SULFUR DIOXIDE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
BISULFITE DIOXIDO DE AZUFRE FERMENICIDE LIQUID FERMENICIDE POWDER SCHWEFELDIOXYD (German) SIARKI DWUTLENEK (Polish) STRAW OIL SULFUR DIOXIDE SULFUR DIOXIDE (ANHYDROUS) SULFUR DIOXIDE (LIQUID) SULFUR DIOXIDE, LIQUEFIED SULFUR OXIDE SULFUR SUPEROXIDE SULFUROUS ACID ANHYDRIDE SULFUROUS ANHYDRIDE SULFUROUS OXIDE SULPHUR DIOXIDE SULPHUR DIOXIDE, LIQUEFIED SCHWEFELDIOXYD SIARKI DWUTLENEK
IDENTIFIERS
1079-Sulfur dioxide 1079-Sulfur dioxide, liquefied 1079-Sulphur dioxide 1079-Sulphur dioxide, liquefied
SYNONYM REFERENCE
- (Ariel GlobalView, 2002; CHRIS , 2002; HSDB , 2002; Lewis, 2000; RTECS , 2002)
USES/FORMS/SOURCES
Sulfur dioxide is used as a preservative for fruits and vegetables, as a disinfectant in breweries, granaries and food factories, for bleaching textile fibers, straw, wicker ware, gelatin, glue, beet sugars, and as a solvent (Ashford, 1994; Budavari, 2000). It is also used in the manufacture of sodium sulfate and sulfuric acid (Harbison, 1998). Sulfur dioxide is used as a dechlorination reagent (drinking water and effluent); in treating wood pulp for paper manufacturing; in ore and metal refining; extraction of lubricating oils; as a food additive (dried fruits and vegetables, meats, soups, and sauces); in refrigeration; in tanning; and as a reducing agent (AAR, 2000; ACGIH, 1991; Ashford, 1994; Budavari, 2000; CGA, 1999; Harbison, 1998; Hathaway et al, 1996). The majority of sulfur dioxide produced for captive use is employed in the sulfuric acid and wood pulp industries (ATSDR, 1998).
PHARMACEUTICALS - Bronchodilator aerosols have been demonstrated to release 0.1 to 6 ppm of sulfur dioxide when nebulized (Koepke et al, 1983). Sulfur dioxide is a colorless, nonflammable gas that is easily compressed to a liquid; it is supplied commercially as a liquid. It possesses a sharp, irritating, pungent odor (Budavari, 2000; CHRIS , 2002; Lewis, 2001; NIOSH , 2002). Available grades include commercial, USP, technical, refrigeration, food-grade and anhydrous (99.98% minimum) (CGA, 1999; Lewis, 2001). Specifications for food-grade sulfur dioxide are as follows (CGA, 1999):
Sulfur dioxide is formed when sulfur-containing materials are burned in air (Bingham et al, 2001; CGA, 1999; Lewis, 2001). It is also derived from the roasting of pyrites in a special furnace (Lewis, 2001). The gas is readily liquefied by cooling with ice and salt or at a pressure of three atm (Lewis, 2001). Selective absorption of sulfur dioxide from cleaned gas, followed by drying and liquefaction is also used for sulfur dioxide gases resulting from metallurgic and smelting operations (GCA, 1999). Sulfur dioxide is a by-product of fossil fuel combustion, petroleum refining, and paper manufacturing. It is also released during volcanic eruptions and naturally-occurring fires (Harbison, 1998). Point sources such as coal- and oil-fueled power plants and metal smelters are the main source of industrial airborne sulfur dioxide (Goldfrank, 1998). It is a common pollutant in urban areas (Baxter et al, 2000). It is one of the most frequently encountered irritant gasses (Bingham et al, 2001; CGA, 1999). Sulfur dioxide is a major contributor to acid rain (Franklin et al, 1985; (Goldfrank, 1998).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Sulfur dioxide (SO2) is an irritant colorless, nonflammable gas at room temperature with a characteristic pungent odor to warn of its presence. It is manufactured into sulfuric acid. It is mostly produced by the combustion of elemental sulfur, though it can also be generated by heating sulfide ores. Sulfuric dioxide is also used as a produce preservative, disinfectant, bleaching agent, and dechlorination reagent.
- TOXICOLOGY: Sulfur dioxide readily converts to sulfurous acid (H2SO3) upon contact with water. It also has irritant effects on the mucosa of the nasopharynx, respiratory tract, and conjunctiva, as well as causing bronchoconstriction.
- EPIDEMIOLOGY: Sulfur dioxide is commonly used in certain industries but significant acute exposures are rarely reported to poison centers. It is a major air pollutant from automobiles, smelters, and certain industrial plants.
ACUTE TOXICITY: Acute exposures may cause typical irritant gas symptoms such as burning of the eyes, nose, and throat, lacrimation, and cough. More severe symptoms include wheezing, a chemical bronchitis and laryngospasm. With severe exposures, patients may develop a chemical pneumonitis and noncardiogenic pulmonary edema. Exposures to levels of 400 to 500 ppm are considered immediately life-threatening. After exposure to high concentrations, victims who survive may develop residual obstructive or restrictive lung disease, reactive airway disease syndrome, or chronic bronchitis. DERMAL EXPOSURE: Dermal exposures from liquefied sulfur dioxide (boiling point -10 degree C or 14 degrees F) may cause serious skin (chemical burn) and frostbite injuries. OCULAR EXPOSURE: Eye exposures to sulfur dioxide may start with eye irritation from the formation of sulfurous acid. However, exposure to liquefied sulfur dioxide can cause severe corneal damage that can lead to blindness.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (ERG, 2004)
TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Vapors are extremely irritating and corrosive. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Fire will produce irritating, corrosive and/or toxic gases. Runoff from fire control may cause pollution.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Sulfur dioxide readily converts to sulfurous acid (H2SO3) upon contact with water. It also has irritant effects on the mucosa of the nasopharynx, respiratory tract, and conjunctiva, as well as causing bronchoconstriction. EPIDEMIOLOGY: Sulfur dioxide is commonly used in certain industries but significant acute exposures are rarely reported to poison centers. It is a major air pollutant from automobiles, smelters, and certain industrial plants. ACUTE TOXICITY: Acute exposures may cause typical irritant gas symptoms such as burning of the eyes, nose, and throat, lacrimation, and cough. More severe symptoms include wheezing, a chemical bronchitis and laryngospasm. With severe exposures, patients may develop a chemical pneumonitis and noncardiogenic pulmonary edema. Exposures to levels of 400 to 500 ppm are considered immediately life-threatening. After exposure to high concentrations, victims who survive may develop residual obstructive or restrictive lung disease, reactive airway disease syndrome, or chronic bronchitis. DERMAL EXPOSURE: Dermal exposures from liquefied sulfur dioxide (boiling point -10 degree C or 14 degrees F) may cause serious skin (chemical burn) and frostbite injuries. OCULAR EXPOSURE: Eye exposures to sulfur dioxide may start with eye irritation from the formation of sulfurous acid. However, exposure to liquefied sulfur dioxide can cause severe corneal damage that can lead to blindness.
