VINYL CHLORIDE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
CHLORETHENE CHLORETHYLENE CHLOROETHENE 1-CHLOROETHYLENE CHLOROETHYLENE CHLORURE DE VINYLE (French) CHLORURO DI VINILE (Italian) ETHENE, CHLORO- ETHYLENE, CHLORO- ETHYLENE MONOCHLORIDE MONOCHLOROETHENE MONOCHLOROETHYLENE MONOVINYL CHLORIDE (MVC) MVC POLYVINYL CHLORIDE TROVIDUR VC VCL VCM VINILE (CLORURO DI) (Italian) VINYLCHLORID (German) VINYL CHLORIDE VINYL CHLORIDE, INHIBITED VINYL CHLORIDE MONOMER VINYL CHLORIDE, STABILIZED VINYL C MONOMER VINYL MONOMER VINYLE(CHLORURE DE) (French) WINYLU CHLOREK (Polish) CHLORURE DE VINYL (FRENCH) MONOCHLOROETHENE VINILE (CLORURO DI) (ITALIAN) SP 60 VINILE (CHLORURO DI) (ITALIAN)
IDENTIFIERS
1086-Vinyl chloride, inhibited 1086-Vinyl chloride, stabilized
IMO CLASSIFICATION:2.0 - Vinyl Chloride, inhibited STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:51139
SYNONYM REFERENCE
- (CGA, 1999; CHRIS , 2001; HSDB , 2001; IATA, 2001; IPCS, 1999b; Lewis, 1998; NFPA, 1997; RTECS , 2001; Verschueren, 2000)
USES/FORMS/SOURCES
Vinyl chloride is used to make plastics, adhesives, as a raw material, mainly (98%) in the manufacture of polyvinyl chloride (PVC) resins, and in the production of vinyl chloride and vinyl acetate copolymers. Because PVC is one of the most energy-efficient materials, it is used to make a wide variety of end-use products such as automotive parts and accessories, furniture, packaging materials, pipes, wall coverings, and wire coatings. Vinyl chloride has also been used as an aerosol propellant (AAR, 1998; ACGIH, 1992; ATSDR, 1997; Baselt, 2000; Baxter et al, 2000; Bingham et al, 2001; Budavari, 2000a; CGA, 1999a; IPCS, 1999b; Lewis, 1997; Lewis, 1998). "The use of vinyl chloride as an aerosol propellant, refrigerant, or a component of pharmaceuticals or cosmetics was banned in the US in 1974" (ACGIH, 1992). PVC is found in a variety of hospital products including: intravenous (IV) bags and tubing umbilical artery catheters blood bags and infusion tubing enteral nutrition feeding bags nasogastric tubes peritoneal dialysis bags and tubing tubing used in cardiopulmonary bypass (CPB) procedures tubing used in extracorporeal membrane oxygenation tubing used during hemodialysis
The technical grade of vinyl chloride is of 99.9 mole percent purity in the liquid phase (CGA, 1999a; Lewis, 1997) or 99.9 percent by weight since the 1960s (IPCS, 1999a). The commercial grade contains 1 to 2 percent of impurities (HSDB, 2001). IMPURITIES: Water (at maximum of 120 mg/kg), hydrochloric acid (at maximum of 1 mg/kg), and acetylene (1-10 mg/kg) can be present as impurities (CGA, 1999a; IPCS, 1999a). Dioxins can be formed as contaminants (IPCS, 1999a). Other impurities include (HSDB, 2001; IPCS, 1999a): - acetaldehyde
- 1,3-butadiene
- butane
- butene
- 1-butyne-3-ene (vinyl acetylene)
- chloroethane
- chlorophene
- chloromethane
- diacetylene
- 1,2-dichloroethane ethene (ethylene)
- hydrogen peroxide
- methyl chloride
- propadiene (allene)
- propene
- propine
- vinyl acetylene
ADDITIVES, sometimes added as stablizers (HSDB, 2001): Hydroquinone butyl catechol phenol
Vinyl chloride is produced by the dehydrochloronation of ethylene dichloride with alcoholic potassium, by the halogenation of ethylene, and by the addition reaction of acetylene and anhydrous hydrogen chloride (Ashford, 1994; Budavari, 2000a; CGA, 1999; Lewis, 1997). Vinyl chloride is one component of cigarette smoke (ACGIH, 1992). Although job-related exposure is usually through inhalation and dermal contact, non-occupational exposure is through drinking water and consumer products (Lewis, 1998).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- SUMMARY: In acute exposure, deaths are most often due to CNS and respiratory depression. The primary toxic hazard is exposure to vinyl chloride monomer (VCM) gas rather than to poly vinyl chloride (PVC) products (except during pyrolysis). There may be a long latent period between exposure and symptom onset.
- ACUTE: The nervous system is the primary target of acute vinyl chloride exposure. Signs and symptoms following ingestion include weakness; ataxia; inebriation; headache; fatigue; numbness; tingling and pallor or cyanosis of the extremities; nausea; abdominal pain; GI bleeding; visual disturbances; cardiac dysrhythmias; narcosis and death. Vinyl chloride is a severe irritant of the eyes, skin, and mucous membranes.
- CHRONIC: Enhanced collagen deposition and thickening of the subepidermal layer of the skin, Raynaud's phenomenon, hepatomegaly, hepatic fibrosis, splenomegaly, thrombocytopenia, sensory-motor polyneuropathy, trigeminal sensory neuropathy, minor pyramidal signs, cerebellar and extrapyramidal motor disorders, degenerative bone changes, and acro-osteolysis may occur with chronic exposure to vinyl chloride. Vinyl chloride is a known human carcinogen and has caused angiosarcoma of the liver in heavily exposed workers.
- DERMAL: Direct contact with liquid vinyl chloride or escaping gas can cause frostbite injury.
- INHALATION: Inhalation may cause CNS and respiratory depression and seizures.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
Vapors may cause dizziness or asphyxiation without warning. Some may be toxic if inhaled at high concentrations. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Fire may produce irritating and/or toxic gases.
ACUTE CLINICAL EFFECTS
- With an acute oral LD50 of 500 mg/kg in rats, the acute toxicity of VCM is relatively low (RTECS , 1996) (ACGIH, 1992).
- VCM is absorbed via inhalation or by dermal exposure. As this substance is a gas at room temperature, ingestion of VCM is unlikely; the most common route of exposure is inhalation (Finkel, 1983) (ACGIH, 1992)(Clayton & Clayton, 1994).
- The vapors are moderately irritating to the eyes. A single instance of human corneal injury was reported, which healed completely in 48 hours (Grant, 1986). VCM is a skin irritant (Schwartz et al, 1957).
- The nervous system is the primary target of acute vinyl chloride toxicity (ATSDR, 1990). Exposure to airborne concentrations greater than 800 to 1,000 ppm can produce headache, dizziness, ataxia, inebriation, euphoria, fatigue, numbness and tingling of the extremities, drowsiness, and visual disturbances (ATSDR, 1989) (ACGIH, 1992)(HSDB , 1996). VCM has narcotic properties and may cause unconsciousness in concentrations of 10,000 to 20,000 ppm (Walker, 1981; Hathaway et al, 1991). Seizures may occur in deep anesthesia induced with VCM (Danziger, 1960).
