Medical Management Guidelines for Vinyl Chloride
(C[SUB]2[/SUB]H[SUB]3[/SUB]Cl)
CAS# 75-01-4
UN# 1086
PDF Versionpdf icon[250 KB]
Synonyms include chloroethene, chloroethylene, 1-chloroethylene, ethylene monochloride, monochloroethylene, monovinyl chloride, MVC, VC, VCM, and vinyl chloride monomer.
- Persons exposed only to vinyl chloride gas pose no risk of secondary contamination. Persons whose clothing or skin is contaminated with pressurized liquid vinyl chloride can secondarily contaminate rescuers by direct contact or through off-gassing of vapor.
- At all ambient temperatures, vinyl chloride is an extremely flammable and potentially explosive gas that is heavier than air. It has a mild, sweet odor, but odor is not an adequate warning of hazardous concentrations.
- Inhalation is the major route of vinyl chloride exposure; absorption is rapid and nearly complete. Gastrointestinal absorption is unlikely as vinyl chloride is a gas at room temperature. Dermal absorption is negligible.
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General Information
Description
At room temperature, vinyl chloride is a colorless, highly flammable, potentially explosive gas. It has a faint sweet odor. The odor threshold for vinyl chloride is about 3,000 ppm in air, depending on the individual. When confined under high pressure in special containers, vinyl chloride exists in a liquefied state. It is shipped and handled this way. When burned or heated to a high enough temperature, vinyl chloride decomposes to hydrogen chloride, carbon monoxide, carbon dioxide, and traces of phosgene. Vinyl chloride should be stored in a cool, dry, well ventilated location, separate from oxidizing materials and accelerants. Phenol is often added as a stabilizer.
Routes of Exposure
INHALATION
Inhalation is the primary route of exposure, and vinyl chloride is readily absorbed from the lungs. Its odor threshold is too high to provide an adequate warning of hazardous concentrations. The odor of vinyl chloride becomes detectable at around 3,000 ppm and the OSHA PEL is 1 ppm (8-hour TWA). Therefore, workers can be overexposed to vinyl chloride without being aware of its presence. A 5-minute exposure to airborne concentrations of 8,000 ppm can cause dizziness. As airborne levels increase to 20,000 ppm, effects can include drowsiness, loss of coordination, visual and auditory abnormalities, disorientation, nausea, headache, and burning or tingling of the extremities. Exposure to higher concentrations of vinyl chloride for longer durations can cause death, presumably due to central nervous system (CNS) and respiratory depression. The gas is heavier than air and can cause asphyxiation in poorly ventilated or enclosed spaces.
Children exposed to the same levels of vinyl chloride as adults may receive a larger dose because they have greater lung surface area:body weight ratios and increased minute volumes:weight ratios. In addition, they may be exposed to higher levels than adults in the same location because of their short stature and the higher levels of vinyl chloride found nearer to the ground.
SKIN/EYE CONTACT
Direct skin contact with escaping compressed gas or liquid vinyl chloride can cause frostbite injury, but systemic absorption is negligible. Direct ocular exposure to vinyl chloride vapor can cause localized burns or irritation of the conjunctiva and cornea.
INGESTION
Ingestion of vinyl chloride is unlikely because it is a gas at room temperature. Small amounts can dissolve in other liquids, but in such small concentrations that acute toxicity is unlikely.
Sources/Uses
Annual production levels of vinyl chloride continue to increase, with 14.98 billion pounds produced in the United States in 1995. Vinyl chloride is produced by chlorinating ethylene to produce 1,2-dichloroethane, which is then subjected to high pressures and temperatures. This causes pyrolysis (thermal cracking) of the 1,2-dichloroethane to produce the vinyl chloride monomer. Most vinyl chloride is polymerized to form polyvinyl chloride (PVC), a material used to manufacture automotive parts and accessories, furniture, packaging materials, pipes, wall coverings, and wire coatings. Vinyl chloride is also used as an intermediate in the production of other chlorinated compounds and as a component in mixed-monomer plastics. Historically, it was used as a solvent, propellant, and refrigerant, and it was once evaluated as a potential anesthetic.
Standards and Guidelines
OSHA PEL (permissible exposure limit) = 1 ppm (averaged over an 8-hour workshift)
NIOSH IDLH (immediately dangerous to life or health) = not yet determined; vinyl chloride is treated as a human carcinogen.
Physical Properties
Description: colorless gas with a sweet odor at room temperature; colorless liquid when contained under pressure or cooled.
Warning properties: inadequate (odor threshold of about 3,000 ppm; varies significantly among individuals)
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)
Flash point: -108.4 °F (-78 °C)
Incompatibilities
Vinyl chloride self-polymerizes explosively if peroxidation occurs (e.g., if heated, exposed to sunlight, or mixed with air and contaminants). Avoid contact with oxygen, strong oxidizing agents, aluminum, copper, iron, and steel.
