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CHEMINFO Record Number: 206
CCOHS Chemical Name: Vinyl chloride

Ethylene monochloride
Vinyl chloride monomer
Vinyl C monomer

Chemical Name French: Chlorure de vinyle
CAS Registry Number: 75-01-4
UN/NA Number(s): 1086
RTECS Number(s): KU9625000
EU EINECS/ELINCS Number: 200-831-0
Chemical Family: Halogenated aliphatic hydrocarbon / unsaturated halogenated aliphatic hydrocarbon / haloalkene / monohaloalkene / monochloroalkene / halogenated ethylene / monochloroethylene / vinyl halide / vinyl chloride
Molecular Formula: C2-H3-Cl
Structural Formula: CH2=CH-Cl


Appearance and Odour:
Colourless gas with a pleasant, sweet, ethereal odour; colourless liquid below -14 deg C (7 deg F) (22,23)

Odour Threshold:
Reported values vary widely; 10-20 ppm (method not given) (24); 2000 ppm (method not given) (8); 3000 ppm (method not given) (4)

Warning Properties:
POOR - reported values vary widely and are above the TLV

Vinyl chloride is available in various grades and typically has a minimum purity of 99.9 mole percent in the liquid phase. It is shipped as a liquefied compressed gas under its own vapour pressure of 234 kPa at 21.1 deg C (70 deg F).(13,22,25) It may contain small amounts of acetylene, acetaldehyde, 1,3-butadiene, 1- and 2-butene, ethylene, ethylene dichloride, propylene, vinyl acetylene, methyl chloride, hydrogen chloride or water as impurities.(26,27) It is normally stabilized (inhibited) with phenol (40-100 ppm) to prevent polymerization.(22,23,27)

Uses and Occurrences:
It is used mainly for the manufacture of polyvinyl chloride (PVC) plastics and resins, and vinyl chloride copolymers. It is used as a comonomer with vinyl acetate or vinylidene chloride in the production of resins. It is also used for the production of chlorinated solvents, such as methyl chloroform and 1,1,1-trichloroethane, and other chemicals; and in the production of adhesives.(22,27,28)


Colourless gas with a pleasant, sweet, ethereal odour; colourless liquid below -14 deg C (7 deg F). EXTREMELY FLAMMABLE GAS. Gas is heavier and colder than air and may spread long distances. Distant ignition and flashback are possible. Can decompose at high temperatures forming toxic gases such as hydrogen chloride, phosgene and acetylene. COMPRESSED GAS. Confined space hazard. DANGEROUSLY REACTIVE. Gas or uninhibited liquid may polymerize explosively when exposed to air, sunlight (ultraviolet light), elevated temperatures, and the presence of incompatible materials, such as peroxides and other oxidizing materials. May form explosive peroxides in the presence of air or oxygen. Mild central nervous system depressant. Very high concentrations may cause headache, nausea, dizziness, drowsiness, incoordination and confusion. May cause frostbite. CANCER HAZARD - can cause cancer, based on human information. MUTAGEN - may cause genetic damage.


Effects of Short-Term (Acute) Exposure

Irritation and odour do not provide adequate warning of exposure to low concentrations of vinyl chloride. Current occupational exposure limits are 1-5 ppm. Very high concentrations (greater than 8000 ppm) cause depression of the central nervous system (CNS). The most commonly observed CNS effects are weakness, dizziness, nausea, fatigue, headache, incoordination and loss of consciousness. Severe exposures can result in death. Studies with volunteers show that the earliest effects (dizziness) begin to appear at 8000 ppm.(1) Significantly higher concentrations (16000 to 25000 ppm) have resulted in dizziness, lightheadedness, headaches and disorientation.(1,2) Even higher exposures would produce unconsciousness and death. Two deaths have been reported from short-term exposure to vinyl chloride in confined spaces.(3)
Relatively high vinyl chloride concentrations (a few hundred ppm and higher) are associated with significant long-term health effects. Refer to "Effects of Long-Term (Chronic) Exposure" below for additional information.

