Absorption, Distribution and Excretion
Vinyl chloride dissolved in oil or water is absorbed very rapidly after gavage in rats. Peak serum vinyl chloride concentrations are observed within 10 minutes of administration. Absorption of vinyl chloride in the human lungs also appears to be rapid, and the percentage absorbed is independent of the inhaled concentration. …In adult male volunteers wearing gas masks exposed to 2.9, 5.8, 11.6, or 23.1 ppm (7.5, 15, 30, or 60 mg/m³) of vinyl chloride for 6 hours, an average of approximately 42% of the inhaled vinyl chloride remained in the body. Lung absorption is partly dependent on the blood/air partition coefficient, which is 1.16 for vinyl chloride. Animal data indicate that vinyl chloride is readily and rapidly absorbed by the lungs and gastrointestinal tract. Conversely, skin absorption of atmospheric vinyl chloride may be insignificant. In monkeys, only 0.023–0.031% of the total available vinyl chloride was absorbed via the skin, while in rats, almost all of it was absorbed after a single oral dose of vinyl chloride aqueous solution (44–92 mg/kg body weight). When rats were exposed to vinyl chloride at initial concentrations below 260 mg/m³ (100 ppm), approximately 40% of the inhaled (14)C-vinyl chloride was absorbed by the lungs. The main elimination routes of vinyl chloride and its metabolites are exhalation and urinary excretion, respectively. Therefore, thiodiglycolic acid has been reported as the main vinyl chloride metabolite detected in the urine of workers exposed to vinyl chloride. The level of thiodiglycolic acid in urine is positively correlated with the concentration of vinyl chloride in the air (concentration > 5 ppm).
For more data on the absorption, distribution, and excretion (complete) of vinyl chloride (18 in total), please visit the HSDB record page.

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Metabolism/Metabolites
Vinyl chloride is primarily metabolized rapidly in the liver, and this metabolism is saturated. The first step in vinyl chloride metabolism is oxidation, primarily mediated by human cytochrome P450 (CYP) 2E1, to generate highly reactive vinyl chloride oxide, which can spontaneously rearrange to chloroacetaldehyde. Vinyl chloride oxide and chloroacetaldehyde bind to glutathione (GSH), ultimately producing the major urinary metabolites N-acetyl-S-(2-hydroxyethyl)cysteine and thiodiglycolic acid. Vinyl chloride oxide and chloroacetaldehyde can be detoxified into glycolaldehyde by microsomal epoxide hydrolase (mEH) and into the urinary metabolite chloroacetic acid by aldehyde dehydrogenase 2 (ALDH2), respectively. After oral administration of (14)C-vinyl chloride, (14)C-carbon dioxide, (14)C-urea, and glutamate were identified as minor metabolites. After rats inhaled (14)C-vinyl chloride, three urinary metabolites were detected: N-acetyl-S-(2-hydroxyethyl)cysteine, thiodiglycolic acid, and an unidentified substance.
The major (14)C urinary metabolites following oral administration of (14)C-vinyl chloride in male rats were N-acetyl-S-(2-hydroxyethyl)cysteine, N-acetyl-S-vinylcysteine, and thiodiglycolic acid, along with small amounts of urea, glutamic acid, chloroacetic acid, and trace amounts of methionine and serine. The proportions of the three major metabolites in rat urine appeared to be unaffected by dose or route of administration.
For more complete data on the metabolism/metabolites of vinyl chloride (10 metabolites in total), please visit the HSDB record page.
Known human metabolites of vinyl chloride include 2-chloroethylene oxide.
Vinyl chloride is primarily absorbed through inhalation or ingestion and rapidly distributed throughout the body. It is primarily metabolized in the liver by cytochrome P-450 monooxygenases, first producing vinyl chloride oxide, then chloroacetaldehyde, both of which are the major toxic metabolites. Chloroacetaldehyde is further converted to chloroethanol and monochloroacetic acid. Detoxification occurs in synergy with glutathione, primarily producing thiodiglycolic acid, which is excreted in the urine. High doses of vinyl chloride can also be exhaled. (L3, T5)

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Biological half-life
Based on limited data: fairly rapid; [TDR, p. 1224]
The pulmonary elimination patterns of 10 ppm and 1000 ppm vinyl chloride exhibit similar first-order kinetics, with half-lives of 20.4 min and 22.4 min, respectively. The initial half-lives of ¹⁴C radioactive material in urine are 4.6 h and 4.1 h, respectively.

