CHLORINE GAS
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
IDENTIFIERS
SYNONYM REFERENCE
- (Bingham et al, 2001; HSDB , 2001)RTECS, 2001
USES/FORMS/SOURCES
Chlorine is used to manufacture other chemicals. These include solvents such as carbon tetrachloride, trichloroethylene, 1,1,1-trichloroethane, tetrachloroethylene, and methylene chloride, pesticides and herbicides, plastics, vinyl chloride, and vinylidene chloride. It is also used in making refrigerants and propellants such as halocarbons and methyl chloride (CGA, 1999; HSDB , 2001). Many other chemicals are produced from chlorine including other chlorinated hydrocarbons, polychloroprene (neoprene), polyvinyl chloride, hydrogen chloride, ethylene dichloride, hypochlorous acid, metallic chlorides, chlorinated benzenes, phosgene, chloroform, chlorinated paraffins, chloracetic acid, and chlorinated lime. It is an important reagent in synthetic chemistry (Bingham et al, 2001; Budavari, 2000; HSDB , 2001; Lewis, 1997). Chlorine is used to make sodium hypochlorite, an ingredient in bleach, deodorizers and disinfectants. Chlorine is used to bleach pulp, paper, and fabrics (CGA, 1999; OHM/TADS , 2001).
Chlorine is employed in purifying drinking and swimming water, for sanitation of industrial and sewage wastes and other disinfecting uses, and as a ring chlorination/oxidation reagent (Ashford, 1994; Bingham et al, 2001; CGA, 1999; HSDB , 2001; OHM/TADS , 2001). Chlorine is used for detinning and dezincing iron, metal fluxing, and for degassing of aluminum melts (Budavari, 2000; CGA, 1999; Hathaway et al, 1996). A limited use for chlorine is in processing meats, fish, and fresh produce. Miscellaneous uses include the production of pharmaceuticals, cosmetics, lubricants, flame proofers, adhesives, food additives, and hydraulic fluids, in special batteries with zinc and lithium, and its use in shrink-proofing wool (ACGIH, 1991; Bingham et al, 2001; Lewis, 1997). It has been used as a poisonous gas for military purposes under the name bertholite (Budavari, 2000). The extinct nuclide Cl-36 is used to determine the geological age of meteors (Budavari, 2000).
Chlorine is available in a semiconductor, high purity grade at 99.5% purity (liquid phase); a liquefied gas grade; a research grade with a minimum purity of 99.99%; a water works grade, and technical gas and liquid grades (HSDB , 2001; Lewis, 1997).
Chlorine is not found free in nature due to its reactivity with other chemicals. Instead, it is found as sodium chloride in land locked lakes, as rock salt in underground deposits, in brines, and in natural deposits of sylvite and carnallite (Bingham et al, 2001). Swimming pool chlorinator tablets or pellets may result in chlorine gas exposure (Wood et al, 1987). For mixtures producing chlorine gas, see the SODIUM HYPOCHLORITE management.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Chlorine is a greenish-yellow, noncombustible gas at room temperature and atmospheric pressure. It is used in industrial bleaching operations, sewage treatment, swimming pool chlorination tablets, and chemical warfare. It can be generated when bleach is mixed with other cleaning products.
- TOXICOLOGY: The primary effects are due to local tissue injury rather than to systemic absorption. Cellular injury is believed to result from the oxidation of functional groups in cell components, from reactions with tissue water to form hypochlorous acid and hydrochloric acid, and from the generation of free oxygen radicals. Although the idea that chlorine causes direct tissue damage by generating free oxygen radicals was once accepted, this idea is now controversial.
- EPIDEMIOLOGY: Chlorine gas is one of the most common single-irritant inhalation exposures, occupationally and environmentally. In a recent study of 323 cases of inhalation exposures reported to poison control centers, the largest single exposure (21%) was caused by mixing bleach with other products.
MILD TO MODERATE POISONING: Cough, shortness of breath, chest pain, burning sensation in the throat and substernal area, nausea or vomiting, ocular and nasal irritation, choking, muscle weakness, dizziness, abdominal discomfort, and headache. SEVERE POISONING: Upper airway edema, laryngospasm, severe pulmonary edema, pneumonia, persistent hypoxemia, respiratory failure, acute lung injury, and metabolic acidosis. PREDISPOSING FACTORS: Patients with asthma, reactive airways, or COPD may develop respiratory irritation at lower concentrations.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
TOXIC; may be fatal if inhaled or absorbed through skin. Fire will produce irritating, corrosive and/or toxic gases. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Runoff from fire control may cause pollution.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: The primary effects are due to local tissue injury rather than to systemic absorption. Cellular injury is believed to result from the oxidation of functional groups in cell components, from reactions with tissue water to form hypochlorous acid and hydrochloric acid, and from the generation of free oxygen radicals. Although the idea that chlorine causes direct tissue damage by generating free oxygen radicals was once accepted, this idea is now controversial. EPIDEMIOLOGY: Chlorine gas is one of the most common single-irritant inhalation exposures, occupationally and environmentally. In a recent study of 323 cases of inhalation exposures reported to poison control centers, the largest single exposure (21%) was caused by mixing bleach with other products. MILD TO MODERATE POISONING: Cough, shortness of breath, chest pain, burning sensation in the throat and substernal area, nausea or vomiting, ocular and nasal irritation, choking, muscle weakness, dizziness, abdominal discomfort, and headache. SEVERE POISONING: Upper airway edema, laryngospasm, severe pulmonary edema, pneumonia, persistent hypoxemia, respiratory failure, acute lung injury, and metabolic acidosis. PREDISPOSING FACTORS: Patients with asthma, reactive airways, or COPD may develop respiratory irritation at lower concentrations.
- The main concern in acute exposure to chlorine is its effect on the respiratory system (Das & Blanc, 1993).
- Exposures in the range of 1 to 3 parts per million (ppm) can produce definite irritation (Hathaway et al, 1996; ACGIH, 1991; ILO, 1983). Effects of acute exposure to chlorine include irritation and corrosion of mucus membranes, skin, eyes, and the respiratory tract (CGA, 1999; Das & Blanc, 1993). Sensory irritation by chlorine is mediated by the trigeminal tract, and considerable accommodation can occur (Winder, 2001).
- Inhaled chlorine gas can induce asthma because of its irritant properties (Taylor & Venables, 1984). Chlorine-induced bronchoconstriction may be of the reflex cholinergic type, not involving allergic mediation (Winder, 2001).
