Sulfur Dioxide

H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H331: Toxic if inhaled [Danger Acute toxicity, inhalation]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

P260, P261, P264, P270, P271, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P321, P363, P403+P233, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 16.2% (425 of 2617) of reports.

H280 (19.3%): Contains gas under pressure; may explode if heated [Warning Gases under pressure]

H314 (83.7%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H331 (82.2%): Toxic if inhaled [Danger Acute toxicity, inhalation]

P260, P261, P264, P271, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P363, P403+P233, P405, P410+P403, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 2617 reports by companies from 31 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Reported as not meeting GHS hazard criteria per 425 of 2617 reports by companies.

There are 30 notifications provided by 2192 of 2617 reports by companies with hazard statement code(s).

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H280: Contains gas under pressure; may explode if heated [Warning Gases under pressure]

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

P260, P261, P264, P264+P265, P270, P271, P280, P304+P340, P305+P351+P338, P308+P316, P316, P319, P321, P337+P317, P403+P233, P405, P410+P403, and P501 (click each P-code to see the statement)

P260, P261, P264, P271, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P363, P403+P233, P405, and P501 (click each P-code to see the statement)

H318: Causes serious eye damage [Danger Serious eye damage/eye irritation]

P260, P261, P264, P264+P265, P271, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P321, P363, P403+P233, P405, and P501 (click each P-code to see the statement)

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

ON FROSTBITE: rinse with plenty of water, do NOT remove clothes. Refer for medical attention .

Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer for medical attention.

Note: Persons with asthma, subnormal pulmonary function, or cardiovascular disease are at greater risk.

Signs and Symptoms of Acute Sulfur Dioxide Exposure: Sulfur dioxide may irritate the eyes and respiratory tract. Signs and symptoms of acute exposure to sulfur dioxide may be severe and include coughing, choking, dyspnea (shortness of breath), sneezing, wheezing, and chest discomfort. Upper airway edema (swelling) or obstruction, bronchoconstriction, pneumonia, pulmonary edema, and respiratory paralysis may occur. Fatigue may be noted. Gastrointestinal effects may include nausea, vomiting, and abdominal pain. Cyanosis (blue tint to skin and mucous membranes) may be noted following exposure to sulfur dioxide.

Emergency Life-Support Procedures: Acute exposure to sulfur dioxide may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination.

Inhalation Exposure:

1. Move victims to fresh air. Emergency personnel should avoid self-exposure to sulfur dioxide.

2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.

3. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

4. Transport to a health care facility.

Dermal/Eye Exposure:

1. Remove victims from exposure. Emergency personnel should avoid self- exposure to sulfur dioxide.

3. Remove contaminated clothing as soon as possible.

4. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes.

5. Wash exposed skin areas with soap and water.

6. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

7. Transport to a health care facility.

Ingestion Exposure: No information is available. (EPA, 1998)

General First Aid:

· Call 911 or emergency medical service.

· Ensure that medical personnel are aware of the material(s) involved, take precautions to protect themselves and avoid contamination.

· Move victim to fresh air if it can be done safely.

· Administer oxygen if breathing is difficult.

· If victim is not breathing:

-- DO NOT perform mouth-to-mouth resuscitation; the victim may have ingested or inhaled the substance.

-- If equipped and pulse detected, wash face and mouth, then give artificial respiration using a proper respiratory medical device (bag-valve mask, pocket mask equipped with a one-way valve or other device).

-- If no pulse detected or no respiratory medical device available, provide continuous compressions. Conduct a pulse check every two minutes or monitor for any signs of spontaneous respirations.

· Remove and isolate contaminated clothing and shoes.

· For minor skin contact, avoid spreading material on unaffected skin.

· In case of contact with substance, remove immediately by flushing skin or eyes with running water for at least 20 minutes.

· For severe burns, immediate medical attention is required.

· Effects of exposure (inhalation, ingestion, or skin contact) to substance may be delayed.

· Keep victim calm and warm.

· Keep victim under observation.

· For further assistance, contact your local Poison Control Center.

· Note: Basic Life Support (BLS) and Advanced Life Support (ALS) should be done by trained professionals.

Specific First Aid:

· In case of contact with liquefied gas, only medical personnel should attempt thawing frosted parts.

· In case of skin contact with hydrogen fluoride, anhydrous (UN1052), if calcium gluconate gel is available, rinse 5 minutes, then apply gel. Otherwise, continue rinsing until medical treatment is available.

Wear self-contained breathing apparatus and full protective clothing. Move container from fire area. Stay away from ends of tanks. Cool containers that are exposed to flames with water from the side until well after the fire is out. Isolate area until gas has dispersed. Keep unnecessary people away.

