fire from protected location or maximum possible distance. Use water spray, dry chemical, foam, or carbon dioxide. Use water spray to keep fire-exposed containers cool. Use flooding quantities of water as fog. /Vinyl chloride, inhibited/

Vinyl chloride should be stored in cool well-ventilated areas, out of direct sunlight. It is usually stored under pressure and handled as a liquid. It must be kept away from sparks, flames and other ignition sources.

Store in cool, dry, well-ventilated location. Separate from oxidizing materials. /Vinyl chloride, inhibited/

Store in a secure poison location. Prior to working with this chemical you should be trained on its proper handling and storage. Before entering confined space where this chemical may be present, check to make sure that an explosive concentration does not exist. Vinyl chloride must be stored to avoid contact with oxidizers (such as perchlorates, peroxides, permanganates, chlorates, and nitrates), since violent reactions occur. Sources of ignition, such as smoking and open flames, are prohibited where vinyl chloride is handled, used, or stored. Metal containers involving the transfer of 5 gallons of vinyl chloride should be grounded and bonded. Drums must be equipped with self-closing valves, pressure vacuum bungs, and flame arresters. Use only nonsparking tools and equipment, especially when opening and closing containers of vinyl chloride. Wherever vinyl chloride is used, handled, manufactured, or stored, use explosion-proof electrical equipment and fittings. Procedures for the handling, use, and storage of cylinders should be in compliance with OSHA 1910.101 and 1910.169, as with the recommendations of the Compressed Gas Association. A regulated, marked area should be established where this chemical is handled, used, or stored in compliance with OSHA Standard 1910.1045.

Containers of vinyl chloride shall be legibly labeled either: VINYL CHLORIDE: EXTREMELY FLAMMABLE GAS UNDER PRESSURE: CANCER SUSPECT AGENT or ... with the additional legend CANCER-SUSPECT AGENT applied near the label or placard.

For more Storage Conditions (Complete) data for Vinyl chloride (6 total), please visit the HSDB record page.

Leaks should be stopped as soon as possible. All sources of ignition must be eliminated. Vinyl chloride vapor can travel to an ignition source and flash back causing a flash fire. Because of the explosive hazard, fire at a leak must not be extinguished unless the leak is simultaneously closed. In the event of a spillage, liquid should be contained and discharges to streams or sewer system prevented. People performing the clean-up should have full protective equipment and positive-pressure breathing apparatus.

Evacuate and restrict persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Establish forced ventilation to keep levels below explosive limit. Ventilate area of leak to disperse the gas. Stop the flow of gas if it can be done safely. If source of leak is a cylinder and the leak cannot be stopped in place, remove leaking cylinder to a safe place in the open air, and repair leak or allow cylinder to empty. Keep this chemical out of confined space, such as a sewer, because of the possibility of explosion, unless the sewer is designed to prevent the buildup of explosive concentrations. It may be necessary to contain and dispose of this chemical as a hazardous waste.

Land Spill: Construct barriers to contain spill. Absorb small amounts of spill with natural or synthetic sorbents, shovel into containers with covers.

Water Spill: Contain contaminated water with dams or natural barriers.

For more Cleanup Methods (Complete) data for Vinyl chloride (6 total), please visit the HSDB record page.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U043 and D043, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Incineration, preferably after mixing with another combustible fuel. Care must be exercised to assure complete combustion to prevent the formation of phosgene. An acid scrubber is necessary to remove the halo acids produced.

PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/

For more Disposal Methods (Complete) data for Vinyl chloride (13 total), please visit the HSDB record page.

A strong correlation was found between vinyl chloride (VC) concentration at working places and the increased excretion of thiodiglycolic acid of 18 exposed workers. The values obtained were in the range of 0.14-7.00 ppm. The excretion of thiodigylcolic acid, measured by gas chromatography-mass spectrometry analysis, amounted to 0.3-4.0 mg/L.