Skin Contact:
Frostbite can occur due to the extremely rapid evaporation of the liquid.(4) Symptoms of mild frostbite include numbness, prickling and itching in the affected area. Symptoms of more severe frostbite include a burning sensation and stiffness of the affected area. The skin may become waxy white or yellow. Blistering, tissue death and gangrene may also develop in severe cases.
There is one case report of a worker who had the liquefied gas sprayed on his hands. Initially his hands felt numb, but within a short period of time there was marked redness and swelling which developed into second degree burns.(4)

Eye Contact:
Frostbite can occur due to the extremely rapid evaporation of the liquid. Permanent eye damage or blindness could result. In one fatal inhalation case, there were local burns to the eye from the liquefied gas sprayed out of an open valve.(4) Eye irritation has not been observed in animals exposed to very high gas concentrations.

Ingestion is not an applicable route of exposure for gases.

Effects of Long-Term (Chronic) Exposure

Numerous human population studies and case reports have led to the identification of significant long-term health effects, which are sometimes collectively referred to as "Vinyl chloride disease". Most of these effects resulted from inhalation exposures which occurred before major reductions in workplace exposures during the 1970's. While it is difficult to accurately estimate actual exposures during this time, typical concentrations may have been several hundred ppm, with peak exposures of several thousand ppm.(5) Current occupational exposure limits are typically in the range of 1 to 5 ppm. Liver/spleen, vascular, skeletal, immune system, skin, respiratory, blood and nervous system effects have all been associated with long-term, higher level vinyl chloride exposure.

Nervous System:
Signs of damage to the nervous system in the extremities (the hands, arms, legs and feet) have been observed some studies of vinyl chloride workers. The condition is referred to as peripheral neuropathy. The most frequently reported symptoms are tingling/numbness and warmth in the hands and feet, weakness, and pain in the fingers. In one study, slight peripheral neuropathy was observed in 70% of a group of exposed workers. Other studies have involved workers who also had Raynaud's Phenomenon and/or acroosteolysis. It is possible that some of the reported symptoms may be related to these disorders rather than peripheral neuropathy and the disorders are most probably inter-related.(4)

Lungs/Respiratory System:
The available information gives conflicting results. Several studies found no increase in respiratory disease while other studies and case reports have found effects, such as an increased incidence of emphysema, pulmonary fibrosis and abnormal X-ray results. No conclusions can be drawn as there are limitations to these studies, such as exposure to other chemicals and the inclusion of smokers.(4,6,8) A recent study of a large group found a statistically significant increase in deaths due to emphysema.(9)

Skin effects have been observed in a small percentage of vinyl chloride workers in several studies. The skin becomes thick and has a whitish, scaly appearance, possibly due to collagen deposits. These effects are by far most often observed on the skin of the hands and wrists. Skin effects have almost exclusively been observed in the same workers who have Raynaud's Phenomenon and/or acroosteolysis.(4,5,7,8)

Heart/Blood Vessels:
(RAYNAUD'S PHENOMENON/SYNDROME): Raynaud's Phenomenon is a condition where the fingers become white and numb following exposure to cold. These symptoms occur because the walls of arteries in the fingers become thick, resulting in impaired blood circulation. Raynaud's phenomenon has most commonly been seen in workers repeatedly and heavily exposed to vinyl chloride while cleaning reactor tanks. Although only a small percentage of vinyl chloride workers have developed Raynaud's Phenomenon, the incidence is higher than in unexposed workers. Some reports indicate that Raynaud's Phenomenon gradually disappears upon removal from exposure.(4-8)

Digestive System:
No conclusions can be drawn from the limited information available. In one study, a very small number of workers with pre- existing liver dysfunction also reported symptoms such as nausea, abdominal distention and heartburn.(10) Another study reported that 99/354 workers had a history of gastritis and ulcers. Some of these workers also had liver and/or spleen enlargement.(11) The results were not compared to a control group.

Severe and characteristic liver damage and liver abnormalities have been reported in a large number of studies. The incidence and severity of the liver effects increases with the concentration and duration of exposure. Animal studies indicate that significant liver changes can be seen at concentrations as low as 50 ppm with a 6 month exposure. Human liver effects may not be recognized early because the changes are not necessarily reflected in standard liver function tests. Enlargement of the spleen (splenomegaly) has also been reported in some studies.(4-8)

Blood/Blood Forming System:
Most studies have reported a mild to severe increase in the number of blood platelets (thrombocytopenia). Some other studies have shown increased levels of plasma proteins.(4,6) In a study of female workers exposed to 0.2 to 130.7 ppm vinyl chloride, a reduced platelet count was observed in the early part of pregnancy. This effect was not seen by the end of pregnancy, following a period of no exposure.(4)