- Sulfur dioxide is an irritant of the respiratory tract, eyes, and skin in acute exposures. Potentially fatal upper airway edema, obstruction, pulmonary edema, and other respiratory effects can occur following significant inhalational exposure (Charan et al, 1979; Harkonen et al, 1983). Perhaps the most sensitive indicator of exposure is BRONCHOCONSTRICTION (ACGIH, 1992). Bronchoconstriction may occur at airborne concentrations as low as 0.1 ppm for 10 minutes (Sheppard, 1981), with nose and throat irritation not noted until 6 ppm (Lewis, 1992). High levels of sulfur dioxide in Spanish pickled onions (765 to 1182 ppm) were responsible for outbreaks of asthma immediately after being eaten by 18 young extrinsic asthmatics (Gastaminza et al, 1995). Acute exposures have produced severe obstructive pulmonary disease which has been unresponsive to bronchodilators and has lasted 3 months after exposure (Clayton & Clayton, 1993).
- The lowest airborne concentration which is irritating to the eyes is 20 ppm; 50 to 100 ppm is the maximum tolerated concentration for 30 to 60 minutes (Lewis, 1992). Concentrations of 100 ppm or greater may cause adverse health effects or endanger life (NIOSH, 1994). Concentrations in the range of 400 to 500 ppm are immediately dangerous to life (Lewis, 1992). Death occurs from suffocation due to reflex spasm of the larynx, airway obstruction, from respiratory paralysis, or from shock (ILO, 1983). Contact with liquefied sulfur dioxide can cause eye burns and corneal damage (Grant, 1986). Frostbite can result from dermal contact with liquefied sulfur dioxide (US DHHS, 1981).
- In a group of 6 workers who were followed up 13 years after an acute exposure to high levels of sulfur dioxide, 5 had abnormal respiratory function (obstruction or combined obstructive and restrictive), and 4 showed bronchial hyperreactivity. The clinical picture was one of reactive airways dysfunction syndrome. Hence acute exposures may have long-lasting, if not permanent, effects (Piirila et al, 1996).
CHRONIC CLINICAL EFFECTS
- Chronic exposure to low levels of sulfur dioxide can produce the same irritant effects as acute exposure. Burning and dryness of the throat, bronchitis, and erosion of dental enamel can also occur with chronic exposure (ILO, 1983).
- While controlled exposures to sulfur dioxide have provoked asthmatic reactions in humans, there was no correlation between emergency room visits for asthma and peaks of sulfur dioxide air pollution in one study (Goldstein & Weinstein, 1986).
- Chronic exposure to concentrations greater than 1 ppm can lead to accelerated decline in pulmonary function, and exposures at or below 2 ppm can cause chronic respiratory disease (Smith et al, 1977). These exposures are below the current TLV (ACGIH(SM), 1996).
- Increased deaths from chronic obstructive lung disease were linked with exposure to pot emissions 20 to 39 years previously in a cohort of Norwegian aluminum smelter workers where sulfur dioxide was one of the most prevalent exposures (Ronneberg, 1995a; Ronneberg, 1995b). These deaths could not be attributed to sulfur dioxide alone because of mixed exposures to COAL TAR PITCH VOLATILES, FLUORIDES, and CARBON MONOXIDE (Ronneberg, 1995a).
- Chronic exposure to sulfur dioxide (mixed with ozone and ammonium sulfate) has altered the immunity of mice (Aranyi, 1983). Chronic exposures have been associated with asthma in humans (Koenig JQ, 1985) and guinea pigs (Kitabataka et al, 1981). Sulfur dioxide, however, did not induce allergic reactions in guinea pigs or rats (Ostapovich, 1975). Inhalation of 2 ppm for 192 days reduced antibody formation in mice, following transient increases (Zarkower, 1972).
- Survival of significant, acute inhalational exposure has been associated with the development of obstructive or restrictive lung disease, bronchitis, or hyperreactive airways (Charan et al, 1979; Harkonen et al, 1983) (Rabinovich et al, 1989).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (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. Remove and isolate contaminated clothing and shoes. In case of contact with liquefied gas, thaw frosted parts with lukewarm water. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. In case of contact with Hydrogen fluoride, anhydrous (UN1052), flush skin and eyes with water for 5 minutes; then, for skin exposures rub on a calcium/jelly combination; for eyes flush with a water/calcium solution for 15 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 (GAS/VAPOR FORM): 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).
SUMMARY 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. Endotracheal intubation, cricothyroidotomy or tracheostomy may be needed if upper airway obstruction is present.
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).
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 of the eye has occurred, DO NOT flush with water; early ophthalmologic consultation should be obtained.
ORAL EXPOSURE Ingestion is unlikely as sulfur dioxide is a gas at room temperature and pressure. However, oral exposure to liquefied sulfur dioxide can cause frostbite injury to the upper gastrointestinal and respiratory tracts. Administer oxygen and maintain airway as clinically indicated. Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
The lowest reported lethal concentrations of sulfur dioxide are 3000 ppm for 5 minutes and 1000 ppm for 10 minutes (RTECS , 2002; Sittig, 1991). Concentrations of 100 ppm to 500 ppm are considered immediately dangerous to life and health (ATSDR, 1999; Bingham et al, 2001; Lewis, 2000; NIOSH , 2002). Baxter et al (2000) reported 300 to 500 ppm as the 30 minute lethal concentration for "mammals" (Baxter et al, 2000). A concentration of 150 ppm over a few-minutes may be lethal to elderly individuals with asthma (Baxter et al, 2000). CASE REPORT: A 76-year-old previously healthy woman with asthma died following an inhalation exposure to sulfur dioxide produced from a sulfite-containing derusting agent. Duplication of the derusting procedure with only 7% to 10% of the derusting agent used by the patient resulted in sulfur dioxide concentrations of 150 ppm (Huber & Loving, 1991).
MAXIMUM TOLERATED EXPOSURE
It should be noted that the toxicity of sulfur dioxide is dependent upon whether it is present in an aerosol, on the humidity, and if there is other particulate matter present. A given concentration of sulfur dioxide is reported to elicit a greater response when inhaled through the mouth than when inspired through the nose (ACGIH, 1991; Bingham et al, 2001). Asthmatics and persons with pulmonary disease are more sensitive to sulfur dioxide in ambient air than are healthy individuals (ACGIH, 1991; Bingham et al, 2001). An estimated 10 to 20% of the adult population is hypersensitive to the adverse effects of sulfur dioxide (HSDB , 2002).