Hepatic

[liver cancer]

Groups each of 25-35 bred Sprague Dawley rats were exposed to vinyl chloride (500 and 2,500 ppm) for 7 hrs daily on days 6-15 of gestation. Some of the mice in the high dose group were given ethanol (15%) in their drinking water on day 6-15 of gestation. The rats were sacrificed on day 21 of gestation and the fetuses examined for visceral and skeletal abnormalities. The dams were examined for corpora lutea, implantations and intrauterine deaths. At the highest dose levels there was significant increase in absolute and relative liver weight. The effect was more pronounced in the group also exposed to ethanol. There was no significant effect on litter size, the number of implantation sites/dam or incidence of absorption in any of the exposed animals. Fetal body weight and crown-rump length were significantly reduced in the 2,500 ppm group in combination with ethanol, but not in the 2500 ppm vinyl chloride alone group. However decreased fetal body weight was observed in rats exposed to 500 ppm vinyl chloride. Unilateral and bilateral dilated uterers were observed in litters of rats exposed to 2500 ppm vinyl chloride. No increase in the incidence of skeletal anomalies were observed in litters of rats exposed to 2500 ppm vinyl chloride. However, rats exposed to both 2500 ppm vinyl chloride and ethanol, showed a significant increase in incidence of spurs, and missing centra of the cervical vertebrae.

Groups each of 15 to 20 bred rabbits (New Zealand) were exposed to 500, or 2500 ppm vinyl chloride for 7 hrs daily on days 6-18 of gestation. Some of the rabbits in the higher dose groups were also exposed to 15% ethanol in their drinking water (days 6-18). On day 29 of gestation the pregnant rabbits were sacrificed, and the fetuses examined for visceral and skeletal abnormalities. The dams were examined for corpora lutea, implantations, and intrauterine deaths. There was no effect on maternal weight gain or liver weight or food consumption in rabbits exposed to 2500 ppm vinyl chloride alone, but those exposed to a combination of vinyl chloride and alcohol showed a significant decrease in weight gain and food consumption. Exposure to vinyl chloride alone did not cause any change in the incidence of reabsorptions, but exposure to vinyl chloride plus ethanol caused a marked increase in the number of resorption. There were no differences in fetal body weight or crown-rump length in the exposed group. Delayed ossification was observed at all dose levels.

Sprague-dawley male rats received either 5% ethanol in drinking water or drinking water only for 4 weeks prior to beginning inhalation of 600 ppm vinyl chloride for 4 hr/day on 5 days/wk for 12 mo. After 60 weeks from the first vinyl chloride exposure, liver tumors were found in 75% of the vinyl chloride-ethanol rats and in 38% of the vinyl chloride-only group.

Vinyl chloride exerts a protective effect on hepatotoxicity when admin with vinylidene chloride.

For more Interactions (Complete) data for Vinyl chloride (8 total), please visit the HSDB record page.

Cancer, Developmental (effects during periods when organs are developing) , Hepatic (Liver), Immunological (Immune System), Neurological (Nervous System)

Hepatic

Liver, central nervous system, blood, respiratory system, lymphatic system

Exposure to vinyl chloride results in liver damage, nerve damage, and immune reactions, as well as depression of the central nervous system and cardiac arrhythmias. Long term exposure may result in damage to the sperm and testes of males. Vinyl chloride is also a known carcinogen. (L3)

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc value of 57(2), indicates that vinyl chloride is expected to have high mobility in soil(SRC). Volatilization of vinyl chloride from moist soil surfaces is expected(SRC) given a Henry's Law constant of 0.0278 atm-cu m/mole(3). The volatilization half-life of vinyl chloride was estimated as 0.2 days when incorporated in a soil at a depth of 1 cm and 0.5 days at a depth of 10 cm(4). Vinyl chloride is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 2980 mm Hg at 25 °C(5). Vinyl chloride had a biodegradation rate of 1.456 ug/g soil/hr in soil from Skellingsted landfill in Holback, Denmark, incubated with methane(6). Vinyl chloride was degraded approximately 50% and 100% in 4 and 11 weeks, respectively, in the presence of sand by methanogenic microorganisms under anaerobic conditions in laboratory scale experiments(7). In the absence of sand 20% and 55% degradation occurred in 4 and 11 weeks, respectively(7). [