- There have been two human fatalities from acute VCM exposure to airborne levels estimated to be greater than 100,000 ppm; deaths were from respiratory failure (CCOHS, 1988). Death is most often due to CNS and respiratory depression. There may be a long latent period between exposure and symptom onset.
- Nausea, vomiting, diarrhea, and abdominal pain, sometimes intense enough to mimic an acute surgical abdomen, may follow ingestion of the liquid (HSDB , 1996). Hematemesis may occur following ingestion (HSDB , 1996).
- In animal studies, VCM lowered the myocardial threshold of dog hearts to epinephrine-induced arrhythmias (Jucker, 1974). Ventricular fibrillation may be a cause of sudden death following acute exposure (HSDB , 1996). This has not been reported in humans, however. Decreased myocardial contractility is associated with anesthetic doses in animals (Belej et al, 1974).
- Direct contact with the liquid or escaping compressed gas can cause frostbite and/or mechanical injury (ACGIH, 1992).
- In a study of human volunteers, 42% of an inhaled dose was retained in the lungs, regardless of the exposure concentration (HSDB , 1996). As much as 12% is excreted in the breath unchanged at concentrations of 1000 ppm, while only 2% is excreted unchanged in the breath with inhalation exposure to 10 ppm (Baselt, 1982). Pulmonary elimination followed first order kinetics, with half-lives of 20.4 and 22.4 minutes with inhalation exposure to 10 and 1000 ppm, respectively (HSDB , 1996).
- VCM is distributed throughout the body by lipids or lipoproteins. The highest concentrations are in the liver and kidneys, followed by the lungs, spleen, and small intestine (ATSDR, 1989).
- In concentrations less than 50 ppm, VCM is metabolized by the alcohol dehydrogenase system. At 50 to 250 ppm, oxidation occurs by the perioxidase-catalase system (Haddad, 1998). At higher levels, the mixed function oxidase system is the major metabolic route.
- Vinyl chloride is metabolized via cytochrome P450 CYP2E1 to form chloroethylene chloride, which is DNA-reactive (Whysner et al, 1996). The primary route of metabolism is: VCM to chloroethylene oxide, which spontaneously reorganizes itself to chloroacetaldehyde, and which is further oxidized to monochloroacetic acid or converted to chloroethanol. Monochloroacetic acid is only seen with exposure to high concentrations (Tamburro, 1978).
CHRONIC CLINICAL EFFECTS
- Allergic contact dermatitis has been associated with exposure to vinyl chloride, but may be due to plasticizers and other additives (Schwartz et al, 1957). Dermatitis occurs in approximately 4.4% of persons with chronic exposure (ACGIH, 1992).
- Fatigue and paresthesias have been reported after chronic exposure (Barlow & Sullivan, 1982). Workers chronically exposed to airborne concentrations of less than 50 ppm have developed axonal peripheral neuropathy (ATSDR, 1989). EEG changes have been seen in VCM workers (ATSDR, 1989; HSDB , 1996).
- A main target organ in chronic exposures is the liver. Direct hepatotoxicity and hepatomegaly are the main noncarcinogenic effects; splenomegaly has also been reported (Walker, 1981).
- Hepatic damage ranges from proliferation of hepatocytes and sinusoidal cells to hepatic angiosarcoma (Harbison, 1998; ATSDR, 1985). Cirrhosis is generally not observed (Popper et al, 1981). The most characteristic effect of long-term exposure to vinyl chloride is induction of the otherwise rare liver tumor, hemangiosarcoma (Harbison, 1998).
- Hepatotoxicity is generally seen after several months or years of exposure to higher VCM concentrations, in the range of 500 to 1000 ppm (ATSDR, 1989). Pathologic porphyrinuria, especially secondary to coproporphyrinuria, is a consistent pathological finding, following chronic exposure, for the recognition of VCM-induced hepatocellular toxicity (Doss et al, 1984).
- Chronic exposure can result in VINYL CHLORIDE DISEASE. A total of 25 cases have been reported (Hathaway et al, 1996). Vinyl chloride disease is characterized by a scleroderma-like condition of the connective tissues of the fingers, Reynaud's phenomenon followed by acro-osteolysis, liver damage, and sometimes hematologic changes and pulmonary effects. ACRO-OSTEOLYSIS involves lytic lesions of the bones; there is a 3 to 5% incidence of this condition in workers who clean PVC reaction chambers (Walker, 1981). Other authors have found a prevalence rate of 2 to 3 percent (Kemp et al, 1986).
- Vinyl chloride disease develops after 1 month to 3 years of exposure, and is reversible after exposure ceases. Wide-field capillary microscopy detected abnormalities in 48 of 152 (31.6%) of VCM workers' hands, and only 3 of 50 (6%) of hands in nonexposed manual workers (Maricq et al, 1976).
- Occupational exposure to high VCM concentrations has been loosely associated with impaired pulmonary function, as measured by carbon monoxide diffusing capacity (TLCO) (Lloyd et al, 1984). "MEAT-WRAPPER'S ASTHMA" occurs in supermarket workers who heat-cut PVC wrap used in wrapping meat, liberating VCM and HYDROGEN CHLORIDE (Anderson, 1974; Stevens, 1974). Meat wrapper's asthma occurs following exposure to PVC pyrolysis products (and possibly to plasticizers) (Falk & Portnoy, 1976). Occupational asthma caused by heat-cutting PVC wrap may be due to release of phthalic anhydrides, not PVC. The actual cause is uncertain.
- Vinyl chloride is thought to cause chronic interstitial pulmonary changes, distinct from those of pneumoconiosis. PVC polymer dust has also been implicated in causing pneumoconiosis (Wagoner, 1983; Cordasco et al, 1980; Soutar, 1980; Mastrangelo, 1981). Chronic exposure may cause pneumoconiosis (Haddad, 1998). An increased risk of lung cancer (large cell carcinomas and adenocarcinomas) has been observed in epidemiological studies (Haddad et al, 1996).
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with liquefied gas, thaw frosted parts with lukewarm water. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID EYE EXPOSURE - If eye tissue is frozen, seek medical attention immediately; if tissue is not frozen, immediately and thoroughly flush the eyes with large amounts of water for at least 15 minutes, occasionally lifting the lower and upper eyelids. If irritation, pain, swelling, lacrimation, or photophobia persist, get medical attention as soon as possible. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection. Contact lens use is not recommended when working with this chemical. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.
DERMAL EXPOSURE - If frostbite has occurred, seek medical attention immediately; do NOT rub the affected areas or flush them with water. In order to prevent further tissue damage, do NOT attempt to remove frozen clothing from frostbitten areas. If frostbite has NOT occurred, immediately and thoroughly wash contaminated skin with soap and water. INHALATION EXPOSURE - Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. TARGET ORGANS - Liver, CNS, blood, respiratory system, and lymphatic system [liver cancer](National Institute for Occupational Safety and Health, 2007; Chemsoft(R) , 2000).