Sulfur dioxide is a severe irritant of the eyes, skin, and upper airways of the respiratory tract. The irritant effects of sulfur dioxide are due to the formation of sulfurous acid which quickly forms when the gas comes into contact with moist surfaces (CGA, 1999; Hathaway et al, 1996). Acute exposures to sulfur dioxide have caused severe obstructive pulmonary disease that is unresponsive to bronchodilators and may last up to 3 months after exposure (Bingham et al, 2001). One hundred ppm is the maximum concentration tolerated for exposures of 30 to 60 minutes in duration. This is also the level established by NIOSH (2002) as immediately dangerous to life and health (Bingham et al, 2001). A healthy individual can tolerate concentrations no greater than 150 ppm for a few minutes (Baxter et al, 2000). Levels of sulfur dioxide in the air of less than 0.25 ppm (0.65 mg/m(3)) do not elicit an airway response in sensitive individuals, presumably because at this concentration, the sulfur dioxide is removed by the nose and mouth ((IARC, 1992)). Healthy individuals did not respond to sulfur dioxide levels less than 1 ppm (Baxter et al, 2000). CASE SERIES: Twelve healthy, young adult males were exposed continuously to sulfur dioxide for 120 hours. No adverse pulmonary effects were reported at exposure levels of 0.3 or 1 ppm, while exposure to 3 ppm caused a slight and reversible increase in airway resistance and decrease in compliance (ACGIH, 1991). In a study where subjects breathed through the mouth, a brief exposure to 1 ppm sulfur dioxide caused no effects (Hathaway et al, 1996). Significant bronchoconstriction was seen in mild asthmatics in response to exposure of 0.5 to 1 ppm sulfur dioxide while engaged in mild exercise. These same subjects adapted to the low levels of sulfur dioxide after repeated short-term exercise in its presence, as evidenced by a decrease in the induced bronchoconstriction (Baxter et al, 2000; Bingham et al, 2001). Inhalation exposure to airborne concentrations of 10 to 50 ppm of sulfur dioxide for 5 to 15 minutes results in irritation of the nose and throat, choking, sneezing, coughing, and reflex bronchoconstriction with increased pulmonary resistance. Workers routinely exposed to sulfur dioxide adapt to irritating concentrations; repeated exposure to an airborne concentration of 10 ppm caused upper respiratory irritation and nosebleeds; these symptoms did not occur at 5 ppm (CGA, 1999; Hathaway et al, 1996; HSDB , 2002). Two miners exposed to concentrations of sulfur dioxide of at least 40 ppm suffered severe airway obstruction, hypoxemia, significantly reduced tolerance to exercise, and ventilation perfusion mismatch. They exhibited evidence of active inflammation as shown by a positive gallium lung scan (HSDB , 2002). Subjects that entered a study-chamber with a 25 ppm concentration of sulfur dioxide in the ambient air found this level to be intolerable on first contact. Those who had been gradually acclimated to this level did not find it as objectionable (HSDB , 2002). Individuals with mild asthma have demonstrated much greater sensitivity to sulfur dioxide exposure (Hathaway et al, 1996). Pulmonary function test changes from baseline have been recorded in exercising asthmatic subjects exposed to airborne concentrations as low as 0.5 to 1 ppm for 2 minutes or longer (Roger et al, 1985; Schachter et al, 1984; Horstman et al, 1988). No such changes were noted in normal subjects (Schachter et al, 1984). Injury to the eye from exposure to sulfur dioxide gas in the ambient air is very uncommon. However, several severe burns to the human eye following contact with liquid sulfur dioxide have been reported (Grant & Schuman, 1993). Liquid sulfur dioxide splashed into the eyes can cause burns and chemical trauma of the cornea and subsequent opacification and vision loss (CGA, 1999; Grant & Schuman, 1993; Hathaway et al, 1996). Liquid sulfur dioxide can cause frostbite and skin burns. Skin irritation may also result when sulfur dioxide converts to sulfurous acid in moist environments (CGA, 1999; Hathaway et al, 1996).
British steel workers were studied for effects from chronic exposure to sulfur dioxide at mean concentrations of 0.35 ppm (0.9 mg/m(3)). No effects were seen at this level (HSDB , 2002). Workers in a United States refrigerator company were studied for the effects of occupational exposure to sulfur dioxide used as a refrigerant. While workers did complain of respiratory symptoms, colds, fatigue and shortness of breath on exertion, no injury to the tracheobronchial tree or alveoli was seen. The exposures were estimated to average from 60 to 90 mg/m(3) (29-32 ppm), with peaks as high as 290 mg/m(3) (100 ppm) (HSDB , 2002). Mortality from asthma and chronic bronchitis has been noted to increase in response to worsening air pollution with sulfur dioxide and to decrease with decreased levels of sulfur dioxide air pollution (Imai et al, 1986). Children exposed to sulfur oxides as air pollutants did not show any statistically significant difference in pulmonary functions, lung growth, or frequency of respiratory disease when compared to controls in a longitudinal study (Dodge et al, 1985). Persons with a long history of exposure to high concentrations of sulfur dioxide may have an increased incidence of chronic bronchitis accompanied by emphysema (HSDB , 2002). Although sulfur dioxide itself is not considered a human carcinogen, it is thought to act as a cancer promoter (Bingham et al, 2001).
- Carcinogenicity Ratings for CAS7446-09-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Sulfur dioxide EPA (U.S. Environmental Protection Agency, 2011): Not Listed 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): 3 ; Listed as: Sulfur dioxide 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Sulfur dioxide 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 CAS7446-09-5 (U.S. Environmental Protection Agency, 2011):
References: ACGIH, 1991 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002 LC- (INHALATION)MOUSE: LC- (INHALATION)RAT: 993 ppm for 20M (OHM/TADS, 2002) 611 ppm for 5H (OHM/TADS, 2002)
LC50- (INHALATION)GUINEA_PIG: 130 ppm for 6.41D (ACGIH, 1991) 1000 ppm for 20H (ACGIH, 1991)
LC50- (INHALATION)MOUSE: 150 ppm for 5.04W (ACGIH, 1991) 3000 ppm for 30M -- convulsions or effect on seizure threshold, change in motor activity 1000 ppm for 4H (ACGIH, 1991)
LC50- (INHALATION)RAT: LCLo- (INHALATION)GUINEA_PIG: LCLo- (INHALATION)HUMAN: LCLo- (INHALATION)RAT: TCLo- (INHALATION)DOG: 1 ppm for 90M/1Y - Intermittent -- structural or functional changes in trachea or bronchi 500 ppm for 2H/21W - Intermittent -- structural or functional changes in trachea or bronchi, respiratory depression
TCLo- (INHALATION)GUINEA_PIG: 10 ppm for 1H/30D - Intermittent -- changes to the liver, kidney, ureter and bladder, biochemical changes (lipids including transport)
TCLo- (INHALATION)HUMAN: TCLo- (INHALATION)MOUSE: female, 5 ppm at 9D prior to mating and 1-14D of pregnancy -- behavioral effects on newborn female, 32 ppm for 24H at 7-18D of pregnancy -- effect on growth statistics, behavioral effects in newborn female, 25 ppm for 7H at 6-15D of pregnancy -- fetotoxicity female, 25 ppm for 7H at 6-15D of pregnancy -- developmental abnormalities of the musculoskeletal system 500 ppm for 5M/30W - Intermittent -- equivocal tumorigenic agent by RTECS criteria, tumors of the respiratory system
TCLo- (INHALATION)RABBIT: female, 70 ppm for 7H at 6-18D of pregnancy -- developmental abnormalities of the musculoskeletal system 200 mg/m(3) for 3H/13W - Intermittent -- cardiac changes, hemorrhage, changes to the liver
TCLo- (INHALATION)RAT: female, 4 mg/m(3) for 24H at 72D prior to mating -- effect on growth statistics of newborn, delayed effects on newborn female, 4 mg/m(3) for 24H -- change in menstrual cycle, parturition affected, female fertility index affected female, 4970 mcg/m(3) for 12H at 12W prior to mating -- menstrual cycle changes, effect on growth statistics of newborn male, 30 ppm for 6H at 21W prior to mating -- effects on testes, epididymis and sperm duct 10 ppm for 24H/14D - Intermittent -- food intake affected, changes to the liver, biochemical changes (lipids including transport) 400 ppm for 3H/6W - Intermittent -- structural or functional change in trachea or bronchi 100 ppm for 5H/28D - Intermittent -- changes to the respiratory system, liver and biochemical changes 500 mcg/m(3) for 96D - Intermittent -- changes in surface EEG, change in motor activity, changes to xanthine, purine or nucleotides including urate 4910 mcg/m(3) for 6H/17W - Intermittent -- pigmented or nucleated red blood cells, effects on cytochrome oxidases (including oxidative phosphorylation) and dehydrogenases
CALCULATIONS
1 mg/m(3) = 0.38 ppm (at 25 degrees C and 760 mmHg) (Clayton & Clayton, 1993) 1 ppm = 2.62 mg/m(3) (at 25 degrees C and 760 mmHg) (Clayton & Clayton, 1993; (IARC, 1992); NIOSH , 2002)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS7446-09-5 (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 CAS7446-09-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS7446-09-5 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS7446-09-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7446-09-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7446-09-5 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7446-09-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS7446-09-5 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS7446-09-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Sulfur Dioxide Reportable Quantity, in pounds: 500 Threshold Planning Quantity, in pounds: Note(s): f f: Chemicals on the original list that do not meet toxicity criteria but because of their acute lethality, high production volume and known risk are considered chemicals of concern ("Other chemicals"). (November 17, 1986, and February 15, 1990.)