- Acute exposure to 3 ppm to 6 ppm can cause a stinging or burning sensation of the eyes, nose, and throat as well as headache, tearing, sneezing, coughing, husky voice, nosebleed, and bloody sputum (Clayton & Clayton, 1994). Exposures in the range of 100 ppm can be lethal, but even concentrations as low as 35 ppm to 50 ppm can be lethal in 60 to 90 minutes (Harbison, 1998; ILO, 1983).
- Exposure to 0.2 ppm to 16 ppm can produce mild mucous membrane irritation, whereas 7 ppm to 8 ppm causes eye irritation, 15 ppm produces throat irritation, and 30 ppm induces cough (Hathaway et al, 1996; ACGIH, 1991).
- Concentrations higher than 50 ppm can induce pneumonitis, and death can occur within minutes of exposure to 400 ppm to 1000 ppm. Chlorine can also occur at concentrations in air sufficient to allow it to act as an asphyxiant (Winder, 2001).
- Pulmonary effects can be delayed in onset and include acute lung injury and intense reflex coughing, which can be painful (Lewis, 1996; ILO, 1983). Immediate effects on pulmonary function testing may be seen, but these are reversible in most cases (Das & Blanc, 1993).
- Respiratory effects in victims of chlorine gassing in World War I were generally thought to be reversible, but this conclusion is clouded by the mixed chemical exposures and unknown contribution of tuberculosis in this population. Increased respiratory symptoms and impaired lung function have been reported in people exposed to sufficiently high levels to have been considered "gassed." Whether chlorine causes irreversible pulmonary effects is controversial (Winder, 2001).
- Chlorine has also been reported to induce irritant asthma, reactive airways dysfunction syndrome, or both. Agents capable of inducing reactive airways dysfunction syndrome typically do so after episodic intense exposure (Winder, 2001).
- Acute exposure to chlorine gas (concentration unknown) for approximately 5 minutes produced bronchiolitis in a previously healthy young adult. The patient was successfully treated; pulmonary function studies repeated at 12 weeks were markedly improved (Parimon et al, 2004).
- Three people who had no history of respiratory symptoms developed intermittent dyspnea on exertion and typical features of reactive airways dysfunction syndrome at least 2.5 years after an acute exposure incident. Typical inflammatory changes were seen in the bronchoalveolar lavage fluid 4 months after the exposure (Schonhofer et al, 1996).
- Inhalation of chlorine gas may cause metabolic acidosis (Szerlip & Singer, 1984).
- Chlorine is extremely irritating to the skin and can cause severe burns (HSDB, 2002).
- The mechanism of chlorine toxicity involves formation of hypochlorous and hydrochloric acids upon reaction of molecular chlorine with water in the body and subsequent ionization. Once inside the cell, the ions can produce oxygen free radicals. The ions and free radicals are highly reactive chemically and can participate in chlorination and oxidation (Winder, 2001).
- Neutrophils can generate reactive chlorine, and chlorine may be involved in inflammation, phagocytosis, and vascular disease (Hazen et al, 1996).
CHRONIC CLINICAL EFFECTS
- Chronic or repeated exposure to chlorine can produce tolerance to sensory irritation (Winder, 2001).
- Chronic exposure to chlorine produces the same effects as acute exposure and also seems to increase susceptibility to lung disease. Exposures below 0.5 ppm are thought to have no long-term effects. Chronic exposure to 1 ppm can cause a moderate but permanent reduction in pulmonary function (ILO, 1983). Short-term exposures above the stated exposure limits have been the main source of concern in occupational settings (Winder, 2001).
With continuing exposure, progressively distal portions of the respiratory system are affected, until the bronchioles and alveoli are involved. In more advanced stages, infiltration, exudation, and hemorrhage can occur, with alveolitis, bronchitis, and obstructive-type loss of respiratory function (Winder, 2001). Pneumonitis can develop, followed by pneumonia after consolidation of exudate. In severe cases, hemorrhagic pneumonia produces loss of lung structure and blood. If an inflammatory reaction has developed, progressive deterioration and fibrosis can occur after exposure has ended (Winder, 2001). In a cross-sectional study, repeated exposure of at least 10 "puffs" (mild gassing incidents) of chlorine over a 3-year period was associated with decreased FEV1 and FVC, as well as increased bronchial responsiveness to a methacholine challenge (Gautrin et al, 1995). In a related longitudinal study of 239 metal production workers, smokers experienced reduction in pulmonary function (FEV1) related to the number of "puffs" experienced in the 2-year period between the 2 assessments (Gautrin et al, 1999).
- Flulike symptoms developed in over 60% of workers after multiple exposures to chlorine gas over a 3- to 6-month period; the most frequent symptoms were throat and eye irritation, cough, headache, and shortness of breath (Courteau et al, 1994).
- Reactive airways dysfunction syndrome developed in a high percentage of workers who had multiple exposures to chlorine in a paper pulp mill. Follow up was 18 to 24 months after the last exposure. Of the affected patients, 82% still had respiratory symptoms, 41% had bronchial hyperresponsiveness, and 23% had evidence of bronchial obstruction on pulmonary function testing (Bherer et al, 1994).
- Hyposmia (reduced sense of smell), bronchitis, and "bleachery disease" (bleichererkrankung) have also been reported from occupational exposure to chlorine. "Bleachery disease" is characterized by premature aging, hemoptysis, and bronchial disease (Winder, 2001).
- Chronic exposure has caused corrosion of the teeth in swimmers (pH of pool water, 2.7) (Centerwall et al, 1986).
- No signs of nasal inflammation or reduction in pulmonary function were seen in 7 human volunteers exposed to random sequences of 0 ppm, 0.1 ppm, 0.3 ppm, and 0.5 ppm chlorine for 6 hours a day for 3 consecutive days at each concentration (Schins et al, 2000).
- Histopathologic signs of irritation and inflammation were seen in the nasal passages of rats and mice exposed to chlorine gas at concentrations up to 2.5 ppm for 6 hours per day, 5 days per week for 2 years (Wolf et al, 1995).
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Clothing frozen to the skin should be thawed before being removed. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Keep victim warm and quiet. Keep victim under observation. Effects of contact or inhalation may be delayed. 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. 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: Eyes, skin, and respiratory system (National Institute for Occupational Safety and Health, 2007).
GENERAL Move victims of inhalation exposure from the toxic environment and administer 100% humidified supplemental oxygen with assisted ventilation as required. Exposed skin and eyes should be copiously flushed with water. Ingestion may result in significant esophageal or gastrointestinal tract irritation or burns, and EMESIS SHOULD NOT BE INDUCED. Cautious gastric lavage followed by administration of activated charcoal may be of benefit if the patient is seen soon after the exposure.