Vinyl chloride is classified as a confirmed human carcinogen by ACGIH, IARC, OSHA, and NIOSH. Rescuers should wear appropriate respiratory and dermal protective equipment and clothing to prevent self-contamination. INHALATION EXPOSURE - INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. Assure adequacy of respirations and oxygenation. Endotracheal intubation may be required if significant CNS or respiratory depression. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
DERMAL EXPOSURE - DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). If frostbite has occurred, DO NOT rub the affected areas, DO NOT flush affected areas with water, or attempt to remove clothing. PREHOSPITAL Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
REWARMING Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000). Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011). Rewarming may be associated with increasing acute pain, requiring narcotic analgesics. For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
WOUND CARE Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day. Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000). The injured extremities should be elevated and should not be allowed to bear weight. In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000). Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010). Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur. Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm. IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010). TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000). IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010). THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011). CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011). CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010). MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
EYE EXPOSURE - DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility. If frostbite injury of the eyes may have occurred from direct exposure to the liquified material or escaping compressed gas, DO NOT flush with water; early ophthalmologic consultation should be obtained.
ORAL EXPOSURE -
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
Exposure to more than 120,000 ppm may be fatal in humans (ILO, 1983). Two vinyl chloride workers died by asphyxiation due to breathing very high levels; concentration levels were not reported (ATSDR, 1997; Baselt, 2000a).
In animal studies, brief exposure to 100,000 to 400,000 ppm was fatal in rats (ATSDR, 1997).
MAXIMUM TOLERATED EXPOSURE
ROUTE OF EXPOSURE Because vinyl chloride is a gas, the most typical route of exposure is inhalation. Occupational exposure to vinyl chloride has been associated with an increased incidence of angiosarcoma of the liver and other malignant tumors, acro-osteolysis, Raynaud syndrome, scleroderma, thrombocytopenia, circulatory disturbances and impaired liver function; very high concentrations cause central nervous system depression. It appears that metabolism of vinyl chloride is necessary before many of its toxic effects occur (Bingham et al, 2001a; Hathaway et al, 1996). "The main route of occupational exposure is via inhalation, and occurs primarily in vinyl chloride or polyvinyl chloride plants" (IPCS, 1999b). Inhalation studies in male human volunteers indicate that absorption was rapid; approximately 42 percent was absorbed. The percentage of VCM retained was independent of its concentration in inspired air (Zenz, 1994). Absorption is rapid by oral exposure (Zenz, 1994). Skin absorption is possible (Sittig, 1991).
CONCENTRATION LEVEL Occupational exposure to vinyl chloride amounted to several thousands of mg/m(3) in the 1940s and 1950s, several hundreds of mg/m(3) in the 1960s and early 1970s, and 13 to 26 mg/m(3) in most countries in the late 1970s (IPCS, 1999b). The reported effects of vinyl chloride have largely been due to the high exposure of workers prior to 1974 (IPCS, 1999a). Early inhalational experiments on human subjects found vinyl chloride to cause CNS depression at 7% to 10% and to cause dangerous arrhythmias at 12 percent (Oster et al, 1947). Humans exposed to 4000 ppm for 5 minutes reported no effects; 8000 ppm for 5 minutes reported some dizziness; and 20,000 ppm for 5 minutes reported dizziness, light-headedness, nausea, and dulling of vision and auditory cues (Hathaway et al, 1996). One 3-minute inhalation exposure at 25,000 ppm was reported to cause confusion, headache, and dizziness (ACGIH, 1992).
CASE SERIES/FIRST RESPONDERS: In 2012, a survey was conducted by the New Jersey Department of Health with the assistance of the CDC and ATSDR to assess the health effects associated with acute exposure of vinyl chloride by emergency responders (n=93) following a release from a train derailment. Of the self-reported symptoms, headache (26%) was a common adverse event. Upper respiratory symptoms (26%) (eg, runny nose, burning nose or throat and hoarseness) and lower respiratory symptoms (22%) (eg, shortness of breath, chest tightness, wheezing, and burning of chest) were also frequently reported. Other clinical events included coughing (15%), neurologic (14%) (ie, dizziness, weakness, and loss of balance), nausea and/or vomiting (14%), increased congestion (11%) and irritation, pain, or burning of the eyes (11%). Twenty-three percent of responders reported that they did not wear any type of personal protective equipment. Of note, air monitoring was not conducted following the release (Brinker et al, 2015).
Reportedly, workers exposed to chronic low concentrations of vinyl chloride showed degenerative bone changes, circulatory disturbances, thrombocytopenia, splenomegaly, hepatomegaly, hepatic fibrosis, and angiosarcoma of the liver (Baselt, 2000a). Vinyl chloride disease has been reported when workers were exposed to several hundred parts per million for periods ranging from months to years. The effects are: enhanced collagen deposition and thickening of the subepidermal layer of the skin; Raynaud's phenomenon (arteriole constriction causing whitening of the fingers and numbness); and, in some cases, acro-osteolysis (resorption of the terminal phalanges) (Hathaway et al, 1996). No new cases of vinyl chloride disease have been reported in the US since 1974, when occupational exposure levels were reduced (Hathaway et al, 1996). Occupational exposure to vinyl chloride has also been associated with an increased incidence of scleroderma and impaired liver function; very high concentrations can cause central nervous system (CNS) depression (Clayton & Clayton, 1994; Hathaway et al, 1996).
Vinyl chloride together with carbon disulfide have been associated with loss of libido and diminished potency in occupationally exposed man. Women 41 to 50 years of age employed in polyvinyl chloride and acrylic glass manufacturing for 21 years or longer showed exposure-associated declines in sexual function without increase in miscarriages or abortions. Higher incidence of preeclampsia in pregnant workers have also been reported (Harbison, 1998).