AQUATIC FATE: Based on a classification scheme(1), a Koc value of 57(2), indicates that vinyl chloride 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 0.0278 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 2 hours and 3 days, respectively(SRC). Vinyl chloride is not expected to undergo hydrolysis in the environment based on reported hydrolysis half-lives of >9.91 years (pH = 7, 25 °C) and >107 years (pH = 7, 10 °C)(5). Vinyl chloride is not likely to photo-degrade in water(5). According to a classification scheme(6), a BCF of <10 measured in fish(7), suggests bioconcentration in aquatic organisms is low. The biodegradation half-life of vinyl chloride in aerobic and anaerobic waters was reported as 28 and 110 days, respectively(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), vinyl chloride, which has a vapor pressure of 2980 mm Hg at 25 °C(2), is expected to exist solely as a gas in the ambient atmosphere. Gas-phase vinyl chloride is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals and ozone(SRC); the half-lives for these reactions in air are estimated to be 2.3 and 46 days(SRC), calculated from respective rate constants of 6.96X10-12(3) and 2.51X10-19(4) cu cm/molecule-sec at 25 °C, respectively. The photolysis half-life of vinyl chloride in air was reported as >3.8 days(5). Vinyl chloride, exposed to light >290 nm for 17 hours was photo-degraded 15.3%(6).

Vinyl chloride was detected at 20 mg/kg in alcoholic beverages which were packaged in products containing vinyl chloride(1,2). Vinyl chloride was detected in edible oils at 0.05 to 2 ppm average and in butter and margarine at unspecified concentrations(2).

Small quantities of chloroethene can be exposed to food by migration of chloroethene monomer present in polyvinyl chloride food wrappings and containers.

The substance can be absorbed into the body by inhalation.

inhalation, skin and/or eye contact (liquid)

Oral (L3) ; inhalation (L3) ; dermal (L3)