- EPA SARA Title III, Community Right-to-Know for CAS7446-09-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS7446-09-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS7446-09-5 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1079 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1079 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS7446-09-5 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Sulfur dioxide gas is a poisonous, corrosive irritant to the respiratory system, eyes, and mucous membranes. Liquid sulfur dioxide can cause frostbite and skin burns. Skin irritation may also result when sulfur dioxide converts to sulfurous acid in moist environments. Liquid sulfur dioxide splashed into the eyes causes corneal burns and opacification resulting in vision loss (AAR, 2000; CGA, 1999; CHRIS , 2002; Grant & Schuman, 1993; Lewis, 2001). In order to prevent injury to personnel or damage to property, only properly trained individuals should be allowed to handle sulfur dioxide. Wear appropriate personal protective clothing, including respiratory protection, when working with or around sulfur dioxide; do not handle broken containers unless wearing appropriate protective clothing (AAR, 2000; CGA, 1999; Grant & Schuman, 1993; Hathaway et al, 1996; Lewis, 2000; NFPA, 1997). All handling, storage and use of compressed gases should be in accordance with Compressed Gas Association Pamphlets P-1-1965, C-6-1968 and C-8-1962 (OSHA, 2002c).
HANDLING
- Avoid contact with sulfur dioxide liquid and gas. Wear appropriate personal protective clothing, including respiratory protection; do not handle broken containers unless wearing appropriate protective clothing. Wash away any sulfur dioxide which may have contacted the body with copious amounts of water or soap and water (AAR, 2000; CGA, 1999; NFPA, 1997). If it is in the eyes, hold eyelids open and flush them out with large amounts of water (CHRIS , 2002; NIOSH , 2002).
- Wear goggles, chemical protective gloves and clothing, and a self-contained breathing apparatus, especially when contact with liquid sulfur dioxide is possible (CHRIS , 2002; HSDB , 2002; NIOSH , 2002).
- If liquid sulfur dioxide comes into contact with skin or the eyes, do not rub the affected area (CHRIS , 2002).
STORAGE
Sulfur dioxide is usually shipped in steel cylinders, pressurized tanks on trucks, rail cars, and barges. Typical containers for bulk shipments of liquefied, compressed sulfur dioxide are single-unit tank cars, multi-unit tank cars (TMUs), and cargo tanks. (CGA, 1999; ITI, 1988; NFPA, 1997; OHM/TADS , 2002; Sittig, 1991). Visual inspection of all compressed gas cylinders should be undertaken to determine that storage containers are in a safe condition (OSHA, 2002c). Compressed gas cylinders, portable tanks, and cargo tanks should have pressure relief devices installed and maintained in accordance with Compressed Gas Association Pamphlets S-1.1-1963 and 1965 addenda and S-1.2-1963 (OSHA, 2002c).
- ROOM/CABINET RECOMMENDATIONS
Store sulfur dioxide in a cool, dry, well-ventilated location (NFPA, 1997; OHM/TADS , 2002) . Eye wash stations should be readily available (HSDB , 2002; Sittig, 1991). Outside or detached, ventilated, fireproof storage is preferred. Protect containers from damage and keep sulfur dioxide below 54 degrees C (130 degrees F) (CHRIS , 2002; ITI, 1995; NFPA, 1997; OHM/TADS , 2002; Sittig, 1991). Because sulfur dioxide liquid expands as the temperature increases, at adequately elevated temperatures it is possible for hydrostatic pressure in a full container to rupture through a pressure relief device and discharge toxic vapors (GCA, 1999). Sulfur dioxide is corrosive in the presence of moisture to carbon steel, copper, aluminum, and brass. Store away from areas constructed with these materials in situations where sulfur dioxide may become moist (CGA, 1999; CHRIS , 2002; NFPA, 1997; NIOSH , 2002). Local exhaust ventilation should be used in areas where there is a point source emission or dispersion of sulfur dioxide in or near a work area (HSDB , 2002). Liquid sulfur dioxide may be stored at one to three atm pressure, or at atmospheric pressure and at -10 degrees C to condense vapors (HSDB , 2002). All handling, storage and use of compressed gases should be in accordance with Compressed Gas Association Pamphlets P-1-1965, C-6-1968 and C-8-1962 (OSHA, 2002c).
Sulfur dioxide forms corrosive hydrochloric acid fumes with air and upon contact with water produces sulfurous acid (Lewis, 2000; NFPA, 1997; NIOSH , 2002). It decomposes at temperatures greater than 60 degrees C (140 degrees F) and forms toxic and corrosive oxides of sulfur. It will attack some plastics, rubber, and coatings (Pohanish & Greene, 1997). Sulfur dioxide reacts violently with alcohols, caustics, amines, water, acrolein, aluminum, chlorine trifluoride, rubidium carbide, tin oxide, diaminolithiumacetylene carbide, as well as many of the compounds listed below (Lewis, 2000; Pohanish & Greene, 1997). It reacts with bromine pentafluoride, carbide diamino, cesium carbide, cesium monoxide, cesium azide, chlorates, chromium, ferrous oxide, fluorine, lithium acetylene, manganese, potassium acetylene carbide, sodium, sodium carbide, stannous oxide (Lewis, 2000; OHM/TADS , 2002; Sittig, 1991; Urben, 1999). It is incompatible with powered alkali metals, water, ammonia, zinc, aluminum, brass, copper, halogens or interhalogens, lithium nitrate, metal acetylides, metal oxides, polymeric tubing, potassium chlorate, sodium hydride (Lewis, 2000; NIOSH , 2002). Explosions may occur on contact with sodium hydride, potassium chlorate at elevated temperatures, ethanol, ether (at cool temperatures; -15 degrees C), fluorine, chlorates, and chlorine trifluoride (Sittig, 1991; Urben, 1999).
Contact with copper, bronze, or alkali metals may cause fire and explosions (Pohanish & Greene, 1997). Diethylzinc added to liquid sulfur dioxide at -15 degrees C resulted in a violent explosion (Urben, 1999).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (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.
- Avoid contact with sulfur dioxide liquid and gas. Wear appropriate personal protective clothing, including respiratory protection; do not handle broken containers unless wearing appropriate protective clothing. Wash away any sulfur dioxide which may have contacted the body with copious amounts of water or soap and water (AAR, 2000; CGA, 1999; NFPA, 1997). If it is in the eyes, hold eyelids open and flush them out with large amounts of water (CHRIS , 2002; NIOSH , 2002).
- Avoid breathing sulfur dioxide vapors; keep upwind of spills or leaks. Wear a positive pressure self-contained breathing apparatus when working with or near sulfur dioxide. Avoid bodily contact with sulfur dioxide liquid; wear appropriate personal protective clothing. Do not handle broken containers unless wearing appropriate personal protective equipment. Wash away any sulfur dioxide which may have contacted the body with copious amounts of water or soap and water. Remove wet or contaminated clothing immediately (AAR, 2000; NFPA, 1997; Sittig, 1991).