- Carcinogenicity Ratings for CAS75-01-4 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Vinyl chloride EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Vinyl chloride EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Vinyl chloride EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Vinyl chloride EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Vinyl chloride IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1 ; Listed as: Vinyl chloride 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Vinyl chloride MAK (DFG, 2002): Category 1 ; Listed as: Vinyl chloride NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS75-01-4 (U.S. Environmental Protection Agency, 2011):
Oral: Inhalation: Drinking Water: Oral: Inhalation: Drinking Water: Oral: Inhalation: Drinking Water: Oral: Inhalation: Drinking Water:
Budavari, 2000 IPCS, 1999b NTP, 1997; OHM/TADS, 2001; RTECS, 2001 LC50- (INHALATION)GUINEA_PIG: 595 mg/L (Budavari, 2000) 595,000 mg/m(3) for 2H (IPCS, 1999b)
LC50- (INHALATION)MOUSE: 293.75 mg/L (Budavari, 2000) 293,000 mg/m(3) for 2H (IPCS, 1999b)
LC50- (INHALATION)RABBIT: 295 mg/L (Budavari, 2000) 295,000 mg/m(3) for 2H (IPCS, 1999b)
LC50- (INHALATION)RAT: 18 pph for 15M -- caused behavioral and respiratory changes 390 mg/L (Budavari, 2000) 390,000 mg/m(3) for 2H (IPCS, 1999b)
LCLo- (INHALATION)GUINEA_PIG: LCLo- (INHALATION)MOUSE: LD50- (ORAL)RAT: TCLo- (INHALATION)HAMSTER: TCLo- (INHALATION)HUMAN: Male, 30 mg/m(3) at 5Y prior to mating -- affected spermatogenesis Male, 200 ppm for 14Y- intermittent -- caused tumors 20 ppm (OHM/TADS, 2001) 500 ppm for 4Y-Intermittent -- carcinogenic effects (NTP, 1997)
TCLo- (INHALATION)MOUSE: Male, 30,000 ppm for 6H at 5D prior to mating -- caused pre-implantation mortality Female, 500 ppm for 7H at 6-15D of pregnancy -- caused fetotoxicity and developmental abnormalities 50 ppm for 30W-intermittent -- caused tumors
TCLo- (INHALATION)RABBIT: Female, 500 ppm for 7H at 6-18D of pregnancy -- affected litter size and musculoskeletal development 9 g/m(3) for 4H/22W -intermittent -- caused cardiac changes 30 mg/m(3) for 26W -intermittent -- affected brain, blood, and musculoskeletal system
TCLo- (INHALATION)RAT: 28,000 ppm for 7H/6W- intermittent -- affected weight gain, transferases, and hepatic microsomal mixed oxidase Female, 10,000 ppm for 4H at 12-18D of pregnancy -- caused tumors 5000 ppm for 7H/52W-intermittent -- affected liver weight, spleen weight, and bladder weight 2000 ppm for 8H/92D-intermittent -- affected liver weight, spleen weight, and leukocyte count 50 ppm for 52W-Intermittent (NTP, 1997) Female, 1500 ppm for 24H at 1-9D of pregnancy -- caused post implantation mortality Female, 500 ppm for 7H at 6-15D of pregnancy -- caused fetotoxicity and developmental abnormalities Female, 250 ppm for 6H at 55D prior to mating -- affected female fertility index Male, 100 ppm for 6H at 26W prior to mating -- affected testes, epididymis, and sperm duct 1 ppm for 4H/52W-intermittent -- caused tumors 400 mg/m(3) for 24H/14W -continuous -- affected muscle spasticity, serum composition, and liver weight
TCLo- (INTRAPERITONEAL)RAT: TD- (INTRAPERITONEAL)RAT: TDLo- (INTRAPERITONEAL)RAT: TDLo- (ORAL)RAT: 23,400 mg/kg for 13W -intermittent -- affected liver weight, blood, and transaminases 3463 mg/kg for 52W-intermittent -- caused tumors 10 g.kg for 52W (NTP, 1997)
TDLo- (SUBCUTANEOUS)RAT:
CALCULATIONS
CONVERSION FACTORS 1 mg/L = 391 ppm (Clayton & Clayton, 1994) 1 ppm = 2.56 mg/m(3) (at 68 degrees F and 760 mmHg) (NIOSH , 2001); 1 ppm = 2.60 mg/m(3) (Verschueren, 2000)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS75-01-4 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS75-01-4 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS75-01-4 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS75-01-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS75-01-4 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS75-01-4 (U.S. Environmental Protection Agency, 2010):
Listed as: Vinyl chloride (D043) Final Reportable Quantity, in pounds (kilograms): Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity Listed as: Vinyl chloride Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Ethene, chloro- Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS75-01-4 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS75-01-4 (U.S. Environmental Protection Agency, 2010b):
Listed as: Ethene, chloro- P or U series number: U043 Footnote: Listed as: Vinyl chloride P or U series number: U043 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS75-01-4 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS75-01-4 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
Listed as: Vinyl chloride Effective Date for Reporting Under 40 CFR 372.30: 1/1/87 Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:
- DOT List of Marine Pollutants for CAS75-01-4 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS75-01-4 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1086 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1086 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS75-01-4 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Vinyl chloride is a very dangerous fire hazard. It is an irritant and moderately toxic if ingested or inhaled. Contact with vinyl chloride liquid may cause frostbite. A regulated, marked area should be established where vinyl chloride is handled, used, or stored. Sources of ignition such as smoking and open flames are prohibited where vinyl chloride is handled, used, or stored. Use only non-sparking tools and equipment, especially when opening and closing containers of vinyl chloride; use explosion-proof electrical equipment and fittings, and ground all electrical lines wherever vinyl chloride is used, handled, manufactured, or stored (CGA, 1999; ITI, 1995; Lewis, 1998; Sittig, 1991).
STORAGE
Store containers in a cool, dry, well-ventilated, non-combustible place; protect containers from physical damage. Typical shipping containers include pressure cylinders, tank cars, and tank barges. Metal containers involving the transfer of 5 gallons or more of vinyl chloride should be grounded and bonded; drums must be equipped with self-closing valves (valves must not be made of copper), pressure vacuum bungs, and flame arresters (Sittig, 1991).
- ROOM/CABINET RECOMMENDATIONS
Store vinyl chloride in outside or detached storage; a standard combustible liquid room should be used for indoor storage. Build ditches or dikes around storage areas to control the liquid in the event of a container rupture; ditches are preferred since vinyl chloride should not be collected directly beneath or surrounding storage tanks (CGA, 1999; ITI, 1995).
Vinyl chloride has violent reactions with oxidizers such as perchlorates, peroxides, permanganates, chlorates, and nitrates; it reacts with aluminum, aluminum alloys, and copper. Elevated temperature, oxidizing materials, or peroxides may cause hazardous polymerization (CGA, 1999; ITI, 1995; NFPA, 1997; Sittig, 1991).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
- Avoid contacting skin with vinyl chloride: It is severe irritant to skin, eyes, and mucous membranes; it can cause skin burns by rapid evaporation and consequent freezing; and it is possible to be absorbed through skin (Lewis, 2000; Sittig, 1991).
- GENERAL RECOMMENDATIONS for hand protection (CCOHS, 1989):
Select a material and style of glove that adequately protects hands from hazard. Review Chemical Manufacturer's MSDS or Label, glove manufacturer's information, and regulatory/advisory agency sources to determine the protective ability of the glove. Inspect and test gloves for defects before using. Follow manufacturer's instructions for glove care and maintenance. Check gloves for proper fit. Wash off all chemical protective gloves with water before removing them. Evaluate material resistance under conditions of use. Variations between products may affect resistance. Maintain gloves carefully.
- Workers who have any disorder of the liver, disorder of the gall bladder, or a past history of jaundice, who are receiving any drug which is potentially injurious to the liver, who have received chloroform or trichlorethylene as an anesthetic, and who are pregnant (liver is particularly sensitive to injury during pregnancy) should avoid exposure to vinyl chloride (a potentially hepatotoxic agent). In addition, workers should avoid alcohol consumption (ILO , 1998). In addition, those who have renal, cardiac, or pulmonary impairments may also be more at risk (HSDB , 2001).
- "A pit or tank must never be entered without adhering to the following safety procedures: never alone, always with a lifeline, and always with a positive pressure supply of fresh air" (IPCS, 1999b).
- Precautions for carcinogens should be strictly followed (HSDB , 2001).
EYE/FACE PROTECTION
- Wear appropriate eye and face protection since vinyl chloride can cause immediate and severe eye and skin irritation.
If eye tissue is frozen or frostbite has occurred on skin, do not rub the area or flush with water, seek medical attention immediately. Otherwise, rinse eye immediately and thoroughly with water for at least 15 minutes, and wash skin with soap and water (NIOSH , 2001).
RESPIRATORY PROTECTION
- Keep upwind; avoid breathing vapors. Wear appropriate personal protective clothing including a positive pressure self-contained breathing apparatus (AAR, 2000; (NFPA, 1997).