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. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
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 the 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).
Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
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 contact with escaping gas may have caused frostbite of the eyes, DO NOT flush with water; early ophthalmologic consultation should be obtained.
ORAL EXPOSURE
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
It has been estimated that at 1 to 3 parts per million (ppm) mild mucous membrane irritation can occur; 5 to 15 ppm will cause moderate irritation of the upper respiratory tract; and 30 ppm will produce immediate chest pain, vomiting, dyspnea and cough. Exposures greater than or equal to 430 ppm chlorine for 30 minutes can be fatal to humans, as can exposures of 34 to 51 ppm for durations of 1 to 1.5 hours (Bingham et al, 2001). It should be noted that some individuals with airway hyperresponsiveness may develop an exaggerated response to even low levels of chlorine (Bingham et al, 2001). In a small study of 6 chlorine-exposed (range of exposure: 30 minutes to 12 hours) workers, it was observed that the development of reactive airway dysfunction syndrome appears unpredictable (Hickmann et al, 2001). LCLo values for human inhalation exposure of 2530 mg/m(3) for 30 minutes and 500 ppm for 5 minutes (RTECS , 2001). A few minutes or a few deep breaths of a level of 1000 ppm is fatal (Bingham et al, 2001; Hathaway et al, 1996; Sittig, 1991).
MAXIMUM TOLERATED EXPOSURE
Chlorine at concentrations at or below 1 parts per million (ppm), which is usually more than is generated in home exposures, has minimal effects. Exposure to sublethal amounts may lead to significant residual lung damage. Restrictive lung defects resolved within 1 month in 4 patients (Ploysongsang et al, 1982), but long-term effects have been reported (Schwartz et al, 1990; Givan et al, 1989; Decker, 1988) . Industrial incidents involving several exposures to chlorine may have delayed-onset pulmonary symptoms. It is possible for a person to be asymptomatic on the first evaluation. Acute lung injury and congestion can develop several hours after the exposure (Bingham et al, 2001). One or two breaths of gas accumulating above swimming pool or spa chlorinator tablets has caused marked respiratory distress and hypoxemia in children (Wood et al, 1987). Exposure to more than 14 ppm for 30 minutes or more may result in severe pulmonary damage (Bingham et al, 2001). Based on the results of a study in 29 men and women, a 2-part standard has been recommended: chlorine concentrations of 0.5 ppm, averaged over 8 hours, should not exceed 2 ppm for any 15-minute period. The study included both smokers and nonsmokers who were exposed to 0, 0.5, 1, or 2 ppm of chlorine over 4- and 8-hour time frames (Bingham et al, 2001; ACGIH, 1991).
- EFFECTS OF EXPOSURE LEVELS (HSDB , 2001; Lewis, 2000; Harbison, 1998; Ellenhorn & Barceloux, 1988):
- NIOSH considers 10 parts per million (ppm) immediately dangerous to life or health (NIOSH , 2001).
- Carcinogenicity Ratings for CAS7782-50-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Chlorine ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Chlorine EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Chlorine 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): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Chlorine MAK (DFG, 2002): Not Listed 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 CAS7782-50-5 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 1x10(-1) mg/kg-day
Inhalation: Drinking Water:
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS7782-50-5 (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 CAS7782-50-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS7782-50-5 (National Institute for Occupational Safety and Health, 2007):
Listed as: Chlorine REL: TWA: STEL: Ceiling: 0.5 ppm (1.45 mg/m(3)) [15-minute] Carcinogen Listing: (Not Listed) Not Listed Skin Designation: Not Listed Note(s):
IDLH: IDLH: 10 ppm Note(s): Not Listed
- OSHA PEL Values for CAS7782-50-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
Listed as: Chlorine Table Z-1 for Chlorine:
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7782-50-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7782-50-5 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7782-50-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS7782-50-5 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS7782-50-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Chlorine Reportable Quantity, in pounds: 10 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS7782-50-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS7782-50-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS7782-50-5 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1017 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1017 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS7782-50-5 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
The Chlorine Emergency Plan (CHLOREP) was established by the Chlorine Institute to improve the effectiveness and efficiency of response to chlorine incidents, industry-wide. Canada and the United States are divided into sectors, each manned with trained personnel on 24-hour alert to handle potential or actual emergencies. They can be contacted through CHEMTREC or CANUTEC (CGA, 1999).
HANDLING
- Equipment for handling moist chlorine at low pressures can be made of glass, porcelain, chemical stoneware, hard rubber, polyvinyl chloride, fiberglass-reinforced polyester, polyvinylidene chloride, fluoride and fully halogenated fluorocarbon resins, or certain alloys. Chlorine contained under high pressure should be stored in lined metallic or compatible metallic containers. Hastelloy C, titanium, and tantalum are commonly used. Titanium is used under restricted conditions for wet chlorine only (CGA, 1999).
STORAGE
Chlorine is stored and shipped as a liquefied gas under pressure. Acceptable containers include steel cylinders, ton containers, tank motor vehicles, tank cars, and tank barges. Pressure relief valves are usually installed in containers (OHM/TADS , 2001; CGA, 1999; NFPA, 1997). Steel piping equipment may be used to carry dry chlorine. Neither gas nor liquid chlorine corrodes steel at normal temperatures. Moisture and elevated temperatures can cause stress corrosion cracking (CGA, 1999). Iron, steel, nickel, silver, tantalum, copper, lead, and platinum are resistant to dry chlorine liquid or gas at temperatures below 121 degrees C (250 degrees F) (CGA, 1999).
For low-pressure applications, moist chlorine may be stored in chemical stoneware, glass, or porcelain containers. Hard rubber, plasticized polyvinyl chloride, glass fiber-reinforced polyester, polyvinylidene chloride or fluoride, or fully halogenated fluorocarbon resin containers may also be used (CGA, 1999). Auxiliary valves and gauges designed specifically for chlorine gas should be used, and stainless steel equipment should not be used. Some stainless steels may fail from corrosion, especially in the presence of moisture or high temperatures (HSDB , 2001; CGA, 1999). Containers should be protected from physical damage and heat. Cylinders should be stored and secured in an upright position (ITI, 1995). Cylinders should never be heated (Budavari, 2000). Permanent storage of chlorine is not recommended, but amounts up to 450 tons stored as liquefied gas under pressure may be safely stored. Large quantities should be stored at atmospheric pressure at low temperatures with appropriate safety devices installed in case of leaks or refrigeration failure (HSDB , 2001).