Immune System:
A small number of studies have shown immune system effects in vinyl chloride workers, generally with higher exposures. The most common findings are increased circulating immune complexes and the presence of an abnormal protein in the blood (cryoglobulinemia). The severity of Raynaud's Phenomenon, acroosteolysis and skin effects has been associated with the extent of immune system abnormalities in some studies, but not others. Therefore, it is thought that these disorders may have an immune basis.(4,6,8)

SKELETAL EFFECTS (ACROOSTEOLYSIS) : Acroosteolysis is a condition that results in the destruction and absorption of the tips of the bones of the end of the fingers. In some cases, other bones (for example, the toes, the sacroiliac joint and the kneecap) are also involved. Acroosteolysis has been observed in a small percentage of vinyl chloride workers in several studies. Like Raynaud's Phenomenon, acroosteolysis has been observed primarily in workers heavily exposed to vinyl chloride. Acroosteolysis has appeared in workers between 5 and 42 months after first exposure. Workers with acroosteolysis have generally showed symptoms of Raynaud's Phenomenon first. It is not clear if this condition is reversible when exposure stops. Two studies showed improvement and two showed progression of the disease.(4-8)


Approximately 30 years after the use of vinyl chloride in industrial production of polyvinyl chloride (PVC) began, there were reports of a high occurrence of a relatively rare cancer, liver angiosarcoma, in vinyl chloride workers. Virtually all relevant human population studies have confirmed this finding. The highest incidence of liver angiosarcoma has been observed in workers with the highest exposure and the longest duration of exposure. Human population studies have also associated vinyl chloride exposure with other forms of liver cancer, cancer of the lung, lymph and blood forming system, and the brain and central nervous system.(4,8,12)
IARC coordinated a large study to investigate the dose-response relationship between liver cancer and exposure to vinyl chloride and to assess the cancer risk for other sites. Results from this large study (12706 subjects) with exposure of at least one year showed an excess of liver cancer including angiosarcoma which was clearly related to time since first exposure, duration of employment and estimated exposure. Other cancer sites investigated were either not higher than expected or were unrelated to vinyl chloride exposure.(14) Another comprehensive industry-wide study of 10173 men who had at least one year of occupational exposure to vinyl chloride also confirmed a significant excess mortality from liver cancer, including angiosarcoma and biliary tract cancer. This study also confirmed an excess of central nervous system and brain cancer.(9)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is carcinogenic to humans (Group 1).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as a confirmed human carcinogen (A1).

The US National Toxicology Program (NTP) has listed this chemical as a known human carcinogen.

This chemical is regulated by the US Occupational Safety and Health Administration (OSHA) as a carcinogen.

Teratogenicity and Embryotoxicity:
A number of human population studies have investigated the possibility of effects on the unborn child in communities with vinyl chloride industries and in people occupationally exposed to vinyl chloride. Many of these studies were poorly conducted. Nevertheless, a statistically significant relationship between developmental effects in children and parental occupation or physical proximity to vinyl chloride industries has not been demonstrated. One study reported no significant developmental effects (fetotoxicity, embryotoxicity or teratogenicity) in the children of mothers who were occupationally exposed to 0.2 to 130.7 ppm vinyl chloride for more than 1 year.(4,15) Animal information is weak but suggests that teratogenic, embryotoxic and fetotoxic effects would not be observed in the absence of maternal toxicity.

Reproductive Toxicity:
An extensive review has concluded that information relating vinyl chloride exposure in the father and possible reproductive effects, such as increased miscarriages in the mother, is sparse, conflicting and inconclusive.(16) One recent study which examined the frequency of miscarriages among wives of workers exposed to vinyl chloride showed no significant differences compared to the wives of unexposed workers.(17) Other possible reproductive effects have included impotence and decreased sexual function in both men and women. No conclusions can be drawn from these studies because of factors such as concurrent exposure to other potentially harmful chemicals and the results were not related to exposure levels or subjected to statistical analysis.(4,15) Animal studies suggest that high concentrations of vinyl chloride may have testicular effects, but no conclusions can be drawn regarding effects on fertility.

Vinyl chloride is mutagenic. There have been numerous studies of the mutagenic effects of vinyl chloride in people with occupational exposure, especially chromosomal aberrations.(4,5,8,12,16,18) A clear correlation between the incidence of chromosomal aberrations and the duration or level of exposure has been observed.(18) Positive results have also been obtained in the somatic cells of live animals and in cultured mammalian cells and bacteria.