Not flammable. Extinguish fires with dry chemical, carbon dioxide, water spray, fog or foam. (EPA, 1998)

In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep cylinder cool by spraying with water. NO direct contact with water. Combat fire from a sheltered position.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. ...Wear self-contained breathing apparatus for firefighting if necessary.

Use water spray to keep fire-exposed containers cool. Extinguish fire using agent suitable for surrounding fire. /Sulfur dioxide, liquefied/

Sulfur oxides

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· Keep unauthorized personnel away.

· Stay upwind, uphill and/or upstream.

· Many gases are heavier than air and will spread along the ground and collect in low or confined areas (sewers, basements, tanks, etc.).

· Ventilate closed spaces before entering, but only if properly trained and equipped.

· 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 contact spilled material.

· Isolate area until gas has dispersed.

Excerpt from ERG Guide 125 [Gases - Toxic and/or Corrosive]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area for at least 100 meters (330 feet) in all directions.

SPILL: See ERG Tables 1 and 3 - Initial Isolation and Protective Action Distances on the UN/NA 1079 datasheet.

FIRE: If tank, rail tank car or highway tank 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. (ERG, 2024)

Immediate precautionary measure

· Isolate spill or leak area for at least 100 meters (330 feet) in all directions.

· For highlighted materials: see Table 1 - Initial Isolation and Protective Action Distances.

· For non-highlighted materials: increase the immediate precautionary measure distance, in the downwind direction, as necessary.

· If tank, rail tank car or highway tank 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.

Small spill:

- ISOLATE in all directions: 100 m (300 ft)

Large spill:

- ISOLATE in all Directions:

-- Rail tank car: 1000 m (3000 ft)

-- Highway tank truck or trailer: 1000 m (3000 ft)

-- Multiple ton cylinders: 500 m (1500 ft)

-- Multiple small cylinders or single ton cylinder: 200 m (600 ft)

- PROTECT people from downwind during DAY time: 0.6 km (0.4 mi)

- PROTECT people from downwind during NIGHT time: 2.6 km (1.6 mi)

- PROTECT people from downwind during DAY time:

-- Rail tank car:

- - - Low wind (< 6 mph (<10 km/h)): 11.0+ km (7.0+ mi)

- - - Moderate wind (6-12 mph (10-20 km/h)): 11.0+ km (7.0+ mi)

- - - High wind (> 12 mph (>20 km/h)): 6.9 km (4.3 mi)

-- Highway tank truck or trailer:

- - - Moderate wind (6-12 mph (10-20 km/h)): 6.0 km (3.8 mi)

- - - High wind (> 12 mph (>20 km/h)): 5.0 km (3.3 mi)

-- Multiple ton cylinders:

Excerpt from ERG Guide 125 [Gases - Toxic and/or Corrosive]:

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 contact spilled material. Isolate area until gas has dispersed. (ERG, 2024)

Ventilation along the floor. Dry.

Storage temp: less than 130 °F

Compressed gas cylinders containing sulfur dioxide should be stored in accordance with 29 CFR 1910.101.

Store in a cool, dry, well-ventilated location. Outside or detached storage is preferred. Isolate from oxidizing materials and alkalies. /Sulfur dioxide, liquefied/

Keep container tightly closed in a dry and well-ventilated place. Contents under pressure. Storage class (TRGS 510): Gases

· Wear positive pressure self-contained breathing apparatus (SCBA).

· Wear chemical protective clothing that is specifically recommended by the manufacturer when there is NO RISK OF FIRE.

· Structural firefighters' protective clothing provides thermal protection but only limited chemical protection.

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

117.0 [ppm]

1.0 [ppm]

AEGL 1: Notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure (Unit: ppm)

AEGL 2: Irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape (Unit: ppm)

AEGL 3: Life-threatening health effects or death (Unit: ppm)

AEGLs Status: Final

0.20 [ppm]

0.75 [ppm]

30 [ppm]

2 ppm (5 mg/m³)

5 ppm (13 mg/m³)

TWA 2 ppm (5 mg/m3) ST 5 ppm (13 mg/m3)

5.0 [ppm]

TWA 5 ppm (13 mg/m3) See Appendix G

100 ppm (NIOSH, 2024)

100.0 [ppm]

Excerpts from Documentation for IDLHs: The maximum concentration for exposures of 0.5 to 1 hour is considered to be 50 to 100 ppm [Henderson and Haggard 1943]. It has been reported that 400 to 500 ppm is considered dangerous for even short periods of exposure [Henderson and Haggard 1943].

See: 7446095

0.25 [ppm]

15 min Short Term Exposure Limit (STEL): 0.25 ppm.

A4; Not classifiable as a human carcinogen.

0.25 ppm as STEL; A4 (not classifiable as a human carcinogen).

0.25 ppm [2008]

1.3 mg/m

2.7 mg/m

Small Fire

· Dry chemical or CO2.

Large Fire

· Water spray, fog or regular foam.