- ROOM/CABINET RECOMMENDATIONS
Chlorine should be stored in a dry, well-ventilated, outside or detached location (OHM/TADS , 2001; NFPA, 1997; ITI, 1995). Storage locations should have a containment vessel or Chlorine Institute Emergency Kit readily available. Emergency response personnel should be trained in their use (CGA, 1999).
Separate chlorine from combustible, organic, or easily oxidizable materials. It should be isolated from ether, ammonia, hydrogen, finely divided metals, hydrocarbons, acetylene, turpentine, and ammonia (OHM/TADS , 2001; NFPA, 1997). Chlorine mixed with moisture is extremely corrosive to bronze, zinc, steel, and iron (Pohanish & Greene, 1997). Chlorine attacks plastics and coatings (Pohanish & Greene, 1997). Dry chlorine and titanium will burn spontaneously on contact (CGA, 1999).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Contact with chlorine in liquid form should be avoided because of the danger of frostbite (NIOSH , 2001; AAR, 2000).
EYE/FACE PROTECTION
- Safety goggles should be worn at all times when in the vicinity of liquid chlorine (CHRIS , 2001).
RESPIRATORY PROTECTION
- 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 7782-50-5.
ENGINEERING CONTROLS
- Local exhaust ventilation can be used to contain vapors at the point of emissions (HSDB , 2001; Zenz, 1994).
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004) Substance does not burn but will support combustion. Vapors from liquefied gas are initially heavier than air and spread along ground. These are strong oxidizers and will react vigorously or explosively with many materials including fuels. May ignite combustibles (wood, paper, oil, clothing, etc.). Some will react violently with air, moist air and/or water. Cylinders exposed to fire may vent and release toxic and/or corrosive gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket.
Chlorine is not combustible, but it is a strong oxidizer and will support the combustion of other materials (Lewis, 1997).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS7782-50-5 (NFPA, 2002):
- INITIATING OR CONTRIBUTING PROPERTIES
Chlorine can be a strong oxidizer in certain circumstances (CGA, 1999; CHRIS , 2001; NFPA, 1997). Most combustible materials will burn in chlorine (CGA, 1999; CHRIS , 2001; NFPA, 1997).
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Water only; no dry chemical, CO2 or Halon®. Contain fire and let burn. If fire must be fought, water spray or fog is recommended. Do not get water inside containers. Move containers from fire area if you can do it without risk. Damaged cylinders should be handled only by specialists.
- TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (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 CAS7782-50-5 (NFPA, 2002):
- Water may be used in flooding quantities as fog and to cool exposed containers (AAR, 2000; (ITI, 1995; OHM/TADS , 2001).
- If a container is leaking during a fire, do not spray water directly on the leak. The reaction with the water forms acids causing the leak to worsen (CGA, 1999).
Combustible materials that burn in chlorine will form irritating and toxic gases (NFPA, 1997). Chlorine may combine with water or steam to produce toxic and corrosive fumes of hydrochloric acid (HSDB , 2001).
EXPLOSION HAZARD
- Chlorine may react explosively or form explosive compounds with many common substances such as acetylene, ether, turpentine, ammonia, fuel gas, hydrogen, and finely divided metals (NIOSH , 2001).
- Mixtures of chlorine and hydrogen, at 5-95%, can explode from contact with almost any form of energy like sunlight, heat, or sparks (Sittig, 1991).
- For more detailed information on the explosive hazards of chlorine, see the REACTIVITY HAZARD section of this management.
DUST/VAPOR HAZARD
- Chlorine gas can be severely irritating if inhaled (CGA, 1999).
- Chlorine gas tends to remain near the ground or settle in low areas because it is approximately 2.5 times heavier than air (AAR, 2000; (CGA, 1999).
- When chlorine reacts with water it produces a poisonous, visible vapor cloud (CHRIS , 2001).
- Vapors are a poison and explosive hazard indoors, outdoors, or in sewers (Sittig, 1991).
REACTIVITY HAZARD
- The halogens, including chlorine, are some of the most chemically reactive elements (Sittig, 1991).
Chlorine combines readily with all elements except the rare gases, (excluding xenon) and nitrogen (Budavari, 2000; HSDB , 2001).
- Chlorine may react explosively or form explosive compounds with many common substances such as acetylene, ether, turpentine, ammonia, fuel gas, hydrogen, and finely divided metals (NIOSH , 2001).
- Chlorine explodes on contact with the following (Lewis, 2000; Pohanish & Greene, 1997):
acetylene + heat or ultraviolet light acetylene alone air + ethylene alcohols molten aluminum ammonia amidosulfuric acid antimony trichloride + tetramethyl silane (at 100 degrees C) benzene + light biuret bromine pentafluoride + heat tert-butyl alcohol butyl rubber + naphtha carbon disulfide + iron catalyst carbon disulfide alone chlorinated pyridine + iron powder 3-chloropropyne cobalt(II) chloride + methanol diborane dibutyl phthalate (at 118 degrees C) dichloro (methyl)arsine (in a sealed container) diethyl ether dimethyl phosphoramidate dioxygen difluoride disilyl oxide 4,4'-dithiodimorpholine ethane over activated carbon (at 350 degrees C) finely divided metals fluorine + sparks gasoline glycerol (above 70 degrees C in a sealed container) hexachlorodisilane (above 300 degrees C) hydrocarbon oils or waxes hydrogen iron(III) chloride + monomers (e.g., styrene) methane over mercury oxide methanol methanol + tetrapyridine cobalt(II) chloride naphtha + sodium hydroxide nitrogen triiodide organic compounds oxygen difluoride white phosphorus (in liquid chlorine) petroleum products phosphorus phosphorus compounds polypropylene + zinc oxide propane (at 300 degrees C) silicones when heated in a sealed container (e.g., polydimethyl siloxane (above 88 degrees C); polymethyl trifluoropropylsiloxane (above 68 degrees C)) stibine synthetic rubber (in liquid chlorine) tetraselenium tetranitride trimethyl thionophosphate turpentine