Toxicologically Synergistic Materials:
In studies with rats, ethanol increased the incidence of liver angiosarcoma causing an earlier onset of tumours and an increased death rate.(4,6,12)

Potential for Accumulation:
Vinyl chloride is rapidly absorbed following inhalation. Significant absorption through the skin does not occur. Once absorbed into the body, the liver converts vinyl chloride to several other chemicals (metabolites). Some metabolites are excreted mainly in the urine, largely within 1 day of absorption. Very little is exhaled as carbon dioxide or eliminated in the feces. Other metabolites, a few of which are more toxic than vinyl chloride, stay in the body longer and are responsible for some of the harmful effects of vinyl chloride, particularly in the liver. Eventually these chemicals are also excreted from the body. Only small amounts of unchanged vinyl chloride are exhaled at low exposure concentrations. If the amount of vinyl chloride exceeds the capacity of the liver, exhalation of unchanged vinyl chloride becomes the major route of excretion.(4)


This chemical is extremely flammable. Take proper precautions (e.g. remove any sources of ignition). Take proper precautions to ensure your own safety before attempting rescue; e.g. wear appropriate protective equipment. Remove source of contamination or have victim move to fresh air. Obtain medical attention immediately.

Skin Contact:
Quickly remove victim from source of contamination and briefly flush with lukewarm, gently flowing water until the chemical is removed. DO NOT attempt to rewarm the affected area on site. DO NOT rub area or apply dry heat. Gently remove clothing or jewelry that may restrict circulation. Carefully cut around clothing that sticks to the skin and remove the rest of the garment. Loosely cover the affected area with a sterile dressing. DO NOT allow victim to drink alcohol or smoke. Quickly transport victim to an emergency care facility.

Eye Contact:
Quickly remove victim from source of contamination. Immediately and briefly flush with lukewarm, gently flowing water until the chemical is removed. DO NOT attempt to rewarm. Cover both eyes with a sterile dressing. DO NOT allow victim to drink alcohol or smoke. Quickly transport victim to an emergency care facility.

Ingestion is not an applicable route of exposure for gases.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures. All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.


Flash Point:
Extremely flammable gas. Can be ignited at all normal temperatures. An open cup flash point of -77.8 deg C (-108 deg F) has been reported.(26,29)

Lower Flammable (Explosive) Limit (LFL/LEL):
3.6-4.0% (23,26,29)

Upper Flammable (Explosive) Limit (UFL/UEL):
20% (26,28); 33% (4,23)

Autoignition (Ignition) Temperature:
472 deg C (882 deg F) (23,26)

Sensitivity to Mechanical Impact:
Stable material. Probably not sensitive.

Sensitivity to Static Charge:
No information is available on the electrical conductivity of vinyl chloride. Vinyl chloride gas in the flammable range may be ignited by a static discharge of sufficient energy. Minimum ignition energy: less than 0.3 millijoules.(30) Discharge of a spray of gas and liquid under pressure from a cylinder generated static charge and ignited the gas.(31)

Combustion and Thermal Decomposition Products:
Above 450 deg C, partial decomposition occurs yielding acetylene and hydrogen chloride, with possible trace amounts of chloroprene. Combustion in air at 510-795 deg C produces hydrogen chloride. Traces of phosgene are formed under oxygen deficient combustion.(26,28)

Fire Hazard Summary:
Extremely flammable gas. Can readily form explosive mixtures with air over a very wide range. Low ignition energy. Hazardous polymerization may occur under fire conditions. Fire-exposed containers may rupture violently due to polymerization. Vinyl chloride gas is uninhibited and may polymerize explosively in a fire and may form polymers in vents and flame arresters, resulting in blockage of vents. Gas is heavier and colder than air and may hug the ground and can travel a considerable distance to a source of ignition and flash back to a leak. During a fire, toxic/corrosive hydrogen chloride and phosgene gases may be generated. Can accumulate in confined spaces, resulting in an toxicity, flammability and explosion hazard.