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 75-01-4.
ENGINEERING CONTROLS
- "Engineering controls are the most effective way of reducing exposure" (IPCS, 1999b).
- The best protection is to enclose operations and provide local exhaust, preferable using a hood with forced ventilation (CGA, 1999; IPCS, 1999b).
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004) EXTREMELY FLAMMABLE. Will be easily ignited by heat, sparks or flames. Will form explosive mixtures with air. Silane will ignite spontaneously in air. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Vapors from liquefied gas are initially heavier than air and spread along ground. Vapors may travel to source of ignition and flash back. Cylinders exposed to fire may vent and release flammable gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket.
Vinyl chloride is a very dangerous fire hazard when exposed to heat, flame, or oxidizers. It is shipped in containers as a liquefied gas under its own vapor pressure. Under fire conditions, closed containers may violently rupture and rocket; flames can flash back to the source of the leak very easily. A fire may restart after it has been extinguished (AAR, 1998a).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS75-01-4 (NFPA, 2002):
- INITIATING OR CONTRIBUTING PROPERTIES
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
- TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Do not direct water at source of leak or safety devices; icing may occur. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS75-01-4 (NFPA, 2002):
- SMALL FIRES: Stop the flow of gas before extinguishing the fire. Use dry chemical or carbon dioxide to extinguish fire (CHRIS , 2001). (AAR, 1998a)
- Fight the fire from a protected place or from the maximum possible distance. Keep upwind and avoid breathing vapors.
- LARGE FIRES: Let the fire burn, as a large fire is practically inextinguishable. Cool all affected containers with flooding quantities of water. Keep run-off water out of sewers and water sources. Keep upwind and avoid breathing vapors. Note that fire may restart and explosive re-ignition may occur unless the fire is allowed to burn out (CGA, 1999; Lewis, 2000).
When heated to decomposition, vinyl chloride emits irritating and highly toxic gases including phosgene, hydrogen chloride, carbon dioxide and carbon monoxide(ACGIH, 1991; Bingham et al, 2001a; OHM/TADS , 2001).
EXPLOSION HAZARD
- Vinyl chloride is heavier than air and is a severe explosion hazard. It is easily ignited and may explode if ignited in an enclosed area. Prolonged exposure of containers to heat or fire may cause vinyl chloride to polymerize and rupture the container (AAR, 2000; CHRIS , 2001; NFPA, 1997).
DUST/VAPOR HAZARD
- When heated to decomposition, vinyl chloride emits irritating and highly toxic gases including phosgene, hydrogen chloride, carbon dioxide and carbon monoxide (ACGIH, 1991; Bingham et al, 2001a; OHM/TADS , 2001).
REACTIVITY HAZARD
- CAUTION: This material may polymerize violently under high temperature conditions or upon contamination with other products. Polymerization will produce heat and high pressure buildup in containers which may lead to an explosion or container rupture (ERG, 2004).
- "At ambient temperatures and in the absence of air, dry purified vinyl chloride is highly stable and non corrosive. At temperatures above 450 degrees C (decomposition temperature), partial decomposition occurs yielding acetylene, hydrogen chloride, and trace amounts of 2-chloro-1,3-butadine (chloroprene). This reaction also occurs by lower temperatures (at 30 degrees C and under) in the presence of sodium or potassium hydroxide" (IPCS, 1999a).
- Vinyl chloride becomes unstable very easily (CGA, 1999; IPCS, 1999a; Lewis, 2000; NIOSH , 2001; Pohanish & Greene, 1997):
It reacts explosively with aluminum or aluminum alloys. It may polymerize explosively when exposed to elevated temperatures or when exposed to pressure. It attacks iron and steel in the presence of moisture due to the formation of hydrochloric acid. It reacts vigorously with oxidizing materials (such as perchlorates, peroxides, permanganates, chlorates, and nitrates). It explodes on contact with oxides of nitrogen.
- It is incompatible with peroxides. It may polymerize explosively when peroxides form after long period of exposure to atmospheric oxygen (due to polymerization of the chloride). Radical polymerization may run out of control (NIOSH , 2001; Urben, 1995).
Polymerization reaction evolves heat (HSDB , 2001; OHM/TADS , 2001). An unstable polyperoxide is formed in vinyl chloride through oxidation by atmospheric oxygen in the presence of any of a variety of contaminants;long-term storage increases the concentration of unstable polyperoxide to hazardous levels (NFPA, 1997).
- Static generated by discharging a spray of vapor and liquid into a fume hood ignited the vapor; discharge of vapor only did not lead to ignition (Urben, 1995).
- Copper or copper alloys can react with acetylene present as impurity to form explosive acetylide (CGA, 1999).
- "There are indications for reactions of vinyl chloride with chlorine or chloride used for water disinfection, thus leading to chloroacetaldehyde and other undesirable compounds (IPCS, 1999a).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- LARGE SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, consider initial evacuation for 1600 meters (1 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks). Keep out of low areas.
- If a fire becomes uncontrollable or a container is exposed to direct flame, consider evacuation of a one-half (1/2) mile radius. If vinyl chloride is leaking but not on fire, consider evacuation from downwind areas based on the amount of vinyl chloride spilled, the location, and weather conditions(AAR, 2000).
- AIHA ERPG Values for CAS75-01-4 (AIHA, 2006):
Listed as Vinyl Chloride ERPG-1 (units = ppm): 50 ERPG-2 (units = ppm): 5000 ERPG-3 (units = ppm): 20,000 Under Ballot, Review, or Consideration: No Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS75-01-4 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Vinyl chloride TEEL-0 (units = ppm): 1 TEEL-1 (units = ppm): 250 TEEL-2 (units = ppm): 1200 TEEL-3 (units = ppm): 4800 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS75-01-4 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS75-01-4 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Stop leak if you can do it without risk. Do not touch or walk through spilled material. Do not direct water at spill or source of leak. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. Isolate area until gas has dispersed.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 116 (ERG, 2004) Keep upwind; avoid breathing vapor/gas(ACGIH, 1991; AAR, 2000). Vinyl chloride is toxic and can asphyxiate by displacement of air. Spilled vinyl chloride is slow to disperse and will collect in low-lying areas due to the high vapor density. A leak from the storage or shipping container can be in the form of liquid or vapor/gas, although the liquid will rapidly "evaporate" to vapor/gas (ACGIH, 1991). Vinyl chloride in air can be recycled, incinerated, or microbially degraded (IPCS, 1999a). Keep liquid form of vinyl chloride out of water. It is lighter than water and will float in water. It also "boils" on water and produces flammable and irritating visible vapor clouds (CHRIS , 2001). Vinyl chloride in water can be removed by stripping, extraction, adsorption, or oxidation. Vinyl chloride in ground water (or soil) can be removed by in situ bioremediation techniques (evaporative and other methods coupled with microbial treatment) (IPCS, 1999a). Evacuate area in the event of a large discharge of vinyl chloride (CHRIS , 2001).