- Chlorine explodes on contact with the following (Lewis, 2000; Pohanish & Greene, 1997): acetylene + heat or ultraviolet lightacetylene aloneair + ethylenealcoholsmolten aluminumammoniaamidosulfuric acidantimony trichloride + tetramethyl silane (at 100 degrees C)benzene + lightbiuretbromine pentafluoride + heattert-butyl alcoholbutyl rubber + naphthacarbon disulfide + iron catalystcarbon disulfide alonechlorinated pyridine + iron powder3-chloropropynecobalt(II) chloride + methanoldiboranedibutyl phthalate (at 118 degrees C)dichloro (methyl)arsine (in a sealed container)diethyl etherdimethyl phosphoramidatedioxygen difluoridedisilyl oxide4,4'-dithiodimorpholineethane over activated carbon (at 350 degrees C)finely divided metalsfluorine + sparksgasolineglycerol (above 70 degrees C in a sealed container)hexachlorodisilane (above 300 degrees C)hydrocarbon oils or waxeshydrogeniron(III) chloride + monomers (e.g., styrene)methane over mercury oxidemethanolmethanol + tetrapyridine cobalt(II) chloridenaphtha + sodium hydroxidenitrogen triiodideorganic compoundsoxygen difluoridewhite phosphorus (in liquid chlorine)petroleum productsphosphorusphosphorus compoundspolypropylene + zinc oxidepropane (at 300 degrees C)silicones when heated in a sealed container (e.g., polydimethyl siloxane (above 88 degrees C); polymethyl trifluoropropylsiloxane (above 68 degrees C))stibinesynthetic rubber (in liquid chlorine)tetraselenium tetranitridetrimethyl thionophosphateturpentine
acetylene + heat or ultraviolet light acetylene alone air + ethylene alcohols molten aluminum ammonia amidosulfuric acid antimony trichloride + tetramethyl silane (at 100 degrees C) benzene + light biuret bromine pentafluoride + heat tert-butyl alcohol butyl rubber + naphtha carbon disulfide + iron catalyst carbon disulfide alone chlorinated pyridine + iron powder 3-chloropropyne cobalt(II) chloride + methanol diborane dibutyl phthalate (at 118 degrees C) dichloro (methyl)arsine (in a sealed container) diethyl ether dimethyl phosphoramidate dioxygen difluoride disilyl oxide 4,4'-dithiodimorpholine ethane over activated carbon (at 350 degrees C) finely divided metals fluorine + sparks gasoline glycerol (above 70 degrees C in a sealed container) hexachlorodisilane (above 300 degrees C) hydrocarbon oils or waxes hydrogen iron(III) chloride + monomers (e.g., styrene) methane over mercury oxide methanol methanol + tetrapyridine cobalt(II) chloride naphtha + sodium hydroxide nitrogen triiodide organic compounds oxygen difluoride white phosphorus (in liquid chlorine) petroleum products phosphorus phosphorus compounds polypropylene + zinc oxide propane (at 300 degrees C) silicones when heated in a sealed container (e.g., polydimethyl siloxane (above 88 degrees C); polymethyl trifluoropropylsiloxane (above 68 degrees C)) stibine synthetic rubber (in liquid chlorine) tetraselenium tetranitride trimethyl thionophosphate turpentine
- Explosive products are formed when chlorine reacts with the following (Lewis, 2000; NFPA, 1994):
alkylthiouronium salts amidosulfuric acid acidic ammonium chloride solutions aziridine bis(2,4-dinitrophenyl) disulfide cyanuric acid phenyl magnesium bromide 2-chloroheptyl 4-nitrophenyl sulfide or its 2,4-dinitro analogue in presence of lithium perchlorate S-ethyl isothiourea + formamidine thiolacetic acid HCl
- Explosive mixtures of chlorine and ethylene are initiated by light, heat, or the presence of mercury, mercury oxide, silver oxide, or lead oxide (at 100 degrees C) (Lewis, 2000).
- Explosive mixtures of chlorine and hydrogen are initiated by sparks, light, heating over 280 degrees C, or the presence of yellow mercuric oxide or nitrogen trichloride (Lewis, 2000).
Explosive mixtures are also formed when chlorine combines with hydrogen along with other gases such as air, hydrogen chloride, or oxygen (Lewis, 2000).
- Ignition or explosive reaction will occur when chlorine combines with the following metals (Lewis, 2000; Pohanish & Greene, 1997):
aluminum antimony powder bismuth powder brass calcium powder copper germanium iron manganese potassium tin vanadium powder
- Ignition or explosive reaction will occur when chlorine combines with the following metals (Lewis, 2000; Pohanish & Greene, 1997): aluminumantimony powderbismuth powderbrasscalcium powdercoppergermaniumironmanganesepotassiumtinvanadium powder
aluminum antimony powder bismuth powder brass calcium powder copper germanium iron manganese potassium tin vanadium powder
- Ignition will occur with the following (Lewis, 2000; NFPA, 1994):
diethyl zinc (on contact) polyisobutylene (at 130 degrees C) metal acetylides metal carbides metal hydrides (e.g. potassium hydride; sodium hydride; copper hydride) metal phosphides (e.g. copper(II) phosphide) methane + oxygen hydrazine hydroxylamine calcium nitride non-metals (e.g., boron; active carbon; silicon; phosphorus) non-metal hydrides (e.g., arsine; phosphine; silane) polymer of oxomonosilane steel (above 200 degrees C or as low as 50 degrees C when impurities are present) sulfides (e.g., arsenic disulfide; boron trisulfide; mercuric sulfide) trialkyl boranes
- Chlorine reacts violently with the following (Lewis, 2000):
- An incandescent reaction occurs when chlorine is warmed with the following (Lewis, 2000; NFPA, 1994):
- A potentially dangerous reaction may occur between chlorine and hydrocarbons + Lewis acids, when toxic and reactive hydrochloric gas is released (Lewis, 2000).
- Chlorine may react with the following, causing fires or explosions upon contact (Lewis, 2000; NFPA, 1997; Pohanish & Greene, 1997):
turpentine illuminating gas polypropylene rubber sulfamic acid As2(CH3)4 UC2 acetaldehyde alcohols alkylisothiourea salts alkyl phosphines aluminum antimony arsenic arsenic compounds AsS2 arsine (AsH3) barium phosphide (Ba3P2) C6H6 bismuth boron BPI2 B2S3 brass (bromium pentafluoride (BrF5) calcium calcium compounds CaC2 + KOH calcium chlorite (Ca(ClO2)2) Ca3N2 Ca3P2 carbon carbon disulfide (CS2) cesium CsHC2 Co2O Cs3N (C + Cr(OCl)2) copper CuH2 CuC2 cuprous acetylide dialklyl phosphines diborane dibutyl phthalate ethyl phosphine diethyl zinc (Zn(C2H5)2) ethane (C2H6) ethylene (C2H4) ethylene imine C2H5PH2 fluorine (F2) germanium glycerol (NH2)2 (H2O + KOH) iodine (I2) hydrocarbons hydroxylamine iron FeC2 lithium Li2C2 Li6C2 magnesium Mg2P3 manganese Mn3P2 HgO HgS mercury Hg3P2 CH4 niobium NI3 OF2 H2SiO (OF2 + Cu) PH3 phosphorus P(SNC)3 P2O3 polychlorinated biphenyls (PCBs) potassium KHC2 KH rubber rubidium RuHC2 silicon SiH2 silver oxide (Ag2O) sodium NaHC2 Na2C2 stannous fluoride (SnF2) SbH3 Sr3P tellurium thorium tin tungsten dioxide (WO2) uranium vanadium zinc ZrC2
- Combustible materials that burn in chlorine will form irritating and toxic gases (NFPA, 1997).