Extinguishing Media:
Use water spray ,carbon dioxide, foam, or dry chemical powder.(23,29) Water will not be effective because it cannot cool vinyl chloride below its flash point. Stop flow of gas.(29)

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid hazardous gas and toxic decomposition products.
For fires involving flammable gases, the best procedure is to stop the flow of gas before attempting to extinguish the fire. To extinguish the fire, while allowing continued flow of the gas, is extremely dangerous. The gas could form an explosive mixture with air and reignite, which may cause far more damage than if the original fire had been allowed to burn. In some cases, extinguishing the fire with carbon dioxide or dry chemical powder may be necessary to permit immediate access to valves to shut off the flow of gas. However, this must be done carefully. If it is not possible to stop the flow of gas and if there is no risk to the surrounding area, it is preferable to allow continued burning, while protecting exposed materials with water spray until the flow of gas can be stopped. Gas clouds may be controlled by water spray or fog. Note that addition of water to any pools of liquefied vinyl chloride may increase evolution of gas. Isolate materials not yet involved in the fire and protect personnel.
Move cylinders from fire area if this can be done without risk. Otherwise, fire-exposed containers, tanks or pipelines should be cooled by application of hose streams and this should begin as soon as possible (within the first several minutes) and should concentrate on any unwetted portions of the container. No part of a cylinder should be subjected to a temperature higher than 52 deg C (approximately 125 deg F). Otherwise, the heat generated by the fire will cause their contents to polymerize. If this is not possible, use unmanned monitor nozzles and immediately evacuate the area. For a massive fire in a large area, use unmanned hose holder or monitor nozzles; if this is not possible withdraw from fire area and allow fire to burn. Stay away from ends of tanks, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire. After the fire has been extinguished, explosives atmospheres may linger. Before entering such an area, especially confined areas, check the atmosphere with an appropriate device.
Vinyl chloride is a confirmed human carcinogen. Do not enter fire area without wearing specialized protective/equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.


NFPA - Health: 2 - Intense or continued (but not chronic) exposure could cause temporary incapacitation or possible residual injury.
NFPA - Flammability: 4 - Will rapidly or completely vaporize at atmospheric pressure and normal ambient temperature, or readily disperse in air and burn readily.
NFPA - Instability: 2 - Undergoes violent chemical change at elevated temperatures and pressures, or reacts violently with water, or may form explosive mixtures with water.


Molecular Weight: 62.50

Conversion Factor:
1 ppm = 2.55 mg/m3; 1 mg/m3 = 0.392 ppm at 25 deg C (calculated)

Physical State: Gas
Melting Point: -154 deg C (-245 deg F) (22,23,26)
Boiling Point: - 13.4 deg C (7.9 deg F) (22,26,28)
Relative Density (Specific Gravity): Not applicable (gas)
Solubility in Water: Slightly soluble in water (110 mg/100 g (26,32); 276 mg/100 mL (4) at 25 deg C)
Solubility in Other Liquids: Very soluble in diethyl ether; soluble in ethanol, benzene, hydrocarbons, chlorinated solvents, oil and most common organic liquids.(13,26,32)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 0.6 (calculated) (27); 1.36 (estimated) (32); 1.99 (estimated) (4)
pH Value: Not available
Vapour Density: 2.15 at 15 deg C (air = 1) (22)
Vapour Pressure: 78 kPa (585 mm Hg) at -20 deg C (26,28); 333 kPa (2500 mm Hg) at 20 deg C (28); 756 kPA (5670 mm Hg) at 50 deg C (28)
Saturation Vapour Concentration: Not applicable at normal temperatures; gas.
Evaporation Rate: Not applicable at normal temperatures; gas.
Critical Temperature: 158.4 deg C (317.1 deg F) (22)

Other Physical Properties:
VISCOSITY-DYNAMIC: 0.273 mPa.s (0.273 centipoise) at -20 deg C (liquid) (26)
VISCOSITY-KINEMATIC: 0.30 mm2/m (0.30 centistokes) at -20 deg C (calculated)
VISCOSITY-DYNAMIC: 0.01072 mPa.s (0.01072 centipoise) at 20 deg C and 101.33 (gas) (27)
SURFACE TENSION: 23.1 mN/m (23.1 dynes/cm) at -20 deg C (27)
CRITICAL PRESSURE: 5341 kPa abs. (774.7 psia or 52.7 atm.) (22)
TRIPLE POINT: -151.5 deg C (-240.7 deg F) at 0.00124 kPa abs (estimated). (22)


Unstable. The liquid can be stabilized with an inhibitor and in the absence of air and oxygen. The gas may polymerize explosively. Unstable peroxides can form on standing in air, especially in the presence of iron impurities which may arise from the corrosion of cast iron and steel storage containers.(26) Reacts with water to form hydrochloric acid.(28)