Vinyl chloride biodegraded in a methanotrophic attached-film bioreactor. The vinyl chloride removal efficiency ranged from 96.3-99.8% when the reactor was loaded in the range from 1800-9600 mcg/L. The maximum degradation rate was 1 g/L/d (Nelson & Jewell, 1993). Anaerobic degradation (of initial concentration of 400 mcg/L) in an adapted methanogenic aquifer was reported to have a half-life of 4 weeks at 20 degrees C (Verschueren, 2001). The biodegradation rate of vinyl chloride in a soil-water or sediment-water incubation study using natural microbial flora under methanogenic conditions was 100% in 23 days (Dragun, 1988). Laboratory experiments that evaluated vinyl chloride's biodegradation under anaerobic conditions in the presence of sand and methanogenic microorganisms showed a 50% degradation in 4 weeks and a 100% degradation in 11 weeks. When sand was not present, only 20% of the vinyl chloride were degraded in 4 weeks, and only 55% in 11 weeks (HSDB, 2004).
Methylosinus sp.: Vinyl chloride is rapidly metabolized using a resting cell suspension of the soil methylotroph Methylosinus trichosporium OB-3b. The half-life of the reaction, based on chloride ion release, is 0.61 hours. The reaction conditions were pH 7.4, 0.1 M phosphate buffer with a cell density of 0.1 g/ml. The complex metabolic mechanism was found to proceed through an intermediate chloroethylene oxide which is subsequently dechlorinated to ethylene oxide. The study concluded that the organism participates in the hydrolysis of both intermediates (Castro et al, 1992).
Pseudomonas sp.: Vinyl chloride is readily metabolized by a soil Pseudomonas sp. in resting cell suspensions. The process mechanism was established to include a dehalogenation step that entails a direct hydroxylation of the C-Cl bond producing acetaldehyde. This product is further oxidized to hydroxyacetic acid then to carbon dioxide. The half-life for dechlorination, with cells grown on 3-chloropropanol, was 1.3 hours at a cell density of 0.1 g/mL (Castro et al, 1992a).
Mycobacterium aurum and Xanthobacter sp.: Two bacteria, Mycobacterium aurum L1 and Xanthobacter autotrophicus GJ10, were characterized for their effectiveness for removal of vinyl chloride and 2-dichloroethane from waste gases. A mixed culture of the two bacteria proved to be effective for removing and mineralizing both vinyl chloride and 2-dichlorethane. The mixed culture was found to operate at concentrations much higher than the allowable concentrations of these materials in waste gases (Hartmans et al, 1992). The bacterium Xanthobactor (strain Py2) was grown on propylene as the carbon source. The resultant culture degraded several chlorinated alkenes of environmental concern, including vinyl chloride. This study confirmed that alkene monooxygenase was the active enzyme required to catalyze chlorinated alkene degradations (Ensign et al, 1992). Mycobacterium aureum is capable of growth using vinyl chloride as its sole carbon source (Verschueren, 2001).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
A suggested disposal method for vinyl chloride is incineration, preferably after mixing it with another combustible fuel. Combustion should be ensured to go to completion. Formation of phosgene should be avoided. Halo acids produced should be removed with an acid scrubber (Sittig, 1991). Most of the vinyl chloride produced industrially is bound in polyvinyl chloride articles, and incinertion involves a risk of formation of other unwanted chlorinated organic compounds (IPCS, 1999a). The amount of volatile aliphatic hydrocarbons and volatile chlorinated organic compounds decreased when a secondary, 900 degrees C, combustion temperature was used in the waste incineration of vinyl chloride. However, this higher temperature increased the amount of aromatic hydrocarbons produced (Nishikawa et al, 1992). Fluidized bed incineration at a temperature range of 450 to 980 degrees C (residence times of seconds) and rotary kiln incineration at a temperature range of 820 to 1600 degrees C (also with residence times of seconds) may be used (HSDB , 2001).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
ENVIRONMENTAL FATE AND KINETICS
When vinyl chloride is released into the atmosphere, it will exist almost entirely as a vapor in ambient air. Gas-phase vinyl chloride will degrade rapidly through reaction with photochemically-produced hydroxyl radicals. Reaction by-products in the atmosphere include chloroacetaldehyde, hydrogen chloride, chloroethylene epoxide, formaldehyde, formyl chloride, formic acid, and carbon monoxide (Howard, 1989). Reaction with hydroxyl radicals is expected to be rapid, with a half-life of 55 hours, calculated from a rate constant of 6.96x10(-12) cm(3)/molecule-sec at 25 degrees C and a radical concentration of 5x10(5)/cm(3) (HSDB, 2004). Calculated half-lives of the reactions of vinyl chloride with hydroxyl radicals and with ozone in the atmosphere are 1.2 days and 4.0 days, respectively (Verschueren, 2001). Gas-phase vinyl chloride will degrade rapidly by reaction with hydroxyl radicals with an estimated half-life of 1.5 days (Howard, 1989). Approximately 50% of atmospheric vinyl chloride exposed to sunlight disappeared in 0.5 days in September and 2 days in December (Howard, 1989). The rate constant for the vapor phase reaction of vinyl chloride with photochemically-produced hydroxyl radicals was determined to be 6.60x10(-12) cm(3)/molecule-sec (at 26 degrees C), corresponding to a half-life of 1.5 days at an atmospheric concentration of 8x10(5) hydroxyl radicals/cm(3) (Howard, 1989). The half-life of vinyl chloride in air ranges from 9.7-97 hours based on its photooxidation half-life in air (Howard et al, 1991). The half-life of vinyl chloride's photooxidative atmospheric degradation is reduced to 3-7 hours when nitrogen oxides are present, as is the case in photochemical smog situations (de Rooij et al, 2004; HSDB , 2001; Howard, 1989).
Direct photolysis should not be important, since vinyl chloride only weakly absorbs solar radiation (HSDB, 2004).
SURFACE WATER When released into the water, vinyl chloride will volatilize rapidly; volatilization half-lives range from 1 hour to 3 days in a model river and a model lake, respectively. It also may undergo indirect photolysis in sunlit surface waters containing photosensitizers (such as humic acid) or free radicals (HSDB, 2004; OHM/TADS, 2004; Howard, 1989). In a 1 mg/L solution at 35 degrees C, 50% of vinyl chloride volatilized in 26 minutes, and 90% volatilized in 96 minutes. Additional volatilization half-lives were determined as follows: (Verschueren, 2001). Volatilization half-life from a model river (1 m deep, flowing 3 m/sec, wind velocity of 3 m/sec) is estimated at 1 hour, and from a model lake at 3 days (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec) (HSDB, 2004). Though dissolved vinyl chloride will readily evolve into the gas phase, chemical reactions with water impurities may interfere with its release to the atmosphere (HSDB, 2004).
Vinyl chloride is not expected to hydrolyze (over pH range of 4.3 to 9.4) at an environmentally significant rate, to bioconcentrate in aquatic organisms, or to adsorb to suspended solids or sediments (HSDB, 2004; Verschueren, 2001; Howard, 1989) . Vinyl chloride's hydrolysis half-life in water is >= 10 years (Verschueren, 2001). Results from a study on the fate of vinyl chloride in water indicate that its adsorption onto particulate matter is negligible. However, given continual high concentrations of vinyl chloride input into water, aquatic sediment could exhibit long-term storage of low levels of vinyl chloride (HSDB, 2004).