IDENTIFICATION AND USE: Vinyl chloride is a colorless gas or liquid (below 77 degrees F). It is used in the plastics industry to manufacture polyvinyl chloride, and in organic syntheses. It has been used as refrigerant and spray can propellant. HUMAN STUDIES: Vinyl chloride causes angiosarcoma of the liver, and hepatocellular carcinoma. Past occupational exposure to several hundred ppm of vinyl chloride for periods ranging from one month to 3 years has been associated with development of "vinyl chloride disease". Vinyl chloride disease is characterized by acroosteolysis, a condition characterized by lytic lesions of bones (primarily of fingers), scleroderma of the connective tissue in the fingers with dermal thickening, and a Raynaud-like condition with reversible arteriole constriction causing numbness, pallor and cyanosis of the fingers. The attribution of acroosteolysis to vinyl chloride exposure is based almost entirely on case reports and has been estimated to affect <3% of workers involved in the polymerization of vinyl chloride. In patients with chronic occupational exposure, neurological disturbances include sensory-motor polyneuropathy, trigeminal sensory neuropathy, slight pyramidal signs and cerebellar and extrapyramidal motor disorders. Psychiatric disturbances included neurasthenic or depressive syndromes. Sleeplessness and loss of sexual functions were frequently encountered. Pathological EEG alterations were found in a high proportion of patients. A chronic hepatic disorder of porphyrin metabolism was found in 36 workers with vinyl chloride-induced hepatic injury following long-time industrial exposure. Pathologic porphyrinuria, especially secondary coproporphyrinuria with transition to subclinical chronic hepatic porphyria, is a consistent pathobiochemical parameter for the recognition of vinyl chloride hepatic lesions. The major immunological abnormalities reported in vinyl chloride disease patients include hyperimmunoglobulinemia with a polyclonal increase in IgG, cryoglobulinemia, cryofibrinogenemia, and in vivo activation of complement. Vinyl chloride is an occupational carcinogen which caused micronuclei in human cells. There was significant increase in chromosomal abnormalities in cultured peripheral lymphocytes from 57 male workers when compared with controls. Sister chromatid exchange was the more sensitive endpoint for indicating a biological response. ANIMAL STUDIES: Brief (30 minutes) exposures to concentrations of vinyl chloride ranging from 100,000 to 400,000 ppm have been shown to be fatal in rats, guinea pigs and mice. Symptoms of intoxication in rats and mice include muscular incoordination and twitching, CNS depression and respiratory failure. Intense salivation and lacrimation have been noted in rats, guinea pigs and rabbits exposed acutely to high concentrations (375-700 mg/L) of vinyl chloride gas. When placed on skin or in eyes, liquid vinyl chloride may freeze tissue and produce a chemical burn as it evaporates, causing damage to the underlying tissue. Profound CNS depression was reported in guinea-pigs exposed to vinyl chloride at 65,000 mg/cu m for 90 min. Ataxia was observed at this dose level after 5 min of exposure. The anesthetic action of vinyl chloride was also observed in dogs and mice. Investigators reported deep CNS depression in rats and mice exposed to 260,000 mg/cu m for 30 min. The CNS depressant effect was preceded by increased motor activity after 5 min of exposure, twitching of extremities (after 10 min), ataxia (after 15 min) and tremor (after 15 min). Rats exposed to 130,000 mg/cu m for 60 min showed ataxia preceded by hyperactivity but no /CNS depressant/ effect. Forty rabbits were exposed for 4 hours/day on 5 days/week for 12 months to air containing (10,000 ppm) vinyl chloride. Between 9 and 15 months exposure, 12 skin acanthomas and 6 lung adenocarcinomas were seen. No similar tumors occurred in 20 controls after 15 months observation. Rats were exposed to 10,000 ppm vinyl chloride in air for 4 hours/day on 5 days/week for 5 weeks, starting at the age of 13 weeks (120 rats per group) or 1 day (43 and 46 rats). Animals were observed for 135 weeks. One hepatoma was reported in the older rats in newborn rats, 10 angiosarcomas and 15 hepatomas were found. No liver tumors were reported in 249 controls. Vinyl chloride was administered for 7 hr/day on days 6-18 of gestation in mice, rats, and rabbits. It was concluded that although maternal toxicity observed, vinyl chloride alone did not cause significant embryonal or fetal toxicity and was not teratogenic in any of the species at concentrations tested. Vinyl chloride produced a significant increase in the frequency of recessive lethal mutations in male Drosophila melangaster. Mutagenic activity of vinyl chloride was reported in yeast (S. pombe and S. cerevisiae) in the presence of metabolic activation. Vinyl chloride was mutagenic to S. pombe in the "host mediated" assay when mice were treated with an oral dose of 700 mg/kg of vinyl chloride. Using Salmonella tester strains, direct mutagenicity of vinyl chloride was reported at 20% (v/v) in air (200,000 ppm) in the absence of metabolic activation. Mutagenic response was increased by metabolic activation. However, 20% vinyl chloride (v/v in air) was inactive in systems employing S. typhimurium strains TA1536, TA1537 and TA1538. ECOTOXICITY STUDIES: In Daphnia magna exposure, results indicated impacts of vinyl chloride on the regulation of genes related to glutathione-S-transferase (GST), juvenile hormone esterase (JHE), and the vitelline outer layer membrane protein (VMO1).