Hazardous Polymerization:
Uninhibited vinyl chloride or material that is depleted of inhibitor can polymerize violently when exposed to air, sunlight (ultraviolet light), elevated temperatures, and the presence of incompatible materials, such as peroxides and other oxidizing materials.(22,23,29,30) Vinyl chloride tends to self-polymerize explosively if peroxidation occurs, and several industrial explosions have occurred.(31)

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

AIR or OXYGEN (especially in the presence of iron impurities) - forms an unstable polyperoxide, which can explode.(29,31)
STRONG OXIDIZING AGENTS (e.g. nitrogen oxides, nitrates, peroxides, perchlorates, permanganates) - can cause violent polymerization increasing risks of fire and explosion.(23,31)
COPPER AND ITS ALLOYS - may form explosive acetylides from trace impurities of acetylene present in vinyl chloride.(22,23,25)
WATER - reacts to form hydrochloric acid.(28)

Hazardous Decomposition Products:
Peroxides, hydrochloric acid

Conditions to Avoid:
Open flames, sparks, electrostatic discharge, heat and other ignition sources, air, sunlight, low inhibitor concentration and moisture.

Corrosivity to Metals:
Dry vinyl chloride is not corrosive to metals, such as cast iron, steel, stainless steel, nickel and its alloys, and aluminum.(22,23) It attacks brass.(33) In the presence of moisture, it accelerates the corrosion of cast iron, steel, copper and its alloys, and aluminum, especially at elevated temperatures.(22,33) It does not corrode type 316 stainless steel, which is a satisfactory material to use with vinyl chloride.(22,33) /RCM/


LC50 (rat): 33700 ppm (4-hour exposure); cited as 47640 ppm (2-hour exposure) (19)
LC50 (mouse): 19400 ppm (4-hour exposure); cited as 27420 ppm (2-hour exposure) (19)

Eye Irritation:

Eye irritation has not been observed in animals exposed to very high concentrations of the gas.(4)

Effects of Short-Term (Acute) Exposure:

There is a marked difference in species susceptibility, but all species studied experienced central nervous system (CNS) effects. Initially, there is excitation followed by incoordination, drowsiness, unconsciousness, convulsions and accelerated respiration progressing to respiratory failure and death.(4,6) Other changes have been reported following brief exposures to very high concentrations (over 100000 ppm), including marked congestion and bleeding of the lungs (guinea pigs), irregular heart beat (dogs), blood clotting failure (guinea pigs), liver damage and kidney congestion (mice). Lower exposures (50000 ppm) had no observable effects on the liver, kidneys, or nervous system in rats.(4)

Effects of Long-Term (Chronic) Exposure:

In studies using relatively low concentrations (up to 500 ppm), the major finding has been liver toxicity. Necrosis of the liver was observed in rabbits exposed to 200 ppm vinyl chloride for 6 months. No significant effects were observed in rats, rabbits and guinea pigs exposed to 50 ppm for 6 months.(20) Rats exposed to 10 ppm for 6 months developed increased heart and kidney weights. Increased mortality has been reported with exposures from 50 to 250 ppm for 6 to 12 months.(4) However, statistical analysis of the data was not reported.(4) Many other studies have been conducted with higher exposure levels (over 2500 ppm). In these studies, harmful changes were observed in the respiratory system, the liver, the heart and blood vessels, the kidneys, and the nervous system.(4,7)

All of the many animal studies reported have been positive for cancer following exposure by any route. The International Agency for Research on Cancer (IARC) has concluded that there is sufficient evidence for carcinogenicity in animals. While there are weaknesses in the reporting and/or conduct of many of studies, the occurrence of cancer is consistently observed.(4,5,8,12) The minimum carcinogenic dose varies by species, but is as low as 10 ppm for rats and 50 ppm for mice.(5) A few studies have examined the possibility that exposure of pregnant animals may result in an increased incidence of cancer in the offspring. No conclusions can be drawn from these studies because of design flaws, such as not using a control group, not conducting statistical evaluation of the results and/or the observation of high mortality in the test animals.(4,21)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
The available information suggests that vinyl chloride does not cause embryotoxicity or teratogenicity at doses that are not maternally toxic.
No conclusions can be drawn from two studies with low exposure levels (15 ppm or less) because the studies were not well conducted or reported. In studies with higher exposure levels (50 to 2500 ppm), developmental effects (for example, reduced fetal weight, delayed ossification, reduced litter size) were observed in mice, rats and rabbits at concentrations that were also maternally toxic. No firm conclusions can be drawn from the one study that showed reduced litter size because only a single concentration of vinyl chloride was tested.(4)