· If it can be done safely, move undamaged containers away from the area around the fire.

· Do not get water inside containers.

· Damaged cylinders should be handled only by specialists.

Fire Involving Tanks

· Fight fire from maximum distance or use unmanned master stream devices 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.

Sulfur dioxide appears as a colorless gas with a choking or suffocating odor. Boiling point -10 °C. Heavier than air. Very toxic by inhalation and may irritate the eyes and mucous membranes. Under prolonged exposure to fire or heat the containers may rupture violently and rocket. Used to manufacture chemicals, in paper pulping, in metal and food processing. Rate of onset: Immediate & Delayed Persistence: Minutes to hours Odor threshold: 1 ppm Source/use/other hazard: Disinfectant and preserving in breweries and food/canning; textile industry; batteries.

Colourless, non-flammable gas with strong pungent suffocating odour

Colorless gas with a characteristic, irritating, pungent odor. [Note: A liquid below 14 degrees F. Shipped as a liquefied compressed gas.] [NIOSH]

COLOURLESS GAS OR COMPRESSED LIQUEFIED GAS WITH PUNGENT ODOUR.

Colorless gas with a characteristic, irritating, pungent odor.

Colorless gas with a characteristic, irritating, pungent odor. [Note: A liquid below 14 °F. Shipped as a liquefied compressed gas.]

Colorless gas or liquid

Colorless gas ... [Note: A liquid below 14 degrees F. Shipped as a liquefied compressed gas]

Strong suffocating odor

... Characteristic, irritating, pungent odor ...

Acid taste

14 °F at 760 mmHg (EPA, 1998)

-10.05 °C

-10.00 °C. @ 760.00 mm Hg

-10.05 °C @760 [mm Hg]

-98.9 °F (EPA, 1998)

-75.5 °C

-75.48 °C

10 % (NIOSH, 2024)

In water, 1.07X10+5 mg/L at 21 °C

Soluble in water

In water: 17.7% at 0 °C; 11.9% at 15 °C; 8.5% at 25 °C; 6.4% at 35 °C

Soluble in water ... forms sulfurous acid (H2SO3)

For more Solubility (Complete) data for Sulfur dioxide (7 total), please visit the HSDB record page.

107 mg/mL at 21 °C

Solubility in water, ml/100ml at 25 °C: 8.5

1.434 (EPA, 1998) - Denser than water; will sink

2.619 g/L

Density: 1.5 /liquid/

Density: 1.434 at 0 °C (liquid); vapor pressure: 2538 mm Hg at 21.1 °C

Relative density (water = 1): 1.4 (liquid, -10 °C)

2.619 @25 °C

2.26(relative gas density)

2.26 (EPA, 1998) - Heavier than air; will sink (Relative to Air)

2.264 at 0 °C (Air = 1)

Relative vapor density (air = 1): 2.25

2432 mmHg at 68 °F (EPA, 1998)

Vapor pressure (kPa): 230 at 10 °C; 330 at 20 °C; 462 at 30 °C; 630 at 40 °C

Vapor pressure, kPa at 20 °C: 330

750 [mm Hg] @-10.3 °C

Dissolves in water to form sulfurous acid, a corrosive liquid. Moist sulfur dioxide is very corrosive due to the slow formation of sulfuric acid [Handling Chemicals Safely 1980 p. 876].

Acids, Strong Non-oxidizing

Reducing Agents, Weak

Water-Reactive

SULFUR DIOXIDE is acidic. Reacts exothermically with bases such as amines, amides, metal oxides, and hydroxides. Frequently used as a reducing agent although it is not a powerful one. Acts as a reducing bleach to decolorize many materials. Can act as an oxidizing agent. Supports combustion of powdered aluminum [Mellor 5:209-212 1946-47]. Reacts explosively with fluorine [Mellor 2:1 1946-47]. Supports burning of manganese [Mellor 12:187 1946-47]. Readily liquefied by compression. Contact between the liquid and water may result in vigorous or violent boiling and extremely rapid vaporization. If the water is hot an explosion may occur. Pressures may build to dangerous levels if the liquid contacts water in a closed container [Handling Chemicals Safely 1980]. Supports incandescent combustion of monocesium acetylide, monopotassium acetylide, cesium oxide, iron(II) oxide, tin oxide, and lead oxide [Mellor]. Ethylene oxide and SO2 can react violently in pyridine solution with pressurization if ethylene oxide is in excess (Nolan, 1983, Case History 51).

Will react with water or steam to produce toxic and corrosive fumes.

Monocesium or monopotassium acetylides, and the ammoniate of monolithium acetylide, all ignite and incandesce in unheated sulfur dioxide. The dimetal derivatives including sodium acetylide appear to be less reactive, needing heat before ignition occurs.