- Wear goggles, chemical protective gloves and clothing, and a self-contained breathing apparatus, especially when contact with liquid sulfur dioxide is possible (CHRIS , 2002; HSDB , 2002; NIOSH , 2002).
EYE/FACE PROTECTION
- Protect eyes against contact with liquid sulfur dioxide by wearing safety goggles or face-shield; provide emergency eyewash facilities (Sittig, 1991).
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 7446-09-5.
ENGINEERING CONTROLS
- Local exhaust ventilation should be used in areas where there is a point source emission or dispersion of sulfur dioxide in or near a work area (HSDB , 2002).
- Any area of sulfur dioxide contamination should be ventilated to allow for the dispersion of the vapors (HSDB , 2002).
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (ERG, 2004) Some may burn, but none ignite readily. Vapors from liquefied gas are initially heavier than air and spread along ground. Some of these materials may react violently with 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.
Sulfur dioxide is not flammable. If sulfur dioxide is involved in a fire, extinguish the fire with an agent that is suitable for the type of surrounding fire. Cool affected containers with flooding quantities of water; apply water from as far away as possible. Use water spray to knock down vapors. Sulfur dioxide will react with water or steam to produce toxic and corrosive fumes. Wear respiratory protection and personal protective equipment at all times (AAR, 2000; Lewis, 2000; NFPA, 1997; OHM/TADS , 2002; Sittig, 1991). Containers of sulfur dioxide may explode in the heat of a fire. When containers are involved in a fire, move them from the fire area if it can be done without undue risk. Stay away from the ends of the containers, as they may rupture and release irritating, toxic sulfur dioxide gas (CHRIS , 2002; Sittig, 1991). Contact with some copper, bronze or alkali metals can cause fire and explosions (Pohanish & Greene, 1997). Cesium azide will ignite on contact with sulfur dioxide. Ignition may occur from the reaction of bromine pentafluoride and sulfur dioxide (Urben, 1999).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS7446-09-5 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (ERG, 2004)
Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Do not get water inside containers. Damaged cylinders should be handled only by specialists.
- TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (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.
- NFPA Extinguishing Methods for CAS7446-09-5 (NFPA, 2002):
Sulfur dioxide is not flammable; however, it will react with water or steam to produce toxic and corrosive fumes (NFPA, 1997; Lewis, 2000). Containers involved in a fire may rupture, releasing highly toxic and irritating sulfur dioxide gas (CHRIS , 2002).
EXPLOSION HAZARD
- Sulfur dioxide is, in itself, a stable compound (OHM/TADS , 2002).
- Contact with copper, bronze, or alkali metals may cause fire and explosions. Sulfur dioxide reacts violently with alcohols, caustics, amines, and water (NFPA, 1997; Pohanish & Greene, 1997). Explosions may occur from the contact of sulfur dioxide with potassium chlorate at elevated temperatures, ethanol, ether, fluorine, chlorine trifluoride and chlorates (Sittig, 1991).
- During preparation of zinc ethylsulfinate, the addition of diethylzinc to liquid sulfur dioxide at -15 degrees C caused a violently explosive reaction (Urben, 1999).
- Halogens and interhalogens can produce ignition or a violent reaction with sulfur dioxide (NFPA, 1997).
- Lithium nitrate and propylene may undergo explosive polymerization with sulfur dioxide (NFPA, 1997).
- Sodium can cause a violent reaction with sulfur dioxide (NFPA, 1997).
- An explosive reaction may occur with sulfur dioxide and nitric acid (NFPA, 1997).
- Sodium hydride and sulfur dioxide may result in an explosive reaction (HSDB , 2002; NFPA, 1997; Sittig, 1991).
- Sulfur dioxide and propene contained in a glass pressure bottle at 20 degrees C polymerized explosively (HSDB , 2002).
- Containers may rupture or explode if exposed to the heat of a fire (CHRIS , 2002).
DUST/VAPOR HAZARD
- Sulfur dioxide gas is a severe irritant of the eyes, skin, and upper airways of the respiratory tract; the vapors are very toxic by inhalation. The irritant effects of sulfur dioxide are due to the formation of sulfurous acid which quickly forms when the gas comes into contact with moist surfaces (AAR, 2000; CGA, 1999; Hathaway et al, 1996).
- Sulfur dioxide forms corrosive hydrochloric acid fumes with air. It decomposes above 60 degrees C (140 degrees F) and forms toxic and corrosive oxides of sulfur (Pohanish & Greene, 1997). Because sulfur dioxide liquid expands as the temperature increases, at adequately elevated temperatures it is possible for hydrostatic pressure in a full container rupture through a pressure relief device and discharge toxic vapors (GCA, 1999).
- Asthmatics and persons with pulmonary disease are more sensitive to sulfur dioxide in ambient air than are healthy individuals. As little as 0.5 to 1 ppm sulfur dioxide can cause significant bronchoconstriction in sensitive individuals engaged in mild exercise (ACGIH, 1991; Baxter et al, 2000; Bingham et al, 2001). An estimated 10 to 20 percent of the adult population is hypersensitive to the adverse effects of sulfur dioxide (HSDB , 2002).
- Acute exposures to sulfur dioxide have caused severe obstructive pulmonary disease that is unresponsive to bronchodilators and may last up to three months after exposure (Bingham et al, 2001).
- Symptoms of acute exposure to sulfur dioxide gas include: choking, sneezing, coughing, and bronchospasm. Chronic exposure may result in: impaired lung function, bronchitis, hacking cough, nasal irritation and discharge, increased fatigue, changes to the senses of taste and smell, and extended duration of the common cold. Extreme cases of repeated overexposure may result in: dental caries, loss of dental fillings, gum disorders, and tooth destruction. At very high levels of exposure, death can result from systemic acidosis, upper respiratory obstruction secondary to edema, and asphyxiation (CGA, 1999; Harbison, 1998; HSDB , 2002).
REACTIVITY HAZARD
- Sulfur dioxide forms corrosive hydrochloric acid fumes with air and upon contact with water produces sulfurous acid (Lewis, 2000; NFPA, 1997; NIOSH , 2002). It decomposes at temperatures greater than 60 degrees C (140 degrees F) and forms toxic and corrosive oxides of sulfur. It will attack some plastics, rubber, and coatings (Pohanish & Greene, 1997).
- Contact with copper, bronze, or alkali metals may cause fire and explosions. It reacts violently with metals such as aluminum and manganese (Lewis, 2000; NFPA, 1997; Pohanish & Greene, 1997).
Metal acetylides such as monocesium acetylide and monopotassium acetylide ignite and incandesce in unheated sulfur dioxide. Dimetal derivatives such as sodium acetylide need heat before ignition can occur (Urben, 1999). Metal oxides such as cesium oxide, iron(II) oxide, tin oxide, and lead oxide ignite and incandesce when heated in sulfur dioxide gas (Urben, 1999). Finely divided (pyrophoric) chromium incandesces in sulfur dioxide. Pyrophoric manganese burns brilliantly when heated in sulfur dioxide gas (Urben, 1999). Molten sodium reacts violently with either gas or liquid sulfur dioxide. Moist gas sulfur dioxide reacts with cold sodium as vigorously as with water (Urben, 1999).
- Sulfur dioxide reacts violently with alcohols, caustics, amines, chlorates, and water (Lewis, 2000; Pohanish & Greene, 1997).
- Plastic tubing normally capable of withstanding an internal pressure of seven bar failed below two bar when it was used to convey sulfur dioxide gas (Urben, 1999).