Toxicity Summary
Identification and Uses: Vinyl chloride is a colorless gas or liquid (below 77 degrees Fahrenheit). It is used in the plastics industry to produce polyvinyl chloride (PVC) and also in organic synthesis. It has been used as a refrigerant and aerosol can propellant. Human Studies: Vinyl chloride can cause hepatic angiosarcoma and hepatocellular carcinoma. Previous occupational exposure to concentrations of up to several hundred ppm of vinyl chloride, lasting from one month to three years, has been associated with the development of "vinyl chloride disease." Vinyl chloride disease is characterized by acrolysis, a disease characterized by osteolytic lesions of the bones (primarily the fingers); scleroderma of the fingers with thickening of the dermis; and Raynaud's disease-like symptoms, manifested as reversible arteriolar constriction leading to numbness, pallor, and cyanosis of the fingers. The association between acrolysis and vinyl chloride exposure is almost entirely based on case reports, and it is estimated that less than 3% of workers involved in vinyl chloride polymerization are affected. In patients with long-term occupational exposure, neurological disorders include sensorimotor polyneuropathy, trigeminal sensory neuropathy, minimal pyramidal tract signs, and cerebellar and extrapyramidal motor disorders. Mental disorders include neurasthenia or depression. Insomnia and loss of sexual function are also common. A significant proportion of patients exhibit pathological electroencephalogram (EEG) changes. Thirty-six workers with long-term industrial exposure to vinyl chloride leading to liver injury were found to have chronic liver disease related to porphyrin metabolism. Pathological porphyrinuria, especially secondary coprophyrinuria progressing to subclinical chronic hepatic porphyria, is a reliable pathobiochemical marker for identifying vinyl chloride-induced liver injury. Major immunological abnormalities reported in vinyl chloride poisoning patients include hyperimmunoglobulinemia (polyclonal elevation of IgG), cryoglobulinemia, cryofibrinogenemia, and complement activation. Vinyl chloride is an occupational carcinogen that can cause micronucleus formation in human cells. Compared to controls, peripheral blood lymphocytes cultured from 57 male workers showed a significantly increased number of chromosomal abnormalities. Sister chromatid exchange is a more sensitive endpoint indicator of biological responses. Animal studies: Brief (30 minutes) exposure to vinyl chloride at concentrations of 100,000 to 400,000 ppm can cause death in rats, guinea pigs, and mice. Symptoms of poisoning in rats and mice include muscle incoordination and convulsions, central nervous system depression, and respiratory failure. Acute exposure to high concentrations (375–700 mg/L) of vinyl chloride gas in rats, guinea pigs, and rabbits resulted in intense salivation and lacrimation. Contact with liquid vinyl chloride on the skin or eyes can freeze tissue and cause chemical burns during evaporation, damaging underlying tissues. Guinea pigs exposed to 65,000 mg/m³ of vinyl chloride for 90 minutes developed severe central nervous system depression. At this dose, ataxia was observed as early as 5 minutes after exposure. The anesthetic effect of vinyl chloride has also been observed in dogs and mice. Researchers reported that rats and mice exposed to vinyl chloride at a concentration of 260,000 mg/m³ for 30 minutes developed severe central nervous system depression. Prior to the onset of central nervous system depression, increased motor activity appeared 5 minutes after exposure, followed by limb twitching after 10 minutes, ataxia after 15 minutes, and tremor after 15 minutes. Rats exposed to a concentration of 130,000 mg/m³ for 60 minutes developed ataxia, initially exhibiting hyperactivity, but without central nervous system depression. Forty rabbits were exposed to vinyl chloride (10,000 ppm) in the air for 4 hours a day, 5 days a week, for 12 months. During the 9-15 month exposure period, 12 cases of cutaneous acanthoma and 6 cases of lung adenocarcinoma were observed. Twenty control rabbits did not develop similar tumors during the 15-month observation period. Rats were exposed to 10,000 ppm vinyl chloride in the air for 4 hours daily, 5 days a week, for 5 weeks, starting at 13 weeks of age (n=120 per group) or 1 day of age (n=43 and 46 per group, respectively). The observation period was 135 weeks. One case of hepatocellular carcinoma was reported in aged rats, and 10 cases of angiosarcoma and 15 cases of hepatocellular carcinoma were found in newborn rats. No liver tumors were reported in any of the 249 control rats. Vinyl chloride was administered daily for 7 hours from days 6 to 18 of gestation in mice, rats, and rabbits. The conclusion was that although maternal toxicity was observed, vinyl chloride itself did not cause significant embryo- or fetal toxicity and was not teratogenic in any species at the tested concentrations. Vinyl chloride significantly increased the frequency of recessive lethal mutations in male Drosophila melanogaster. Vinyl chloride has been reported to have mutagenic activity against yeasts (Schizosaccharomyces and Saccharomyces cerevisiae) under metabolically activated conditions. In host-mediated mutagenicity studies, vinyl chloride was mutagenic to fissile yeast after oral administration of 700 mg/kg to mice. Using Salmonella test strains, vinyl chloride was directly mutagenic at an airborne concentration of 20% (v/v) (200,000 ppm) without metabolic activation. Metabolic activation enhanced the mutagenic response. However, in systems using Salmonella Typhimurium strains TA1536, TA1537, and TA1538, 20% (v/v) vinyl chloride was inactive. Ecotoxicity studies: In exposure experiments on Daphnia magna, results showed that vinyl chloride affected the regulation of genes related to glutathione S-transferase (GST), juvenile hormone esterase (JHE), and vitelline outer membrane protein (VMO1). Vinyl chloride poisoning exhibits characteristics of many autoimmune diseases. This is thought to be due to the binding of active vinyl chloride intermediate metabolites to immunoglobulins, altering protein structure and initiating an immune response. Metabolites of vinyl chloride, especially vinyl chloride oxides, are mutagenic, and their mechanism of action is through covalent binding to DNA. This forms cyclic vinyl adducts, leading to base pair switching and DNA cross-linking during transcription. Metabolites may also cause oxidative stress and affect tumor suppressor genes, as vinyl chloride is known to cause specific mutations in the p53 and Ki-ras genes. Vinyl chloride metabolites are also thought to have hepatotoxic effects by covalently binding to liver proteins, leading to cytotoxicity. (L3, A65)