- Chlorine may combine with water or steam to produce toxic and corrosive fumes of hydrochloric acid (HSDB , 2001).
- The autoignition temperatures of some halogenated hydrocarbons are considerably reduced in the presence of chlorine compared to those in air. Examples include the following (Urben, 1999):
chloromethane: 215 degrees C (618 degrees C, air) dichloromethane: 262 degrees C (556 degrees C, air) 1,2-dichloropropane: 180 degrees C (555 degrees C, air)
- The autoignition temperatures of some halogenated hydrocarbons are considerably reduced in the presence of chlorine compared to those in air. Examples include the following (Urben, 1999): chloromethane: 215 degrees C (618 degrees C, air)dichloromethane: 262 degrees C (556 degrees C, air)1,2-dichloropropane: 180 degrees C (555 degrees C, air)
chloromethane: 215 degrees C (618 degrees C, air) dichloromethane: 262 degrees C (556 degrees C, air) 1,2-dichloropropane: 180 degrees C (555 degrees C, air)
- Chlorine readily attacks cesium nitride (NFPA, 1997).
- The reaction of chlorine and hydrogen peroxide in strong potassium hydroxide solution results in red luminescence (NFPA, 1997).
- Flaming occurs when liquid chlorine in heptane is added to red phosphorus at 0 degrees C (HSDB , 2001; NFPA, 1997).
- Attacks some plastics and coatings extremely corrosive to iron, steel, copper, bronze, and zinc in the presence of moisture (Pohanish & Greene, 1997).
EVACUATION PROCEDURES
- Initial Isolation and Protective Action Distances (ERG, 2004)
Data presented from the Emergency Response Guidebook Table of Initial Isolation and Protective Action Distances are for use when a spill has occurred and there is no fire. If there is a fire, or if a fire is involved, evacuation information presented under FIRE - PUBLIC SAFETY EVACUATION DISTANCES should be used. Generally, a small spill is one that involves a single, small package such as a drum containing up to approximately 200 liters, a small cylinder, or a small leak from a large package. A large spill is one that involves a spill from a large package, or multiple spills from many small packages. Suggested distances to protect from vapors of toxic-by-inhalation and/or water-reactive materials during the first 30 minutes following the spill.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 100 meters (330 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (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. Ventilate closed spaces before entering.
- Downwind evacuation of one-half mile should be considered based on the amount spilled, location, and weather if this material is leaking but not on fire (AAR, 2000).
- If the spill is a 55 pound drum or smaller, then isolate the area 140 feet in all directions. A larger spill from multiple drums or from a tank needs an evacuation area of 290 feet in all directions. The area should be isolated until the vapors have dispersed (Sittig, 1991).
- AIHA ERPG Values for CAS7782-50-5 (AIHA, 2006):
- DOE TEEL Values for CAS7782-50-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
- AEGL Values for CAS7782-50-5 (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):
Listed as: Chlorine Final Value: AEGL-1 10 min exposure: ppm: 0.5 ppm mg/m3: 1.5 mg/m(3)
30 min exposure: ppm: 0.5 ppm mg/m3: 1.5 mg/m(3)
1 hr exposure: ppm: 0.5 ppm mg/m3: 1.5 mg/m(3)
4 hr exposure: ppm: 0.5 ppm mg/m3: 1.5 mg/m(3)
8 hr exposure: ppm: 0.5 ppm mg/m3: 1.5 mg/m(3)
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Chlorine Final Value: AEGL-2 10 min exposure: ppm: 2.8 ppm mg/m3: 8.1 mg/m(3)
30 min exposure: ppm: 2.8 ppm mg/m3: 8.1 mg/m(3)
1 hr exposure: ppm: 2 ppm mg/m3: 5.8 mg/m(3)
4 hr exposure: ppm: 1 ppm mg/m3: 2.9 mg/m(3)
8 hr exposure: ppm: 0.7 ppm mg/m3: 2 mg/m(3)
Definitions: AEGL-2 is the airborne concentration 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.
Listed as: Chlorine Final Value: AEGL-3 10 min exposure: ppm: 50 ppm mg/m3: 145 mg/m(3)
30 min exposure: ppm: 28 ppm mg/m3: 81 mg/m(3)
1 hr exposure: ppm: 20 ppm mg/m3: 58 mg/m(3)
4 hr exposure: ppm: 10 ppm mg/m3: 29 mg/m(3)
8 hr exposure: ppm: 7.1 ppm mg/m3: 21 mg/m(3)
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS7782-50-5 (National Institute for Occupational Safety and Health, 2007):
IDLH: 10 ppm Note(s): Not Listed
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004) Fully encapsulating, vapor protective clothing should be worn for spills and leaks with no fire. Do not touch or walk through spilled material. Keep combustibles (wood, paper, oil, etc.) away from spilled material. Stop leak if you can do it without risk. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Do not direct water at spill or source of leak. 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. Ventilate the area.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
For leaks from containers, attempt to turn the container so that gas, instead of liquid escapes which will reduce the quantity of chlorine released. A Chlorine Institute Emergency Kit, or a recovery containment vessel, and emergency assistance should be obtained. If possible, pressure in the container should be reduced by removing the chlorine as a gas to process or for disposal. The container should be removed to an isolated, or well ventilated location (CGA, 1999; HSDB , 2001). Liquid spills should be diked for containment and spilled chlorine neutralized. Water spray may be used to knock down chlorine gas vapors but the runoff water is corrosive and should be diked for containment (AAR, 2000). All actions should be in accordance with the Chlorine Emergency Plan established by the Chlorine Institute. The formalized plan is to minimize injuries during a potential or actual incident. The United States and Canada are divided into sectors with trained personnel assigned on 24-alert to handle emergencies if they occur in their area (CGA, 1999).