Vinyl chloride poisoning exhibits many of the characteristics of autoimmune diseases. This is believed to be the result of a reactive vinyl chloride intermediate metabolite binding to an immunoglobulin, altering the protein and initiating an immune response. The metabolites of vinyl chloride, especially choloroethylene oxide, are mutagenic and act by covalently binding to DNA. This produces cyclic etheno-adducts, which cause base-pair transitions during transcription and DNA crosslinks. Metabolites also may cause oxidative stress and affecting tumor supressor genes, as vinyl chloride has been known to produce specific mutations in the p53 and Ki-ras genes. Vinyl chloride metabolites are also believed to exert toxic effects in the liver by covalently binding to liver proteins, resulting in cellular toxicity. (L3, A65)

D043; A solid waste containing vinyl chloride may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

U043; As stipulated in 40 CFR 261.33, when vinyl chloride, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Vinyl chloride is produced, as an intermediate or a final product, by process units covered under this subpart.

Vinyl chloride has been designated as a hazardous air pollutant under section 112 of the Clean Air Act.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Vinyl chloride is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1 lb or 0.454 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

(CA) CALIFORNIA 0.5 ug/L

(DE) DELAWARE 1 ug/L

(FL) FLORIDA 1 ug/L

(NJ) NEW JERSEY 2 ug/L

(WI) WISCONSIN 0.2 ug/L

Vinyl chloride

1

10000

Flammable chemical that can be released at a facility.

(AZ) ARIZONA 0.015 ug/L

(CT) CONNECTICUT 2 ug/L

(ME) MAINE 0.2 ug/L

(MN) MINNESOTA 0.2 ug/L

Maximum contaminant level (MCL) for organic contaminants apply to community and non-transient, non-community water systems: vinyl chloride, MCL 0.002 mg/L.

EPA 2 ug/l

Vinyl chloride carcinogenicity occurs via a genotoxic pathway and is understood in some detail. Vinyl chloride is metabolized to a reactive metabolite, probably chloroethylene oxide, which is believed to be the ultimate carcinogenic metabolite of vinyl chloride. The reactive metabolite then binds to DNA, forming DNA adducts that, if not repaired, ultimately lead to mutations and tumor formation.

There is a large body of data showing that VC acts as a genotoxic carcinogen. After metabolic activation to CEO /chloroethylene oxide/ by CYP2E1, VC exerts various genotoxic effects (including gene mutations and chromosomal aberrations) in different organisms, including bacteria, yeasts, mammalian cells in culture, Drosophila, rodents and humans. Among the mutagenic events induced by VC, base-pair substitutions appear, so far, to be the most frequent. VC in the presence of an activation system has a transforming activity on mammalian (rodent) cells in culture. Studies in vitro have demonstrated that metabolically activated VC and its electrophilic metabolites CEO and CAA /chloroacetaldehyde/ can alkylate nucleic acid bases. 7-OEG, the major DNA adduct formed by VC and CEO does not exhibit promutagenic properties. In contrast, four minor adducts, Epsilon A, Epsilon C, N2,3-Epsilon G and 1,N2-Epsilon G, show promutagenic properties, inducing mainly base-pair substitution mutations and a low level of frameshift mutations.

Based on limited data: fairly rapid; [TDR, p. 1224]

The pattern of pulmonary elimination of 10 and 1000 ppm vinyl chloride was described by apparently similar first-order kinetics, with half-lives of 20.4 and 22.4 minutes respectively. The half lives for the initial phase of excretion of (14)C radioactivity in urine were 4.6 and 4.1 hours, respectively.

Vinyl chloride is primarily and rapidly metabolized in the liver, and this metabolism is saturable. ...The first step in the metabolism of vinyl chloride is oxidation, which is predominantly mediated by human cytochrome P450 (CYP) 2E1, to form the highly reactive chloroethylene oxide, which can spontaneously rearrange to chloroacetaldehyde. ... Conjugation of chloroethylene oxide and chloroacetaldehyde with glutathione (GSH) eventually leads to the major urinary metabolites N-acetyl-S-(2-hydroxyethyl)cysteine and thiodiglycolic acid. Chloroethylene oxide and chloroacetaldehyde can also be detoxified to glycolaldehyde by microsomal epoxide hydrolase (mEH) and to the urinary metabolite chloroacetic acid by aldehyde dehydrogenase 2 (ALDH2), respectively.