Reproductive Toxicity:
It is not possible to conclude that vinyl chloride is a reproductive toxin.
Adverse effects on the testes have been observed in rats. In two studies, adverse effects on the testes were observed in male rats exposed to 100 or 500 ppm for 12 or 10 months, respectively.(4) No conclusions can be drawn from another study in which male rats were exposed to 250 ppm or 1000 ppm for 11 weeks. A significant reduction in the number of pregnant females was noted, but a statistically significant decrease in the number of fertile males was not observed. There was no evidence of pre- or post- implantation loss of embryos in the females.(34) The study did not comment on the presence or absence of toxicity in the exposed animals.

Vinyl chloride is mutagenic, based on positive results (DNA adducts, single strand breaks, chromosomal aberrations) in the somatic cells of live animals exposed by inhalation.
Rats were exposed to 500 ppm vinyl chloride (99.9% pure) for 14 consecutive days (7 hr/d). DNA adducts were observed in the livers, lungs, and brains of young rats, and only in the livers of older rats.(39) Adult male rats were exposed by inhalation to 700 ppm radio-labeled vinyl chloride (purity not specified) for a single 6-hour exposure. Adult female and 11-day-old rats were exposed to 700 ppm radio-labeled vinyl chloride for two 6-hour exposures. Increased DNA alkylation was observed in the liver cells of both the adult and young rats, but at a much higher rate in the younger rats due to the increased rate of cell replication.(43) Other studies have also shown DNA adduct formation in somatic cells following inhalation exposure of rats or mice to vinyl chloride.(40,41,44,45) Female mice were exposed by inhalation to 100, 250 or 500 ppm vinyl chloride (purity not specified) for 4 days (6 hr/d). A dose-dependent increase in single strand breaks in liver cell DNA was observed. DNA adducts were also observed in liver cells. Mice were also exposed to 250 ppm for 2, 4, 6 or 8 hours. Single strand breaks in liver cell DNA were observed in these animals.(47) Female mice were exposed by inhalation to 500 ppm vinyl chloride (greater than 99.9%) for 1-8 weeks (6 hr/d; 5 d/wk). Animals were killed 2 hours after exposure for 39, 60, 117 and 234 hours or 18 hours after exposure for 36, 114 or 231 hours. In animals killed 2 hours after 117 and 234 -hour exposures, single strand breaks (SSB) were observed in DNA from the lungs, liver, and kidneys. When animals were killed 18 hours after exposure for 114 or 231 hours, the SSB levels in the kidneys, lungs and liver remained elevated.(46) Chinese hamsters were exposed by inhalation to 12500, 25000 or 50000 ppm (cited as 1.25, 2.5, or 5%) vinyl chloride (purity not specified) for 6, 12 or 24 hours. There was no mortality observed. A statistically significant, duration dependent increase in chromosomal aberrations was observed at 25000 and 50000 ppm following exposure for 6, 12 or 24 hours. A statistically significant, concentration and duration dependent increase in sister chromatid exchanges was observed following exposure to 12500 or 25000 ppm for 6, 12 or 24 hours.(38) These exposure levels are very high. Negative results have been obtained in mammalian dominant lethality tests.(5,42)
Positive results have been produced in bacteria and cultured mammalian cells, usually in the presence of metabolic activation.(4,5,12,18)