If the spill is a 55 pound drum or smaller, then isolate the area 140 feet in all directions (Sittig, 1991). Chlorine disolves in water in a few hours if the spill occurs more than 4.5 feet below the water's surface followed by an atmospheric vapor cloud (OHM/TADS , 2001). A leak from equipment or piping can be handled by disposing of the remaining chlorine in an alkaline solution (CGA, 1999). Valve leaks that cannot be stopped by tightening the packaging nut or closing the valve and evacuating the outlet piping will require a Chlorine Institute Emergency Kit. Kit A is appropriate for 100 pound to 150 pound cylinders (CGA, 1999). Recovery vessels are commercially available to contain an entire cylinder, if other steps to stop the leak have not proven successful (CGA, 1999). Suitable sorbents for chlorine include activated carbon, polyurethane, polyolefin, and Dowex 1 (HSDB , 2001). All actions should be in accordance with the Chlorine Emergency Plan established by the Chlorine Institute. The formalized plan is to minimize injuries during a potential or actual incident. The United States and Canada are divided into sectors with trained personnel assigned on 24-hour alert to handle emergencies if they occur in their area (CGA, 1999).
Wash beach or shore areas with a sodium thiosulfate solution (OHM/TADS , 2001). Large leaks will require Chlorine Institute Emergency Kits B, for ton containers, and C, for tank cars and trucks (CGA, 1999). In situ amelioration, using sodium thiosulfate and carbon, is effective for cleanup (OHM/TADS , 2001). A larger spill from multiple drums or from a tank needs an evacuation area of 290 feet in all directions. The area should be isolated until the vapors have dispersed (Sittig, 1991). Suitable sorbents for chlorine include activated carbon, polyurethane, polyolefin, and Dowex 1 (HSDB , 2001). All actions should be in accordance with the Chlorine Emergency Plan established by the Chlorine Institute. The formalized plan is to minimize injuries during a potential or actual incident. The United States and Canada are divided into sectors with trained personnel assigned on 24-hour alert to handle emergencies if they occur in their area (CGA, 1999).
"Recovery is an option to disposal for chlorine in the case of gases from aluminum chloride electrolysis and chlorine in wastewaters" (Sittig, 1991). Recovery vessels are commercially available to contain an entire cylinder, if other steps to stop the leak have not proven successful. Chlorine can be recaptured from the recovery vessel (CGA, 1999). 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.
Spilled chlorine may be neutralized in solutions of caustic soda, diluted HCl, or soda ash. Caution should be used because the heat of reaction of chlorine in alkaline solutions is substantial and the caustic solution may burn personnel (CGA, 1999; ITI, 1995). Reducing agents include:(HSDB , 2001; OHM/TADS , 2001): Reducing agents include:(HSDB , 2001; OHM/TADS , 2001): bisulfiteferrous saltcalcium sulfite hemihydratelignite filtratecellulose sulfite liquor from wood pulping Add chlorine to a large volume of concentrated reducer solution, prepared from hypo, a bisulfite, or a ferrous salt and acidified with 3M sulfuric acid. When reduction is complete, neutralize with soda ash, or dilute hydrochloric acid (HSDB , 2001).
To dispose of the contents of a leaking cylinder, force the gas from the leaking cylinder through a piece of flexible tubing connected to the valve outlet, at a moderate rate, into an alkaline solution in an appropriate container. Transport the resulting salt solution to a treatment plant for neutralization and disposal (HSDB , 2001). Environmental regulatory agencies should be consulted prior to land disposal of waste residue or waste sludge containing chlorine (HSDB , 2001). Ultraviolet radiation has been shown to remove up to 99% of the total chlorine in municipal water (HSDB , 2001).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Chlorine may enter the atmosphere during its production, transportation, and use. There are no known natural sources (HSDB , 2001).
- Chlorine is listed on the EPA's hazardous air pollutant (HAP) list of substances known or suspected to cause serious health problems (HSDB , 2001).
ENVIRONMENTAL FATE AND KINETICS
SURFACE WATER Free chlorine released to water is very unstable. It will rapidly oxidize inorganic compounds and will oxidize organic compounds at a slower rate (HSDB , 2001). Chlorine may react with organic precursors found in source waters to produce compounds such as chloroform, which is a potential carcinogen (HSDB , 2001).
ABIOTIC DEGRADATION
- Chlorine loss in seawater has two phases, the rapid initial loss followed by a continual loss at a significantly slower rate. The true organic demand appears to have an influence on the initial loss saturation levels in various natural seawater samples. Seawater with bromine shows distinct losses over a 10-day period. Other studies indicate that the bromide chemical system in seawater accounts for the chlorine loss (HSDB , 2001).
BIOACCUMULATION
ENVIRONMENTAL TOXICITY
- Chlorine is harmful to many forms of aquatic life in concentrations below 0.1 ppm (CGA, 1990).
- Chlorine may adversely affect vegetation by retarding growth and yield (CGA, 1990).