- Sulfur dioxide reacts violently with alcohols, caustics, amines, water, acrolein, aluminum, rubidium carbide, chlorine trifluoride, tin oxide, diaminolithiumacetylene carbide, as well as many of the compounds listed below (Lewis, 2000; Pohanish & Greene, 1997).
It reacts with bromine pentafluoride, carbide diamino, cesium carbide, cesium monoxide, cesium azide, chlorates, chromium, ferrous oxide, fluorine, lithium acetylene, manganese, potassium acetylene carbide, sodium, sodium carbide, and stannous oxide (Lewis, 2000; OHM/TADS , 2002; Sittig, 1991; Urben, 1999). It is incompatible with powered alkali metals, water, ammonia, zinc, aluminum, brass, copper, halogens or interhalogens, lithium nitrate, metal acetylides, metal oxides, polymeric tubing, potassium chlorate, and sodium hydride (Lewis, 2000; NIOSH , 2002). Explosions may occur on contact with sodium hydride, potassium chlorate at elevated temperatures, ethanol, ether (at cool temperatures; -15 degrees C), and chlorine trifluoride (Sittig, 1991; Urben, 1999).
- Diethylzinc added to liquid sulfur dioxide at -15 degrees C resulted in a violent explosion (Urben, 1999).
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. DOT ID No. 1079 - Sulfur dioxide SMALL SPILLS LARGE SPILLS
DOT ID No. 1079 - Sulfur dioxide, liquefied SMALL SPILLS LARGE SPILLS
DOT ID No. 1079 - Sulphur dioxide SMALL SPILLS LARGE SPILLS
DOT ID No. 1079 - Sulphur dioxide, liquefied SMALL SPILLS LARGE SPILLS
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (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 125 (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 125 (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.
- Leaks can be detected by odor or sulfur dioxide alarms. A small leak can be located using a 10 percent ammonia solution sprayed from an aspirator or squeeze bottle in the area where the leak is suspected; dense white fumes will result where the sulfur dioxide reacts with the ammonia (CGA, 1999).
- If sulfur dioxide is leaking, consider evacuation from downwind areas based on the amount of sulfur dioxide spilled, location of the spill, and weather conditions. Keep unnecessary people away from the area (AAR, 2000; Sittig, 1991). Prevent spilled material from entering water sources and sewers; notify local health and pollution control agencies (CHRIS , 2002; HSDB , 2002).
- Only trained and authorized personnel should enter areas of known sulfur dioxide contamination to try and stop the leak. Adequate respiratory equipment should be worn (CGA, 1999). Isolate area until the gas has dispersed (HSDB , 2002).
- Avoid breathing vapors or fumes from this material and stay upwind of fires, spills, or leaks. Avoid contact with liquid (AAR, 2000). Keep out of low areas as sulfur dioxide vapors are heavier than air (CHRIS , 2002).
- Isolate the hazard area until gas has dispersed and keep unnecessary people away (CHRIS , 2002).
- Evacuate the immediate hazard area and restrict entry (CHRIS , 2002).
- If a tank, rail car or tank truck containing sulfur dioxide is on fire, isolate the area for 160 meters (1 miles) in all directions; consider initial evacuation of the same distance (HSDB , 2002).
- AIHA ERPG Values for CAS7446-09-5 (AIHA, 2006):
Listed as Sulfur Dioxide ERPG-1 (units = ppm): 0.3 ERPG-2 (units = ppm): 3 ERPG-3 (units = ppm): 15 Under Ballot, Review, or Consideration: Yes 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 CAS7446-09-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Sulfur dioxide TEEL-0 (units = ppm): 0.2 TEEL-1 (units = ppm): 0.2 TEEL-2 (units = ppm): 0.75 TEEL-3 (units = ppm): 27 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 CAS7446-09-5 (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: Sulfur dioxide Final Value: AEGL-1 10 min exposure: ppm: 0.2 ppm mg/m3: 0.52 mg/m(3)
30 min exposure: ppm: 0.2 ppm mg/m3: 0.52 mg/m(3)
1 hr exposure: ppm: 0.2 ppm mg/m3: 0.52 mg/m(3)
4 hr exposure: ppm: 0.2 ppm mg/m3: 0.52 mg/m(3)
8 hr exposure: ppm: 0.2 ppm mg/m3: 0.52 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: Sulfur dioxide Final Value: AEGL-2 10 min exposure: ppm: 0.75 ppm mg/m3: 1.95 mg/m(3)
30 min exposure: ppm: 0.75 ppm mg/m3: 1.95 mg/m(3)
1 hr exposure: ppm: 0.75 ppm mg/m3: 1.95 mg/m(3)
4 hr exposure: ppm: 0.75 ppm mg/m3: 1.95 mg/m(3)
8 hr exposure: ppm: 0.75 ppm mg/m3: 1.95 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: Sulfur dioxide Final Value: AEGL-3 10 min exposure: ppm: 30 ppm mg/m3: 78 mg/m(3)
30 min exposure: ppm: 30 ppm mg/m3: 78 mg/m(3)
1 hr exposure: ppm: 30 ppm mg/m3: 78 mg/m(3)
4 hr exposure: ppm: 19 ppm mg/m3: 49 mg/m(3)
8 hr exposure: ppm: 9.6 ppm mg/m3: 25 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 CAS7446-09-5 (National Institute for Occupational Safety and Health, 2007):
IDLH: 100 ppm Note(s): Not Listed
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (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. Stop leak if you can do it without risk. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. 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 conact spilled material. Isolate area until gas has dispersed.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 125 (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.
If sulfur dioxide is spilled, keep it out of water sources and sewers. If the spill or leak occurs indoors, ventilate the area and evacuate unnecessary personnel. Attempt to stop the leak if it can be done without undue personnel hazard. Approach spill or leak from upwind. Neutralize spilled sulfur dioxide with crushed limestone, soda ash, or lime (AAR, 2000; NFPA, 1997; Sittig, 1991). Water should never be sprayed at or into a container that is leaking sulfur dioxide. Because the combination of sulfur dioxide and water is very corrosive, the use of water would increase the venting rate of the leak (CGA, 1999). Do not walk through or touch spilled liquid material (HSDB , 2002).
If possible, leaking tanks should be vented to a lime or caustic soda solution. The resultant reduction in pressure may slow the leak enough to permit stopping it (CGA, 1999). If leak cannot be stopped, move leaking containers to safe locations outdoors, if it can be done without undue risk (NFPA, 1997; Sittig, 1991). Spilled material can be neutralized with sodium bicarbonate, limestone, soda ash or lime (AAR, 2000; HSDB , 2002; ITI, 1995; OHM/TADS , 2002). Small spills can be cleaned up by neutralizing material with sodium bicarbonate or soda ash and transferring to a large beaker, then cautiously adding an equal volume of hypochlorite and additional water while stirring (ITI, 1995). For small leaks, seal the cylinders and return them to the supplier (ITI, 1995).