Selected Bibliography:
(1) Lester, D., et al. Effects of single and repeated exposure of humans and rats to vinyl chloride. Paper presented at the 23rd Annual Meeting of the American Industrial Hygiene Association, May, 1962. American Industrial Hygiene Association Journal. Vol. 24 (May-June, 1963). p. 265-275
(2) Patty, F.A., et al. Acute response of guinea pigs to vapors of some new commercial organic compounds: V. Vinyl chloride. Public Health Reports. Vol. 45, no. 34 (Aug. 1930). p. 1963-1971
(3) Danziger, H. Accidental poisoning by vinyl chloride: report of two cases. Canadian Medical Association Journal. Vol 82 (Apr. 16, 1960), p. 828-830
(4) Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for vinyl chloride. Draft. US Department of Health and Human Services, 1995
(5) The mutagenicity and carcinogenicity of vinyl chloride: a historical review and assessment. ECETOC Technical Report No. 31. European Chemical Industry Ecology and Toxicology Centre, July 28, 1988
(6) Mackison, F. Review, summarization, and evaluation of literature to support the update and revision of criteria documents. VIII. Vinyl chloride. National Institute for Occupational Safety and Health, 1977
(7) Holmberg, B., et al. The industrial toxicology of vinyl chloride: A review. Work-Environ-Health. Vol. 11 (1974). p. 138-144
(8) The Report on the Designation of Vinyl Chloride in Ontario. Occupational Health and Safety Division, Ontario Ministry of Labour, Aug. 27, 1981.
(9) Wong, O., et al. An industry-wide epidemiologic study of vinyl chloride workers, 1942-1982. American Journal of Industrial Medicine. Vol. 20, no. 3 (Sept. 1991). p. 317-334
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(11) Lilis, R., et al. Prevalence of disease among vinyl chloride and polyvinyl chloride workers. Annals of the New York Academy of Sciences. Vol. 246 (Jan. 31, 1975). p. 22-41
(12) Vinyl chloride (group 1). In: International Agency for Research on Cancer. IARC monographs on the evaluation of carcinogenic risks to humans. Suppl. 7. Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42. World Health Organization, 1987. p. 373-376
(13) Report on Carcinogens. 11th ed. US Department of Health and Human Services, Public Health Service, National Toxicology Program
(14) Simonato, L., et al. A collaborative study of cancer incidence and mortality among vinyl chloride workers. Scandinavian Journal of Work, Environment and Health. Vol. 17, no. 3 (June 1991). p. 159-169
(15) Tas, S., et al. Occupational hazards for the male reproductive system. Critical Reviews in Toxicology. Vol. 26, issue 3 (May 1996). p. 261-307
(16) Uzych, L. Human male exposure to vinyl chloride and possible teratogenic and mutagenic risks: a review. Human Toxicology. Vol. 7, no. 6 (1988). p. 517-527
(17) Mur, J.M., et al. Spontaneous abortion and exposure to vinyl chloride. Letter. The Lancet. Vol. 339, no. 8785 (Jan. 11, 1992). p. 127-128
(18) Giri, A.K. Genetic toxicology of vinyl chloride: a review. Mutation Research. Vol. 339, no. 1 (Feb. 1995). p. 1-14
(19) Prodan, L., et al. Experimental acute toxicity of vinyl chloride (monochloroethene). Annals of the New York Academy of Sciences. Vol. 246 (Jan. 31, 1975). p. 154-158
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(22) Compressed Gas Association. Handbook of compressed gases. 3rd ed. Van Nostrand Reinhold Company, 1990. p. 576-582
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(27) HSDB record for vinyl chloride. Last updated: 97/03/27
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(46) Walles, S.A.S., et al. Induction of single-strand breaks in DNA of mice after inhalation of vinyl chloride. Cancer Letters. Vol. 25 (1984). p. 13-18
(47) Walles, S.A.S., et al. Induction of single-strand breaks in liver DNA of mice after inhalation of vinyl chloride. In: Methods for detecting DNA damaging agents in humans: applications in cancer epidemiology and prevention. Edited by H. Bartsch, et al. IARC Scientific Publications No. 89. International Agency for Research on Cancer, 1998. p. 227-231

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

Review/Preparation Date: 1997-12-02

Revision Indicators:
US transport 1998-02-01
TLV-TWA 1999-03-01
TLV comments 1999-03-01
TDG 2002-05-29
Extinguishing media 2003-04-17
TLV basis 2004-01-04
PEL-TWA transitional 2004-01-29
PEL transitional comments 2004-01-29
PEL-TWA final 2004-01-29
PEL-STEL final 2004-01-29
PEL final comments 2004-01-29
Toxicological info 2004-03-12
Mutagenicity 2004-03-12
WHMIS detailed classification 2004-03-12
WHMIS health effects 2004-03-12
WHMIS classification comments 2004-03-12
Resistance of materials for PPE 2004-04-06
ERPG-1 2004-06-30
ERPG-2 2004-06-30
ERPG-3 2004-06-30
Bibliography 2005-02-02
Relative density 2006-09-28

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