- (Values are from OHM/TADS, 2001 unless noted otherwise:)
LC25 - (WATER) CARP: 0.15-0.2 mg/L for 12-16D (HSDB, 2001) LC25 - (WATER) CARP: 0.15 ppm for 288H LC28 - (WATER) GREEN SUNFISH (Lepomis cyanellus): 3.0 mg/L for 24H LC50 - (WATER) BLUEGILL SUNFISH (Lepomis macrochirus): 0.44 mg/L for 96H-intermittent (at 15 degrees C) (HSDB, 2001) LC50 - (WATER) CHANNEL CATFISH (Ictalurus punctatus), Fingerling: 0.07 mg/L for 96H (HSDB, 2001) LC50 - (WATER) COHO SALMON (Oncorhynchus kisutch): 208 mcg/L for 1H (HSDB, 2001) LC50 - (WATER) DAPHNIA PULEX: 0.49 mg/L for 96H (HSDB, 2001) LC50 - (WATER) EMERALD SHINER, Yearling: 0.23 mg/L for 30M (Lake Superior) (HSDB, 2001) LC50 - (WATER) EMERALD SHINER, Adult: 0.28 mg/L for 30M (Lake Superior) (HSDB, 2001) LC50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 0.07-0.15 ppm for 96H LC50 - (WATER) FATHEAD MINNOW (Pimephales promelas): >0.79 ppm for 1H LC50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 0.26 ppm for 12H LC50 - (WATER) GAMBUSIA AFFINIS: 1.59 mg/L for 30M (HSDB, 2001) LC50 - (WATER) GAMBUSIA AFFINIS: 0.84 mg/L for 1H (HSDB, 2001) LC50 - (WATER) LARGEMOUTH BASS (Micropterus salmoides): 0.74 g/L for 1H (HSDB, 2001) LC50 - (WATER) LARGEMOUTH BASS (Micropterus salmoides): > 0.74 ppm for 1H LC50 - (WATER) LARGEMOUTH BASS (Micropterus salmoides): 0.365 ppm for 12H LC50 - (WATER) WATER FLEA (Daphnia magna): 0.097 mg/L for 30M (HSDB, 2001) LC50 - (WATER) WATER FLEA (Daphnia magna): 0.063 mg/L for 1H (HSDB, 2001) LC50 - (WATER) WATER FLEA (Daphnia magna): 0.017 mg/L for 46H (HSDB, 2001) LC50 - (WATER) YELLOW PERCH: 0.88 mg/L for 1H (HSDB, 2001) LC50 - (WATER) YELLOW PERCH: > 0.88 ppm for 1H LC50 - (WATER) YELLOW PERCH: 0.494 ppm for 12H LC100 - (WATER) CLAM, Larval: 0.5 mg/L for 100H (HSDB, 2001) LC100 - (WATER) BROWN TROUT: 0.04 ppm for 2M LD - (WATER) BULLFROG, Tadpole: 2 ppm for 12H; 76 degrees F (OHM/TADS, 2001) LD - (WATER) TROUT: 0.3 ppm for 2H (OHM/TADS, 2001) LD - (WATER) TROUT: 1 ppm for 1H (OHM/TADS, 2001) LD50 - (WATER) PLAICE, Larvae: 0.026 ppm for 48H LD50 - (WATER) PLAICE, Larvae: 0.024 ppm for 96H TL50 - (WATER) COHO SALMON (Oncorhynchus kisutch): 0.083 ppm for 168H TL50 - (WATER) BLACK BULLHEAD: 0.099 ppm for 96H TL50 - (WATER) BROOK TROUT: 0.083 ppm for 168H TL50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 0.1 mg/L for 96H (HSDB, 2001) TL50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 0.082-0.115 ppm for 168H TL50 - (WATER) KERATELLA COCHLEARIS: 0.019 mg/L for 4H (HSDB, 2001) TL50 - (WATER) LARGEMOUTH BASS (Salmo gairdnerii): 0.205 ppm for 168H TL50 - (WATER) RAINBOW TROUT: 0.14-0.29 ppm for 96H TL50 - (WATER) SMALLMOUTH BASS: 0.261 ppm for 168H TL50 - (WATER) WALLEYE: 0.15 ppm for 168H TL50 - (WATER) WHITE SUCKER: 0.132 ppm for 168H TLm - (WATER) GOLD FISH (Carassius auratus): 0.17 mg/L for 24H-intermittent chlorination (at 17-25 degrees C) (HSDB, 2001) TLm - (WATER) GRASS SHRIMP: 0.22 mg/L for 96H (HSDB, 2001) TLm - (WATER) OCEAN SPOT: 0.14 mg/L for 24H (HSDB, 2001) TLm - (WATER) RAINBOW TROUT (Salmo gairdnerii): 0.08 mg/L for 168H (HSDB, 2001) TLm - (WATER) TROUT: 0.08 ppm for 168H
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Chlorine is a greenish-yellow diatomic gas with an irritating, pungent, or suffocating odor (Budavari, 2000; Lewis, 1997; NIOSH , 2001).
- It condenses to an clear amber liquid at minus 35 degrees C and may also take the form of rhombic crystals (ACGIH, 1991; Lewis, 1997).
VAPOR PRESSURE
- 5 atm (at 10.3 degrees C) (Weast, 1989)
- 4800 mmHg (at 20 degrees C) (Lewis, 2000)
- 6.8 atm (at 68 degrees F) (NIOSH , 2001)
- 5.83X10(+3) mmHg (at 25 degrees C) (HSDB , 2001)
- 28.533 psia (at -17.8 degrees C; 0 degrees F) (CGA, 1999)
- 42.730 psia (at -6.7 degrees C; 20 degrees F) (CGA, 1999)
- 61.767 psia (at -4.4 degrees C; 40 degrees F) (CGA, 1999)
- 118.16 psia (26.7 degrees C; 80 degrees F) (CGA, 1999)
- 205.70 psia (48.9 degrees C; 120 degrees F) (CGA, 1999)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
1.4085 (at 20 degrees C and 6.864 atm) (liquid) (Budavari, 2000; HSDB, 2001) 2.485 (at 0 degrees; 32 degrees F) (1 atm) (gas) (CGA, 1999b) 1.57 (at -34 degrees C) (NFPA, 1997a) 1.5649 (at -35 degrees C and 0.9949 atm) (Budavari, 2000) 1.56 (at -35 degrees C) (Lewis, 1997a)
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
1.5649 g/mL (at -35 degrees C and 0.9949 atm) (liquid) (Budavari, 2000) 1.4085 g/mL (at 20 degrees C and 6.864 atm) (liquid) (Budavari, 2000) 1.47 g/mL (at 0 degrees C and 3.65 atm) (liquid) (Lewis, 2000) 0.20057 lb/ft(3) (at 0 degrees; 32 degrees F) (gas) (CGA, 1999b) 3.21 g/L (at 0 degrees C; 1 atm) (air=1.29) (Lewis, 1997a)
FREEZING/MELTING POINT
-105.5 degrees C (HSDB, 2001) -149.76 degrees F (at 1 atm) (CGA, 1999a)
BOILING POINT
- -34.05 degrees C (Budavari, 2000)
- -34 degrees C; -29 degrees F (NFPA, 1997; NIOSH , 2001)
- -34.1 C; -29.3 F (at 760 mmHg) (OSHA, 1978)
- -34.04 degrees C (HSDB , 2001)
- -29.15 degrees F (at 1 atm) (CGA, 1999)
- -34.9 degrees C (Lewis, 2000)
FLASH POINT
- Not Applicable (NIOSH , 2001)
EXPLOSIVE LIMITS
SOLUBILITY
310 mL/100 mL (at 10 degrees C) (HSDB , 2001; Weast, 1989) 1.46 g/100 mL (at 0 degrees C) (HDSB, 2001; (Weast, 1989) 177 mL/100 mL (at 30 degrees C) (HDSB, 2001; (Weast, 1989) 0.57 g/100 mL (at 30 degrees C) (HDSB, 2001; (Weast, 1989) 0.7% (by weight) (NIOSH , 2001) 0.7 g/100 mL (at 20 degrees C/68 degrees F) (OSHA, 1978)
OTHER/PHYSICAL
GAS: 1.0008 (Weast, 1989; HSDB , 2001) LIQUID: 1.367 (Weast, 1989; HSDB , 2001)
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