Chloroethene, chloroethylene, 1-chloroethylene, ethylene monochloride, monochloroethylene, mono vinyl chloride, MVC, VC, VCM, and vinyl chloride monomer are all synonyms.

  • There is no risk of secondary contamination for people exposed only to vinyl chloride gas. It is possible for people whose clothing or skin is contaminated with pressurized liquid vinyl chloride to contaminate rescuers through direct contact or off-gassing.
  • Vinyl chloride is a highly flammable and explosive gas at all ambient temperatures. There is a mild, sweet smell to it. However, odor is not an adequate warning of hazardous concentrations.
  • Vinyl chloride is primarily absorbed through inhalation; absorption is rapid and nearly complete. Because vinyl chloride is a gas at room temperature, it is unlikely to be absorbed through the digestive system. It is not absorbed through the skin.

General Information


Gases such as vinyl chloride are colourless, highly flammable, and potentially explosive at room temperature. 

There is a faint sweet smell to it. Depending on the individual, vinyl chloride has an odor threshold of about 3,000 ppm in air. When confined under high pressure in special containers, vinyl chloride becomes liquefied. This is how it is shipped and handled. Hydrogen chloride, carbon monoxide, carbon dioxide, and phosgene are produced when vinyl chloride is burned or heated to a high enough temperature. Store vinyl chloride in a cool, dry, well-ventilated location, away from oxidizing materials. Stabilizers often contain phenol.

Routes of Exposure


Vinyl chloride is readily absorbed from the lungs by inhalation. As a result, its odor threshold is too high to provide an adequate warning of hazardous concentrations. Around 3,000 parts per million of vinyl chloride are detectable, and the OSHA PEL is 1 part per million (8-hour TWA). 

As a result, workers can be overexposed to vinyl chloride without being aware of it. Airborne concentrations of 8,000 ppm can cause dizziness after five minutes. Airborne levels above 20,000 ppm can cause drowsiness, loss of coordination, visual and auditory abnormalities, disorientation, nausea, headaches, and burning or tingling in the extremities. The central nervous system (CNS) and respiratory system can be affected by prolonged exposure to higher concentrations of vinyl chloride. In poorly ventilated or enclosed spaces, the gas can cause asphyxiation.

Because children have greater lung surface area: body weight ratios and greater minute volumes: and weight ratios, they may receive a higher dose of vinyl chloride. As a result of their short stature and the higher levels of vinyl chloride near the ground, they may be exposed to higher levels than adults in the same location.


Frostbite can be caused by direct contact with escaping compressed gas or liquid vinyl chloride, but systemic absorption is very low. Conjunctivitis and corneal irritation can result from direct ocular exposure to vinyl chloride vapor.


Vinyl chloride is a gas at room temperature, so it is unlikely to be ingested. 

A small amount can dissolve in other liquids, but at such a low concentration that acute toxicity is unlikely.


Vinyl chloride production levels in the United States continue to rise, with 14.98 billion pounds produced in 1995. Chlorinating ethylene produces 1,2-dichloroethane, which is then subjected to high pressures and temperatures to produce vinyl chloride. Vinyl chloride monomer is produced by pyrolysis (thermal cracking) of 1,2-dichloroethane.

 Most vinyl chloride is polymerized into polyvinyl chloride (PVC), a material used in automotive parts and accessories, furniture, packaging materials, pipes, wall coverings, and wire coatings. Other chlorinated compounds can also be produced from vinyl chloride, and mixed-monomer plastics can be produced from it as well. Once evaluated as a potential anaesthetic, it was used as a solvent, propellant, and refrigerant.

Standards and Guidelines

PEL (permissible exposure limit) = 1 ppm (averaged over an 8-hour shift).

NIOSH IDLH (immediately dangerous to life or health) = not yet determined; vinyl chloride is considered a human carcinogen.

Physical Properties


At room temperature, it is a colourless gas with a sweet odour; under pressure and when cooled, it becomes a colourless liquid.

The odor threshold varies significantly among individuals (about 3,000 ppm).

  • Boiling point 7.9 °F (-13.4 °C)
  • Freezing Point: -244.8 °F (-153.8 °C)
  • Specific gravity: 0.9106 (liquid) at 68 °F (20 °C) (water = 1.00)
  • Vapor pressure: 2,530 mm Hg at 68 °F (20 °C)
  • Vapor density: 2.16 (air = 1.00)
  • Water solubility: (1,100 to 2,763 mg/L at 77 °F [25 °C])
  • Flammability: highly flammable and explosive gas; flammability range is 3.6% to 33% (concentration in air)
  • Flashpoint: -108.4 °F (-78 °C)


When peroxidation occurs (e.g., when heated, when exposed to sunlight, or when mixed with air and contaminants), vinyl chloride self-polymerizes explosively. Aluminium, copper, iron, and steel should not be in contact with oxygen or strong oxidizing agents.

Health Effects

  • Acute exposure to vinyl chloride primarily affects the central nervous system. Signs and symptoms include dizziness, ataxia, inebriation, fatigue, numbness and tingling of the extremities, visual disturbances, coma, and death.
  • Acute exposure to vinyl chloride primarily affects the central nervous systemspiratory tract. Escaping compressed gas or liquid can cause frostbite or irritation of the skin and eyes.
  • Acute exposure to vinyl chloride primarily affects the central nervous systemic, neurologic or behavioural symptoms, and changes to the skin and bones of the hand.
  • Acute exposure to vinyl chloride primarily affects the central nervous system interaction of the parent compound with neural membranes. Other effects appear to be caused by the interaction of reactive intermediates with macromolecules.

Acute Exposure

Exposure to vinyl chloride primarily affects the central nervous system on lipids and protein components of neural membranes that interrupt signal transmission. Reactive metabolic intermediates may also cause specific target organ toxicity by covalently bonding to tissue or initiating destructive chain reactions such as lipid peroxidation. 

As a result of acute exposure to vinyl chloride, the central nervous system is the primary target of symptom onset. Vinyl chloride is rapidly metabolized and the metabolites are eliminated in the urine.

CNS is the primary target of vinyl chloride acute exposure adults. Different protocols for managing their care may be needed.