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Toxicity Data
LC50 (rat) = 180,000/15m
LD50: 500 mg/kg (oral, rat) (T15)

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Interactions
Twenty-five Sprague Dawley rats were randomly divided into groups and exposed to vinyl chloride (500 and 2,500 ppm) for 7 hours daily from day 6 to day 15 of gestation. In the high-dose group, some mice drank water containing 15% ethanol from day 6 to 15 of gestation. Rats were sacrificed on day 21 of gestation, and the internal organs and skeletal abnormalities of the fetuses were examined. The corpus luteum, implantation, and intrauterine mortality of the mothers were examined. In the highest-dose group, both absolute and relative liver weight were significantly increased. This effect was more pronounced in the groups co-exposed to ethanol. The number of pups, the number of implantation sites per mother, or the rate of resorption were not significantly affected in any of the exposure groups. In the 2500 ppm vinyl chloride combined with ethanol group, fetal weight and crown-rump length were significantly reduced, but this was not observed in the group exposed to 2500 ppm vinyl chloride alone. However, a decrease in fetal weight was observed in rats exposed to 500 ppm vinyl chloride. Unilateral and bilateral uterine dilatation were observed in pups born to rats exposed to 2500 ppm vinyl chloride. No increased incidence of skeletal malformations was observed in pups born to rats exposed to 2500 ppm vinyl chloride. However, rats simultaneously exposed to 2500 ppm vinyl chloride and ethanol showed a significantly increased incidence of cervical vertebral osteophytes and vertebral body loss.
15 to 20 New Zealand rabbits per group were exposed to 500 ppm or 2500 ppm vinyl chloride for 7 hours daily from day 6 to day 18 of gestation. Some rabbits in the high-dose group also had 15% ethanol added to their drinking water (from day 6 to day 18 of gestation). On day 29 of gestation, pregnant does were sacrificed, and the internal organs and skeletal abnormalities of the fetuses were examined. The corpus luteum, implantation status, and intrauterine mortality of the does were also examined. Rabbits exposed to 2500 ppm vinyl chloride alone did not experience any effect on the weight gain, liver weight, or food consumption of the does; however, rabbits exposed to the mixture of vinyl chloride and ethanol showed a significant decrease in both weight gain and food consumption. Exposure to vinyl chloride alone did not change the rate of absorption, but exposure to the mixture of vinyl chloride and ethanol resulted in a significant increase in the amount absorbed. There were no differences in fetal weight or crown-rump length among the exposed groups. Delayed ossification was observed at all dose levels. Sprague-Dawley male rats were given either water containing 5% ethanol or plain water for the first 4 weeks before starting inhalation of 600 ppm vinyl chloride (4 hours daily, 5 days a week, for 12 months). Sixty weeks after initial exposure to vinyl chloride, the incidence of liver tumors was 75% in the vinyl chloride-ethanol group and 38% in the vinyl chloride-only group. Vinyl chloride, when used in combination with vinylidene chloride, has a protective effect against hepatotoxicity. For more complete data on vinyl chloride interactions (8 items total), please visit the HSDB record page. Non-human toxicity values: Oral LD50 in rats: 500 mg/kg