Reactions between vinyl chloride and many salts may generate complexes that have a greater water solubility than vinyl chloride itself. Therefore, the presence of salts in water can influence the total amount of vinyl chloride in the aquatic system (HSDB, 2004). Vinyl chloride has the potential to react with chlorine in water, thereby generating more highly chlorinated compounds. This may be the case in environments such as municipal water chlorination facilities (HSDB, 2004).
TERRESTRIAL Vinyl chloride is expected to volatilize rapidly from moist soil, and may also volatilize from dry soil. Any vinyl chloride that does not evaporate will be very mobile in soil and may leach into groundwater. Under normal environmental conditions, it is not expected to hydrolyze in soils (HSDB, 2004; Howard, 1989). Volatilization half-lives have been estimated at approximately 0.2 days from a soil depth of 1 centimeter, and 0.5 days from a soil depth of 10 centimeters (HSDB, 2004; Verschueren, 2001).
ABIOTIC DEGRADATION
- Because of its volatility, vinyl chloride exists almost entirely in the gas-phase in the environment. It degrades rapidly in the atmosphere through reaction with photochemically-produced hydroxyl radicals and ozone. Vinyl chloride will volatilize quickly from water and soil surfaces. It is not expected to adsorb to suspended solids or sediments. In soils, material that does not vaporize will be highly mobile, and may leach into groundwater (HSDB, 2004; Howard, 1989).
- Photodissociation does not appear to be a major degradation process. Photooxidation has been reported to remove vinyl chloride rapidly from the troposphere with a half-life of a few hours (HSDB, 2004).
- Direct photolysis in water is expected to be, at best, a very slow degradation process. However, in the presence of photosensitizers or free-radical sources, such as humic material, acetone or hydrogen peroxide, vinyl chloride has been shown to decompose rapidly when irradiated with ultraviolet light (HSDB, 2004).
- Reactions with molecular oxygen at temperatures and oxygen concentrations present in natural waters will not contribute significantly to the degradation (HSDB, 2004).
BIODEGRADATION
- The scientific judgement of the half-life of vinyl chloride in soil ranges from 672-4320 hours (4 weeks - 6 months) based on estimated unacclimated aqueous aerobic biodegradation half-life (Howard et al, 1991).
- The scientific judgement of the half-life of vinyl chloride in surface waters ranges from 672 - 4320 hours (4 weeks - 6 months) based on estimated unacclimated aqueous aerobic biodegradation half-life (Howard et al, 1991).
- The scientific judgement of the half-life of vinyl chloride in ground water ranges from 1344-69,000 hours (8 weeks - 95 months) based on estimated unacclimated aqueous aerobic biodegradation half-life (low half-life) and an estimated half-life for anaerobic biodegradation of vinyl chloride from a ground water field study of chlorinated ethenes (Howard et al, 1991).
- Biodegradation under anaerobic conditions, such as in flooded soil or groundwater, may occur. However, existing data indicate that vinyl chloride is not readily degraded in aerobic systems, such as natural waters (HSDB, 2004; Howard, 1989).
BIOACCUMULATION
A bioconcentration factor (BCF) for aquatic organisms of approximately 7 was estimated based on the water solubility of 2736 mg/L (IPCS, 1999a; Howard, 1989) . A BCF of 2.8 for aquatic organisms was calculated based on log octanol/water partition coefficient (log Kow) of 0.9 (IPCS, 1999a). A BCF of 5.7 for aquatic microorganisms was calculated based on an octanol/water partition coefficient (Kow) of 1.23 (IPCS, 1999a).
ENVIRONMENTAL TOXICITY
EC20 - FISH: 14,520 mcg/L -- estimated (IPCS, 1999a) LC50 - BLUEGILL (Lepomis macrochirus): 1220 mg/L for 96H (de Rooij et al, 2004) LC50 - LARGEMOUTH BASS (Micropterus salmoides): 1060 mg/L for 96H (de Rooij et al, 2004) LC50 - ZEBRA DANIO (Brachydanio rerio): 240 mg/L for 24H (IPCS, 1999a) LC50 - ZEBRA DANIO (Brachydanio rerio): 210 mg/L for 96H -- >99% purity; semi-static, closed system (de Rooij et al, 2004) NOAEC - FRESHWATER FISH: 128 mg/L (IPCS, 1999a) NOAEC - FRESHWATER FISH: 0.088 - 29 mg/L (IPCS, 1999a) NOEC - ZEBRA DANIO (Brachydanio rerio): 128 mg/L for 96H -- >99% purity; semi-static, closed system (de Rooij et al, 2004)
- EC50 - ANAEROBIC MICROORGANISM: 40 mg/L for 3.5 days -- based on inhibition of respiration in a batch assay (IPCS, 1999b)
- IC50 - PROTOZOA (Tetrahymena pyriformis): 540 mg/L; 8.6 mmol/L -- caused a reduction in population doubling time (IPCS, 1999a)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- It is a colorless gas. However, it can be stored as liquid under pressure at ambient temperature (most frequently compressed as a liquified gas under its own vapor pressure during shipping or storage) or under atmospheric pressure at a temperature below its boiling point (such as a during handling) (AAR, 2000; (CHRIS , 2001; Lewis, 1998).
If high temperature is expected at atmospheric pressure, 40-100 ppm of phenol is used as inhibitor of polymerization. It can polymerize in the presence of air sunlight, or heat (CHRIS , 2001).
- Vinyl chloride is highly flammable, and at high concentrations exhibits a pleasant, ether-like, or faintly sweet odor (CGA, 1999; NIOSH , 2001).