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Health Effects
- The primary target of vinyl chloride acute exposure is the CNS. Signs and symptoms include dizziness, ataxia, inebriation, fatigue, numbness and tingling of the extremities, visual disturbances, coma, and death.
- Vinyl chloride can irritate the eyes, mucous membranes, and respiratory tract. Escaping compressed gas or liquid can cause frostbite or irritation of the skin and eyes.
- Chronic exposure can cause permanent liver injury and liver cancer, neurologic or behavioral symptoms, and changes to the skin and bones of the hand.
- Vinyl chloride's acute CNS effects are likely to be caused by interaction of the parent compound with neural membranes. Other effects appear to be caused by interaction of reactive intermediates with macromolecules.
Acute Exposure
Vinyl chloride is thought to depress the CNS via a solvent effect on lipids and protein components of neural membranes that interrupts 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. There may be a latent period of hours to days between exposure and symptom onset. Vinyl chloride is rapidly metabolized and the metabolites are eliminated in the urine.
Children do not always respond to chemicals in the same way that adults do. Different protocols for managing their care may be needed.
CNS
The CNS is the primary target of vinyl chloride acute toxicity. The symptoms reported most commonly stem from the anesthetic properties of vinyl chloride; these symptoms include dizziness, ataxia, fatigue, drowsiness, headache, and loss of consciousness. With inhalation exposure, signs and symptoms increase in severity over a range of 8,000 to 20,000 ppm in air. Exposure to higher concentrations for longer durations can cause death, presumably due to CNS and respiratory depression. Sublethal CNS effects resolve quickly when the victim is removed from further exposure.
RESPIRATORY
Vinyl chloride gas inhalation can cause mild respiratory tract irritation, wheezing, and chemical bronchitis. These effects are transient and resolve quickly following removal from exposure. Death may result from respiratory depression.
Exposure to certain chemicals can lead to Reactive Airway Dysfunction Syndrome (RADS), a chemically- or irritant-induced type of asthma.
Children may be more vulnerable because of relatively increased minute ventilation per kg and failure to evacuate an area promptly when exposed.
Hydrocarbon pneumonitis may be a problem in children.
CARDIOVASCULAR
Vinyl chloride may lower the myocardial threshold to the dysrhythmogenic effects of catecholamines; it might predispose patients to ventricular ectopy and fibrillation. In experimental animals, exposure to vinyl chloride has led to ECG abnormalities, including ventricular ectopy, heart block, and T-wave inversions.
DERMAL
Exposure to escaping compressed gas or liquid can cause frostbite injury with redness, blistering, and scaling. Contact dermatitis has also been reported.
OCULAR
Exposure to escaping compressed gas or liquid can cause frostbite injury with corneal and conjunctival irritation or burns. High concentrations of vapor can cause eye irritation.
GASTROINTESTINAL
Nausea, vomiting, diarrhea, and epigastric pain have been reported with ingestion.
POTENTIAL SEQUELAE
Patients exposed to significant amounts of vinyl chloride may not develop symptoms immediately and should be monitored for CNS and respiratory depression and liver and kidney damage for 24 to 48 hours.
Chronic Exposure
Prolonged absorption of vinyl chloride can induce hepatotoxicity and hepatic cancers, including angiosarcoma. Portal hypertension and cirrhosis can occur. Vinyl chloride toxicity is thought to result from the binding of reactive epoxide metabolites to hepatic DNA. Other effects of chronic exposure include sensory-motor polyneuropathy; pyramidal, extrapyramidal, and cerebellar abnormalities; neuropsychiatric symptoms such as sleep disorders, loss of libido, headaches, and irritability; EEG alterations; and immunopathologic phenomena such as purpura and thrombocytopenia. Vinyl chloride disease is a syndrome consisting of Raynaud's phenomenon, acroosteolysis (dissolution of the bones of the terminal phalanges and sacroiliac joints), and scleroderma-like skin changes.
CARCINOGENICITY
The U.S. Department of Health and Human Services (DHHS) and the International Agency for Research on Cancer (IARC) have classified vinyl chloride as a known human carcinogen. Vinyl chloride has caused angiosarcoma of the liver in heavily exposed
REPRODUCTIVE AND DEVELOPMENTAL EFFECTS
Vinyl chloride is included in
Reproductive and Developmental Toxicants, a 1991 report published by the U.S. General Accounting Office (GAO) that lists 30 chemicals of concern because of widely acknowledged reproductive and developmental consequences. However, there is no conclusive evidence of reproductive or developmental effects in humans. A few case reports describe decreased libido or fertility in men with chronic occupational exposure, and some animal studies also support this finding. Some studies in experimental animals have reported developmental toxicity associated with high-dose exposures, but vinyl chloride is not considered a developmental toxicant.
Special consideration regarding the exposure of pregnant women is warranted, since vinyl chloride has been shown to be a genotoxin; thus, medical counseling is recommended for the acutely exposed pregnant women.
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https://wwwn.cdc.gov/TSP/MMG/MMGDetails.aspx?mmgid=278&toxid=51