Vinyl chloride is a colorless, flammable, and unstable gas with a slightly sweet taste. It is a synthetic substance and not naturally occurring. Vinyl chloride can be produced by the decomposition of substances such as trichloroethane, trichloroethylene, and tetrachloroethylene. Vinyl chloride is used to manufacture polyvinyl chloride (PVC). PVC is used to manufacture various plastic products, including pipes, wire and cable coatings, and packaging materials. Vinyl chloride is also known as vinyl chloride, vinyl chloride, and monochloroethylene. According to California labor laws, vinyl chloride may be carcinogenic. Vinyl chloride is a colorless gas with a sweet taste and is flammable. It is usually transported as a liquefied gas, relying on its own vapor pressure. Contact with unsealed liquids can cause frostbite due to evaporative cooling. Leaks may be liquid or vapor. Vapors are heavier than air and can cause asphyxiation due to air displacement. Prolonged exposure to fire or high temperatures may cause containers to rupture violently and spray out. It is a suspected carcinogen. It is used in the manufacture of plastics, adhesives, and other chemicals. Vinyl chloride is a monohalogenated ethylene, where one hydrogen atom in the ethylene molecule is replaced by a chlorine atom. It is a carcinogen. It is a type of vinyl chloride compound, a monohalogenated vinyl group, and a gaseous molecular entity. Vinyl chloride is a chlorinated hydrocarbon that exists as a colorless, highly flammable gas with a slightly sweet taste. When heated, it decomposes, releasing toxic gases such as carbon dioxide, carbon monoxide, hydrogen chloride, and phosgene. Vinyl chloride is primarily used to manufacture polyvinyl chloride (PVC), which is then used to produce plastics. Exposure to this substance can affect the central and peripheral nervous systems and cause liver damage. Long-term exposure to vinyl chloride can lead to a range of symptoms characterized by Raynaud's phenomenon, joint and muscle pain, and scleroderma-like skin changes. Vinyl chloride is a known human carcinogen, associated with an increased risk of liver cancer (primarily hepatic angiosarcoma), but also linked to brain cancer, lung cancer, and cancers of the lymphatic and hematopoietic systems. (NCI05) Vinyl chloride is a man-made organic compound formed by the decomposition of trichloroethane, trichloroethylene, and tetrachloroethylene, among other substances. Its monomeric form is highly toxic and therefore primarily used in polymer production. At room temperature, it is a flammable, colorless, sweet-tasting gas, but it is easily condensed and is usually stored in liquid form. It is one of the components of cigarettes. (L3)
Vinyl chloride was once used as an aerosol propellant and is also a starting material for polyethylene resin. Toxicity studies have shown that vinyl chloride can cause a variety of adverse reactions, especially liver tumors.
See also: Polyvinyl chloride (related substances).
Mechanism of Action

The carcinogenicity of vinyl chloride occurs through a genotoxic pathway, the mechanism of which is well understood. Vinyl chloride is metabolized into an active metabolite, possibly vinyl chloride oxide, which is considered the final carcinogenic metabolite of vinyl chloride. This active metabolite then binds to DNA, forming DNA adducts, which, if not repaired, eventually lead to mutations and tumor formation.
A large amount of data indicates that vinyl chloride is a genotoxic carcinogen. After being activated by CYP2E1 metabolism to vinyl chloride oxide, vinyl chloride exerts a variety of genotoxic effects (including gene mutations and chromosomal aberrations) in various organisms, including bacteria, yeast, cultured mammalian cells, fruit flies, rodents, and humans. Among the VC-induced mutations, base pair substitution appears to be the most common. VC exhibits transformative activity in cultured mammalian (rodent) cells in the presence of an activated system. In vitro studies have shown that metabolically activated VC and its electrophilic metabolites CEO and CAA (chloroacetaldehyde) can alkylate nucleic acid bases. The major DNA adduct 7-OEG formed by VC and CEO is not mutagenic. Conversely, four minor adducts, namely εA, εC, N2,3-εG, and 1,N2-εG, are mutagenic, primarily inducing base pair substitution mutations and a small number of frameshift mutations.

(C2-H3-CL)X-

62.4987

64.008

9002-86-2

26793-37-3;25037-47-2;9002-86-2

6338

Colorless gas or liquid (below 77 degrees F) [Note: Shipped as a liquefied compressed gas]

1.4 g/mL at 25 °C(lit.)

-245 °F (NTP, 1992)
-153.84 °C
-154 °C
-256 °F
-256 °F

1.245

0

0

0

3

10.3

0

ClC([H])=C([H])[H]

BZHJMEDXRYGGRV-UHFFFAOYSA-N

InChI=1S/C2H3Cl/c1-2-3/h2H,1H2

chloroethene

Chloroethylene homopolymerise; Polyvinyl chloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)