VAPOR PRESSURE
- 2660 mmHg (at 25 degrees C) (ATSDR, 1997; Howard, 1989) Verschueren, 2000)
- 2600 mmHg (at 25 degrees C) (Lewis, 2000)
- 2530 mmHg (at 20 degrees C) (ACGIH, 1991; (ATSDR, 1997; Bingham et al, 2001a; Budavari, 2000)
- 2524 mmHg (at 20 degrees C) (NFPA, 1997)
- 2300 mmHg (at 20 degrees C) (Lewis, 1997)
- 580 mmHg (at -20 degrees C) (Verschueren, 2000)
- 400 mmHg at (-28 degrees C) (OHM/TADS, 2001)
- 240 mmHg at (-40 degrees C) (Verschueren, 2000)
- 788 kPa ; 114.3 psig (at 54.4 degrees C; 130 degrees F) (CGA, 1999)
- 62.3 kPa ; 90.3 psig (at 46.1 degrees C; 115 degrees F) (CGA, 1999)
- 519 kPa; 75.3 psig (at 40.6 degrees C; 105 degrees F) (CGA, 1999)
- 243 kPa; 35.3 psig (at 21.1 degrees C; 70 degrees F) (CGA, 1999)
- 3.3 atm (at 68 degrees F) (NIOSH , 2001)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
0.9106 (at 20/4 degrees C) (ACGIH, 1991; (Bingham et al, 2001a; Budavari, 2000) LIQUID: 0.9121 (at 20/20 degrees C) (Lewis, 1997) LIQUID: 0.9195 (at 15/4 degrees C) (Lewis, 2000) 0.91 (at 15/4 degrees C) (Verschueren, 2000)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
0.9106 g/cm(3) (at 20 degrees C) (ATSDR, 1997) 0.9195 g/cm(3) (at 15 degrees C) (ATSDR, 1997) 0.969 g/cm(3) (at -14.2 degrees C) (ATSDR, 1997) 0.97 kg/L (at -14 degrees C) (Ashford, 1994a) GAS: 2.56 kg/m(3); 0.160 lb/ft(3) (at 21.1 degrees C; 70 degrees F) (CGA, 1999) LIQUID: 908.41 kg/m(3); 56.71 lb/ft(3) (at 21.1 degrees C; 70 degrees F) (CGA, 1999) LIQUID: 0.969 kg/m(3) (at -13 degrees C) (CHRIS , 2001) LIQUID: 871.08 kg/m(3); 54.38 lb/ft(3) (at 40.6 degrees C; 105 degrees F) (CGA, 1999) LIQUID: 860.03 kg/m(3); 53.69 lb/ft(3) (at 46.1 degrees C; 115 degrees F) (CGA, 1999) LIQUID: 842.73 kg/m(3); 52.61 lb/ft(3) (at 54.4 degrees C; 130 degrees F) (CGA, 1999)
FREEZING/MELTING POINT
-153.8 degrees C (ACGIH, 1991) -153.8 degrees C; -244.8 degrees F; -119.4 K (CHRIS , 2001) -159.7 degrees C; -256 degrees F (Lewis, 1997; Lewis, 2000; NIOSH , 2001)
-153.8 degrees C (ATSDR, 1997; Budavari, 2000; Howard, 1989) -160 degrees C (ITI, 1995) OHM/TADS, 2001) -153.9 degrees C; -245 degrees F (NFPA, 1997) -154 degrees C; -245 degrees F (CGA, 1999) Liquefies at 21.6 degrees C (ITI, 1995)
BOILING POINT
- -13.37 degrees C (ATSDR, 1997; Budavari, 2000; Howard, 1989)
- -13.9 degrees C (Lewis, 1997; Lewis, 1998; Lewis, 2000)
- -16 degrees C (Ashford, 1994a)
- -14 degrees C (ITI, 1995)
- -13.4 degrees C; 7.93 degrees F (ACGIH, 1991; (CGA, 1999)
- -13.8 degrees C; 7.2 degrees F; 259.4 K (CHRIS , 2001)
- -14 degrees C; 7 degrees F (NFPA, 1997)
FLASH POINT
- -78 degrees C (ITI, 1995) OHM/TADS, 2001)
- -77 degrees C; -108 degrees F (Lewis, 1997)
- 17.6 degrees F (Cleveland open cup) (Lewis, 2000)
- -77.8 degrees C (open cup) (ACGIH, 1991)
- -77.8 degrees C; -108.4 degrees F (open cup) (CGA, 1999; NFPA, 1997)
- -110 degrees F (open cup) (CHRIS , 2001)
- -78 degrees C; -112 degrees F (closed cup) (Budavari, 2000)
AUTOIGNITION TEMPERATURE
- 472.22 degrees C; 881.6 degrees F (ATSDR, 1993) OHM/TADS, 2001)
EXPLOSIVE LIMITS
3.6% (ITI, 1995; NFPA, 1997; NIOSH , 2001; Sittig, 1991) 3.8 % (in air; at 20 degrees C) (IPCS, 1999a) 4% (ACGIH, 1991; (Bingham et al, 2001a; CGA, 1999; IPCS, 1999a; Lewis, 1997; Lewis, 2000)
22% (ACGIH, 1991; (Bingham et al, 2001a; CGA, 1999; IPCS, 1999a; Lewis, 1997; Lewis, 2000) OHM/TADS, 2001) 29.3 degrees C (in air; at 20 degrees C) (ICPS, 1999a) 33.0% (ITI, 1995; NFPA, 1997; NIOSH , 2001)
SOLUBILITY
Slightly soluble (ACGIH, 1991; (Budavari, 2000; Lewis, 1997; Lewis, 2000; NFPA, 1997). 1100 mg/L (at 25 degrees C) (ATSDR, 1997; Bingham et al, 2001a) Verschueren, 2000) 2763 mg/L (at 25 degrees C) (Howard, 1989) 0.11% (at 25 degrees C; 77 degrees F) (CGA, 1999; NIOSH , 2001) 2700 mg/L (HSDB , 2001)
Liquid form of vinyl chloride is lighter than water and will float in water. It will also "boil" on water and produce flammable and irritating visible vapor cloud (CHRIS , 2001).
Soluble/ miscible with oxygenated and chlorinated solvents, such as alcohol, ether or carbon tetrachloride (ACGIH, 1991; (Ashford, 1994a; Budavari, 2000). Soluble in benzene (Budavari, 2000).
OCTANOL/WATER PARTITION COEFFICIENT
- Log Kow = 0.6 (calculated) (HSDB , 2001)
- Log Kow = 1.36 (calculated) (ATSDR, 1997; IPCS, 1999a)
- Log Kow = 1.38 (calculated) (Howard, 1989)
HENRY'S CONSTANT
- 1.07x10(-2) atm-m(3)/mol (Howard, 1989)
- 1.2 atm-m(3)/mol (at 10 degrees C) (ATSDR, 1997)
- 3.55x10(5) atm (at 20 degrees C) (Corbitt, 1990)
- 0.0560 atm/m(3)-mole (HSDB , 2001)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
"The actual vapor concentrations that can be detected have never been adequately determined and vary from one individual to another, in impurities in the sample, and probably in duration of exposure" (Bingham et al, 2001a). "Although vinyl chloride has a faintly sweet odor at high concentrations, the odor is of no value in preventing excessive exposure" (Bingham et al, 2001a). 3.4 ppm in water (ATSDR, 1993; Sittig, 1991) 260 ppm in air (CHRIS , 2001; Sittig, 1991) 3000 ppm in air (ATSDR, 1997; Sittig, 1991) 4000 ppm in air (Sittig, 1991)
- ORGANIC CARBON PARTITION COEFFICIENT
23.1 dyn/cm (at -20 degrees C) (HSDB , 2001) 16.0 dynes/cm; 0.0160 N/m (estimated) (at 25 degrees C) (CHRIS , 2001)
774.7 psia; 52.7 atm; 5.34 MN/m(2); 5341.37 kPa abs (CGA, 1999; CHRIS , 2001) 5600 kPa (IPCS, 1999a) 5755 kPa; 57.55 bar; 834.7 psia; 56.8 atm (HSDB , 2001)
156 degrees C (IPCS, 1999a) 158.4 degrees C; 317.1 degrees F; 431.6 K (CHRIS , 2001) 151.5 degrees C; 304.6 degrees F; 424.61 K (HSDB , 2001)
75.94 kJ/kg; 32.65 Btu/lb (at -153.9 degrees C) (CGA, 1999) 18.14 cal/g (CHRIS , 2001) 75.94 kJ/kg; 32.65 Btu/lb (at melting point) (CGA, 1999)
- LIQUID WATER INTERFACIAL TENSION
GAS: 0.01072 cP (at 20 degrees C and 101.325 kPa) (HSDB , 2001) LIQUID: 0.280 cP (at -20 degrees C) (HSDB , 2001)
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