Following oral administration of (14)C-vinyl chloride, (14)C-carbon dioxide, (14)C-labelled urea and glutamic acid were identified as minor metabolites.

After inhalation of (14)C vinyl chloride by rats ... three urinary metabolites have been detected: N-acetyl-S-(2-hydroxyethyl)cysteine, thiodiglycolic acid, and an unidentified substance.

The principal (14)C urinary metabolites of orally administered (14)C-vinyl chloride, in the male rat, are N-acetyl-S-(2 hydroxyethyl)cysteine, N-acetyl-S-vinylcysteine and thiodiglycollic acid and lesser amounts of urea, glutamic acid, chloracetic acid and traces of methione and serine. The proportions of the three major urinary metabolites in the rat appear to be unaffected by either the dose, or the route of administration.

For more Metabolism/Metabolites (Complete) data for Vinyl chloride (10 total), please visit the HSDB record page.

VINYL CHLORIDE has known human metabolites that include 2-Chlorooxirane.

Vinyl chloride dissolved in either oil or water when administered to rats by gavage, was absorbed extremely rapidly. Peak blood serum concentrations of vinyl chloride were observed within 10 minutes of dosing.

Pulmonary absorption of vinyl chloride in humans appeared to be rapid and the percentage absorbed was independent of the concentration inhaled. ... Adult male volunteers exposed for 6 hr to 2.9, 5.8, 11.6 or 23.1 ppm (7.5, 15, 30 or 60 mg/cu m) by gas mask retained on average approximately 42% of inhaled vinyl chloride. Pulmonary uptake is determined in part by the blood:air partition coefficient, which is 1.16 for vinyl chloride.

Animal data have demonstrated that pulmonary and gastrointestinal absorption of vinyl chloride occurs readily and rapidly. On the contrary, dermal absorption of airborne vinyl chloride is probably not significant. In monkeys, ... only 0.023-0.031% of the total available vinyl chloride was absorbed by the dermal route, whereas absorption in rats was virtually complete following single oral doses (44-92 mg/kg bw) of vinyl chloride in aqueous solution. When rats were exposed to initial concentrations of < 260 mg/cu m (100 ppm), about 40% of inhaled (14)C-vinyl chloride was absorbed by the lung.

The main routes of elimination of vinyl chloride and its metabolites are exhalation and urinary excretion, respectively. Accordingly, thiodiglycolic acid has been reported to be the major metabolite of vinyl chloride detected in the urine of exposed workers. Urinary levels of thiodiglycolic acid were correlated with levels of vinyl chloride in the air at concentrations of > 5 ppm.

For more Absorption, Distribution and Excretion (Complete) data for Vinyl chloride (18 total), please visit the HSDB record page.

Most of the vinyl chloride produced is used to make polyvinyl chloride (PVC), a material widely used in automotive parts, packaging products, pipes, construction materials, furniture, and a variety of other products.

The highest exposures to vinyl chloride occurred in polyvinyl chloride polymerization plants during reactor vessel cleaning. [LaDou, p. 520]

See 29 CFR 1910.1017;

Smoking cigarettes [Category: Food & Drugs]

About 99% of the global vinyl chloride capacity is used for the production of poly(vinyl chloride) (PVC) and its copolymers.

In the plastics industry to manufacture polyvinyl chloride; in organic syntheses. Has been used as refrigerant, spray can propellant.

Commercial grade contains 1-2% impurities: water, non-volatile residues, acetaldehyde, hydrogen chloride, hydrogen peroxide, and methyl chloride.

Specifications for a typical commercial product call for maxima in mg/kg by weight of the following impurities: unsaturated hydrocarbons - 10; acetaldehyde - 2; dichloro compounds - 16; water - 15 ; hydrogen chloride - 2; nonvolatiles - 200; iron - 0.4. Phenol at levels of 25-50 mg/kg by weight is used as a stabilizer to prevent polymerization.