Pass sulfur dioxide gas through a large tank or drum of soda ash solution and add calcium hypochlorite cautiously. Dilute and neutralize with 6 mol hydrochloric acid or 6 mol sodium hydroxide. Contact sewage treatment facility for guidance on disposal (ITI, 1995; OHM/TADS , 2002). Add equal parts soda ash to liquid sulfur dioxide and dilute with water creating a slurry (gaseous sulfur dioxide can be bubbled into a soda ash and water mixture). Add calcium hypochlorite cautiously. Dilute and neutralize with 6 mol hydrochloric acid or 6 mol sodium hydroxide. Let solution sit for one hour. Contact sewage treatment facility for guidance on disposal (ITI, 1995; OHM/TADS , 2002; Sittig, 1991). Spill areas on beaches/shores should be restored through washing with a mild caustic (OHM/TADS , 2002). At the time of review, land treatment and sanitary landfill practices are subject to significant revision. Always consult with applicable environmental regulatory and pollution control agencies prior to implementing disposal of sulfur dioxide (HSDB , 2002). 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.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
ENVIRONMENTAL FATE AND KINETICS
Due to its high vapor pressure, sulfur dioxide generally exists as a gas in the ambient atmosphere. Some amounts emitted into the atmosphere will move unchanged into soil, water, grass and other vegetation (ATSDR, 1998). When sulfur dioxide gas is released from point sources (i.e., smoke stacks from petroleum refining plants), it travels vertically for some distance before spreading laterally. Dispersion is influenced by wind direction, velocity, inversion and turbulence (Bingham et al, 2001).
Direct uptake to non-acidic surfaces (e.g., some crop and forests species, oceans, and other moist surfaces) is the most significant dry removal process for atmospheric sulfur dioxide (HSDB, 2004; ATSDR, 1998). When released into the atmosphere, sulfur dioxide is deposited to the ground through both precipitation and dry deposition. Dry deposition is more important in areas of high sulfur dioxide concentrations, where it is expected to occur more or less continuously. The residence time for sulfur dioxide in the atmosphere is between 2.5 and 10 days, depending on the region's climate, as well as type, intensity, duration and frequency of precipitation (HSDB, 2004; Bingham et al, 2001; ATSDR, 1998; Dragun, 1988). The removal rate of sulfur dioxide in the atmosphere through wet deposition is approximately 4% per hour (HSDB, 2004). In the atmosphere, sulfur dioxide below cloud level is intercepted by falling drops of precipitation or it diffuses into precipitation. In-cloud processes include coagulation, diffusional uptake of sulfur dioxide, and sulfate particles acting as condensation nuclei. These in-cloud processes dominate in air when below-cloud sulfur dioxide concentrations are low (HSDB, 2004). The dissolution of sulfur dioxide in precipitation is shown to increase in the presence of magnesium and iron ions, in high pH solutions, and at high temperatures (ATSDR, 1998). A decrease in temperature from 25 degrees C to 8 degrees C decreased sulfur dioxide absorption rates 5- to 10-fold. Typical removal rates by this process were between 0.08 and 2% per hour (ATSDR, 1998).
Gas-phase oxidation reaction rates range from 0.5 to 5% per hour in sunlight. In less polluted air, the reaction occurs more slowly. Because this reaction involves photochemically-produced reactants, its significance decreases in the winter and at night. Direct photooxidation of sulfur dioxide is not considered important (HSDB, 2004). Oxidation of sulfur dioxide in the gas phase occurs thorough reaction with hydroxyl radicals. This reaction rate has been characterized at greater than 1% per hour, making it a significant mechanism for conversion (ATSDR, 1998). Photochemical or catalytic oxidation oxidizes sulfur dioxide to sulfur trioxide and sulfate in the atmosphere (ATSDR, 1998). Rate constants for oxidation of sulfur dioxide by gases (including O2, O2-, O3, NO2-, NO3, N2O5 and OH) range from 2 x 10(-24) to 4 x 10(-3) cm(3)/molecule-sec, with the reaction of dinitrogen pentaoxide as the most rapid (ATSDR, 1998). Liquid-phase oxidation, catalyzed by metal ions (e.g., manganese, iron), is an important degradation process in air with sufficiently high sulfur dioxide concentrations. Atmospheric liquid-phase oxidation reactions involving ozone and hydrogen peroxide may also be important fate processes, although reaction rates for these processes are unknown (HSDB, 2004). Plant leaves also contribute to the removal of sulfur dioxide from air, especially under dry conditions (ATSDR, 1998). Sulfur dioxide in moist air or fog combines with water to form sulfurous acid, which is slowly oxidized to sulfuric acid (Bingham et al, 2001; ATSDR, 1998).
SURFACE WATER Spring melt of accumulated winter snowpack (which in itself is a poor receptor of sulfur dioxide gases and particulate compounds) can result in a rapid, short-term influx of acidic, high-sulfate water to freshwater systems, with a generally harmful effect on fish and aquatic life (HSDB, 2004). Oceans act as a good sink for atmospheric sulfur dioxide (HSDB, 2004). Dissolved sulfur dioxide in ocean surface waters may be slowly oxidized to the sulfate anion, due to the presence of dissolved oxygen and metal salts. Oxidation occurs less rapidly in freshwater due to its lower salt content (ATSDR, 1998).
TERRESTRIAL Non-acidic, moist surfaces are good sinks for direct uptake of gaseous sulfur dioxide. Dry, snow-covered surfaces and soils provide less efficient uptake conditions (HSDB, 2004). Adsorption to soils is dependent upon soil pH and moisture content (HSDB, 2004; ATSDR, 1998).
ABIOTIC DEGRADATION
- Sulfur dioxide is expected to exist entirely as a vapor in the atmosphere. It is removed through direct uptake to non-acidic surfaces and wet and dry deposition. It is oxidized through reaction with gases and photochemically-produced radicals. In surface waters, dissolved sulfur dioxide is expected to slowly oxidize to the sulfate anion. Oxidation should occur less rapidly in freshwater than in saltwater due to the lower salt content. Sulfur dioxide may adsorb to soil, depending on its pH and moisture content (HSDB, 2004; ATSDR, 1998).
BIOACCUMULATION
ENVIRONMENTAL TOXICITY
LC - SUNFISH: 16 ppm for 1H (OHM/TADS, 2004) LC - SUNFISH: 16-19 ppm (OHM/TADS, 2004) LC - TROUT: 5 ppm for 1H (OHM/TADS, 2004)
AQUATIC ANIMALS PLANTS Less than 1 ppm of sulfur dioxide in the atmosphere can be injurious to plant foliage (OHM/TADS, 2004). Some crop plants are extremely sensitive to the presence of sulfur dioxide in air. Alfalfa, barley, cotton, and wheat can be damaged at air concentrations of 0.15 to 0.20 ppm. Other crops, such as corn and white potatoes, are more resistant to injury (HSDB, 2004).
Sulfur dioxide inhibited higher plant photosystem II (PSII) activity via the action of sulfate on the binding of chloride and two extrinsic proteins (Beauregard, 1992). PINES: Lipids in Pinus sylvestris L. needles were studied by microscopic and chromatographic methods in polluted industrial areas. Needles from the industrial area showed an increased size or number of lipid bodies. Changes were also detected in the internal membrane system of their mesophyll cell chloroplasts. These changes were not observed in needles from the nonpolluted area (Anttonen, 1992) . DOUGLAS FIR: Sulfur dioxide may have significant effects on photosynthesis and respiration in stands with a low leaf area index (Mohren et al, 1992). ENGLISH OAK: Different sulfur dioxide concentrations of (80, 120, and 160 nL/L) were applied for 32 to 70 days to leaves of Quercus robur L. trees in order to simulate acidic gas deposition. Identification of the proton neutralization mechanism was attempted by following the uptake of nitrogen, the increase in sulfur and carboxylate contents, and the excretion of hydroxyl ions or protons. The results showed that sulfur reduction was not involved in the neutralization of protons generated by sulfur dioxide uptake and that organic acid metabolism had a significant role (Thomas & Runge, 1992).
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Sulfur dioxide is a colorless, irritating, nonflammable gas or liquid with a strong, suffocating odor (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000) Freeman, 1989; (Grant & Schuman, 1993; Lewis, 1998; Lewis, 2000; Lewis, 2001).
PH
- Aqueous solution is slightly acidic (HSDB , 2002)
VAPOR PRESSURE
- 3.2 atm (at 20 degrees C) (Lewis, 2001)
- 3.12 psia; -11.57 psig (at -40.0 degrees C; -40 degrees F) (CGA, 1999)
- 5.88 psia; -8.81 psig (at -28.9 degrees C; -20 degrees F) (CGA, 1999)
- 10.26 psia; -4.43 psig (at -17.8 degrees C; 0 degrees F) (CGA, 1999)
- 13.3 psia; -1.39 psig (at -12.2 degrees C; 10 degrees F) (CGA, 1999)
- 16.9 psia; 2.2 psig (at -6.7 degrees C; 20 degrees F) (CGA, 1999)
- 21.3 psia; 6.6 psig (at -1.1 degrees C; 30 degrees F) (CGA, 1999)
- 26.6 psia; 11.9 psig (at 4.4 degrees C; 40 degrees F) (CGA, 1999)
- 32.9 psia; 18.2 psig (at 10.0 degrees C; 50 degrees F) (CGA, 1999)
- 40.3 psia; 25.6 psig (at 15.6 degrees C; 60 degrees F) (CGA, 1999)
- 49.1 psia; 34.4 psig (at 21.1 degrees C; 70 degrees F) (CGA, 1999)
- 59.8 psia; 44.6 psig (at 26.7 degrees C; 80 degrees F) (CGA, 1999)
- 71.0 psia; 56.3 psig (at 32.2 degrees C; 90 degrees F) (CGA, 1999)
- 84.1 psia; 69.4 psig (at 37.8 degrees C; 100 degrees F) (CGA, 1999)
- 99.1 psia; 84.4 psig (at 43.3 degrees C; 110 degrees F) (CGA, 1999)
- 116.3 psia; 101.6 psig (at 48.9 degrees C; 120 degrees F) (CGA, 1999)
- 135.8 psia; 121.1 psig (at 54.4 degrees C; 130 degrees F) (CGA, 1999)
- 157.7 psia; 143.0 psig (at 60.0 degrees C; 140 degrees F) (CGA, 1999)
- 3.2 atm (at 20 degrees C) (Lewis, 1993; NIOSH , 2002)
- 2538 mmHg (at 21.1 degrees C) (Lewis, 2000)
- 3x10(3) mmHg (at 25 degrees C) (derived) (HSDB , 2002)
- 400 mmHg (at -23 degrees C) (OHM/TADS , 2002)
SPECIFIC GRAVITY
- STANDARD TEMPERATURE AND PRESSURE
(0 degrees C; 32 degrees F and 760 mmHg) LIQUID: 1.436 (at 0/4 degrees C and 23.7 psia) (CGA, 1999) GAS: 2.2638 (at 0 degrees C; 32 degrees F and 1 atm) (CGA, 1999)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
LIQUID: 1.45 (at -10 degrees C) (CHRIS , 2002) LIQUID: 1.434 (at 0 degrees C) (ACGIH, 1991; Lewis, 2000) LIQUID: 1.46 (at -10 degrees C) (ITI, 1995; NFPA, 1997) LIQUID: 1.5 (Budavari, 2000) LIQUID: 1.4337 (at 0 degrees C) (Lewis, 2001) GAS: 2.26 (Baxter et al, 2000; CGA, 1999) GAS: 2.2 (CHRIS , 2002) GAS: 2.264 (at 0 degrees C) (Lewis, 2000) GAS: 2.21 (NFPA, 1997)
DENSITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
LIQUID: 1.5 kg/L (at -20 degrees C) (Ashford, 1994) LIQUID: 95.79 lb/ft(3) (at -40.0 degrees C; -40 degrees F) (CGA, 1999) LIQUID: 94.16 lb/ft(3) (at -28.9 degrees C; -20 degrees F) (CGA, 1999) LIQUID: 94.42 lb/ft(3) (at -17.9 degrees C; 0 degrees F) (CGA, 1999) LIQUID: 91.58 lb/ft(3) (at -12.2 degrees C; 10 degrees F) (CGA, 1999) LIQUID: 90.66 lb/ft(3) (at -6.7 degrees C; 20 degrees F) (CGA, 1999) LIQUID: 89.77 lb/ft(3) (at -1.1 degrees C; 30 degrees F) (CGA, 1999) LIQUID: 88.89 lb/ft(3) (at 4.4 degrees C; 40 degrees F) (CGA, 1999) LIQUID: 87.95 lb/ft(3) (at 10.0 degrees C; 50 degrees F) (CGA, 1999) LIQUID: 87.03 lb/ft(3) (at 15.6 degrees C; 60 degrees F) (CGA, 1999) LIQUID: 86.06 lb/ft(3) (at 21.1 degrees C; 70 degrees F) (CGA, 1999) LIQUID: 85.11 lb/ft(3) (at 26.7 degrees C; 80 degrees F) (CGA, 1999) LIQUID: 84.10 lb/ft(3) (at 32.2 degrees C; 90 degrees F) (CGA, 1999) LIQUID: 83.06 lb/ft(3) (at 37.8 degrees C; 100 degrees F) (CGA, 1999) LIQUID: 82.03 lb/ft(3) (at 43.3 degrees C; 110 degrees F) (CGA, 1999) LIQUID: 80.97 lb/ft(3) (at 48.9 degrees C; 120 degrees F) (CGA, 1999) LIQUID: 79.94 lb/ft(3) (at 54.4 degrees C; 130 degrees F) (CGA, 1999) LIQUID: 78.70 lb/ft(3) (at 60.0 degrees C; 140 degrees F) (CGA, 1999) LIQUID: 2.811 g/l (HSDB , 2002)
FREEZING/MELTING POINT
-76.1 degrees C (Lewis, 2001) -75.9 degrees C; -104.6 degrees F (at 1 atm) (CGA, 1999) -104 degrees F (NIOSH , 2002) -103.9 degrees F; -75.5 degrees C; 197.7 K (CHRIS , 2002)
-72 degrees C (Budavari, 2000; OHM/TADS , 2002) -72.7 degrees C (Clayton & Clayton, 1993) -73 degrees C (Ashford, 1994) -75.5 degrees C (HSDB , 2002; ITI, 1995; Lewis, 2000) -76 degrees C; -104 degrees F (NFPA, 1997) -75.51 degrees (Bingham et al, 2001)
BOILING POINT
- -10 degrees C; 14 degrees F; 263.2 K (Ashford, 1994; Budavari, 2000; CGA, 1999; CHRIS , 2002; Clayton & Clayton, 1993; ITI, 1995; Lewis, 2000; Lewis, 2001; NFPA, 1997; OHM/TADS , 2002)
- -10.05 degrees C (HSDB , 2002)
- -10.06 degrees C (Bingham et al, 2001)
FLASH POINT
- Not Combustible (NFPA, 1997)
AUTOIGNITION TEMPERATURE
SOLUBILITY
It is soluble in alcohol, acetic acid, sulfuric acid, ether, ethyl ether, methyl alcohol, ethyl alcohol, and chloroform (ACGIH, 1991; Ashford, 1994; Budavari, 2000; Clayton & Clayton, 1993). 25% in alcohol (Budavari, 2000) 32% in methanol (Budavari, 2000)
OTHER/PHYSICAL
115.5 kJ/kg; 49.70 Btu/lb (at -75.5 degrees C; -103.9 degrees F) (CGA, 1999) 7.4 kJ/mol (at -75.5 degrees C) (HSDB , 2002) 32.2 cal/g (CHRIS , 2002)
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