The impurities /of vinyl chloride are as follows:/ acetic aldehyde 5 ppm, butane 8 ppm, 1,3-butadiene 10 ppm, chlorophene 10 ppm, diacetylene 4 ppm, vinyl acetylene 10 ppm, propine 3 ppm, methylchloride 100 ppm.

(1978) 4.08X10+11 G

(1983) 3.11X10+11 G

(1985) 4.61X10+11 G

(1987) 8.43X10+8 lb

(1996) 2.2 billion pounds

(1977) 6.05X10+5 G

(1982) 2.30X10+10 G

(1985) 5.89X10+10 G

(1986) 2.06X10+8 lb

2023: 15,000,000,000 - <20,000,000,000 lb

(1977) 2.72X10+12 G

(1982) 2.22X10+12 G

(1985) 4.30X10+12 G

(1986) 8.41X10+9 lb

For more U.S. Production (Complete) data for Vinyl chloride (15 total), please visit the HSDB record page.

MONOMER FOR POLY(VINYL CHLORIDE) RESINS, 85%; EXPORTS, 13.5%; MISCELLANEOUS (MOSTLY COPOLYMER USE), 1.5% (1982)

95% FOR POLYVINYL CHLORIDE HOMOPOLYMER AND COPOLYMER RESIN; 4% FOR SYNTHESIS OF METHYL CHLOROFORM; 1% FOR MISC APPLICATIONS (1972)

91% FOR POLYVINYL CHLORIDE

CHEMICAL PROFILE: Vinyl Chloride. Polyvinyl chloride, 91%; exports, 7%; other, including chlorinated solvents, 2%.

For more Consumption Patterns (Complete) data for Vinyl chloride (7 total), please visit the HSDB record page.

(1) Dehydrochlorination of ethylene dichloride; (2) reaction of acetylene and hydrogen chloride, either as liquids or gases.

Prepared from ethylene dichloride and alcoholic potassium; ... by halogenation of ethylene.

The catalytic hydrochlorination of acetylene is possible in either the gaseous or the liquid phase. The gas-phase reaction dominates in industrial processes. In this process the gaseous reactants are brought into contact with the catalyst at slightly increased pressure (0.1-0.3 MPa) and 100-250 °C (contact time 0.1-1 seconds) and then are quenched and partially liquefied. The reaction products are separated, recycled, or submitted to final purification.

In the crack gas processes for vinyl chloride manufacture, unpurified acetylene produced by high-temperature cracking of naphtha or methane is used. These processes are advantageous in that they do not require the cost-intensive separation of acetylene-ethylene mixtures. The crack gas is fed directly to the hydrochlorinator, and the acetylene is converted to vinyl chloride, which is then separated from the remaining constituents. Because all of the acetylene is consumed, the remaining ethylene is more easily separated, or it can be introduced to a direct chlorination stage, where it is chlorinated to 1,2-dichloroethane, which is subsequently cracked to vinyl chloride. Because almost equimolar amounts of ethylene and acetylene can be achieved in the crack gas, the process can be balanced for chlorine.

Grade: Technical, pure 99.9%

Vinyl chloride monomer is available commercially in cylinders or in bulk and is generally supplied as a liquid under pressure.

Liquefied gas, polymer grade

Chemical Classes -> Volatile organic compounds

Food Contaminant -> CONTAMINANT -> JECFA Functional Classes

Plastics Material and Resin Manufacturing

Ethene, chloro-: ACTIVE

Because it has been confirmed that vinyl chloride monomer is a human and animal carcinogen, sale of propellants and all aerosols containing it was banned in 1974.

The most important vinyl monomer.

Dichloroethane used for pyrolysis to vinyl chloride must be of purity greater than 99.5 wt % because cracking process is highly susceptible to inhibition. It must also be dry to prevent excessive corrosion.