Cesium monoxide, iron(II) oxide, tin oxide, and lead(IV) oxide all ignite and incandesce on heating in /sulfur dioxide/ gas. Finely divided (pyrophoric) chromium incandesces in sulfur dioxide, while pyrophoric manganese burns ... on heating in gas. Molten sodium reacts violently with dry gas or liquid, while moist gas reacts as vigorously as water with cold sodium.

Heated oxide /barium peroxide/ attains incandescence in a rapid stream of ... sulfur dioxide.

For more Hazardous Reactivities and Incompatibilities (Complete) data for Sulfur dioxide (18 total), please visit the HSDB record page.

Powdered alkali metals (such as sodium & potassium), water, ammonia, zinc, aluminum, brass, copper [Note: Reacts with water to form sulfurous acid (H2SO3).]

CDC-ATSDR Toxicological Profile

IDENTIFICATION AND USE: Sulfur dioxide (SO2) is a colorless gas or liquid with a strong suffocating odor. SO2 is used as a fungicide and preservative for grapes. It is also used for the manufacture of corn syrups and molasses, in the manufacture of wine to destroy bacteria, mold, and unwanted yeasts, and for sterilization, and prevents the formation of nitrosamines in beer. SO2 is used to manufacture hydrosulfites, to bleach wood pulp and paper, to process, disinfect, and bleach food, for waste and water treatment, in metal and ore refining, and in oil refining. HUMAN STUDIES: Exposures of less than an hour to SO2 at levels above 10 ppm in air are irritating to the nose and throat, sometimes causing a choking sensation followed by nasal discharge, sneezing, coughing, and increased mucous secretion. Severe injuries of human eyes by sulfur dioxide have been produced only by liquified form. The minimum lethal human exposure is an airborne concentration of 400 ppm for 1 minute. The odor or taste is noticeable at airborne concentrations of 3 to 5 ppm, throat and conjunctival irritation and lacrimation start at 8 to 12 ppm, and symptoms become severe at 50 ppm. Other reported minimum lethal concentrations of sulfur dioxide include 3000 ppm for 5 minutes and 1000 ppm for 10 minutes. Elderly patients with asthma may be more sensitive. A 76-year-old woman with asthma died following inhalation exposure to approximately 150 ppm over a period of minutes. The frequencies of chromosomal aberrations and sister-chromatid exchange (SCE) in peripheral blood lymphocytes of 40 workers chronically exposed to SO2 at a sulfuric acid factory were studied. It was shown that the mean frequency of chromosomal aberrations and the mean frequency of lymphocytes with chromosomal aberrations of the SO2-exposed workers were both higher than controls. In human lymphocytes SO2 caused significant increases in the frequency of sister chromatid exchange and micronuclei and also induced mitotic delays and decreased mitotic index and replication index. The potential risk of low birth-weight baby might be higher in elder women exposed to SO2 during pregnancy. ANIMAL STUDIES: SO2 has been found to be endogenously generated from metabolism of sulfur-containing amino acids in mammals through transamination by aspartate aminotransferase. SO2 has physiological effects on the cardiovascular system, including vasorelaxation and cardiac function regulation. Eye irritation occurs at 6 ppm/4 hr in rabbits. After a 120-hr exposure to SO2 concentration of 1.1 ppm, guinea pigs showed proliferative interstitial pneumonia, bronchitis, and tracheitis and an increased histamine content in the lungs, while exposure to 0.06 ppm of SO2 for one month led to interstitial changes in the respiratory tract. In rats continuously exposed to SO2 for 5 months (0.7 ppm and 7.0 ppm), it increased the activity of serum cholinesterase and aspartate aminotransferase and caused morphological changes in the upper respiratory tract. Prolonged exposure of dogs to high concentrations of SO2 (200 ppm) causes a syndrome similar to human chronic bronchitis, involving chronic airway obstruction, airway inflammation, and symptoms of cough and mucus hypersecretion. In mice, fetal weight was reduced by 5% by exposure to SO2. Ossification of the sternebrae and occipital was retarded, but the incidence of malformations was not significantly increased. In rabbits, the incidence of a few minor skeletal variants was significantly increased in group exposed to SO2. SO2 increased the frequencies of chromosome aberrations and aberrant cells in mouse bone marrow in a dose-dependent manner. SO2 inhalation caused an increase of micronuclei frequencies in the polychromatic erythrocytes. SO2 caused significant, dose-dependent increases in DNA damage by inhalation exposure of mice. ECOTOXICITY STUDIES: SO2 was acutely toxic to fish. Green plants are extremely sensitive to atmospheric sulfur dioxide. Alfalfa, barley, cotton, and wheat can be injured at levels between 0.15 and 0.20 ppm, while potatoes, onions, and corn are far more resistant.

Evaluation: There is inadequate evidence for the carcinogenicity in humans of sulfur dioxide, sulfites, bisulfites and metabisulfites. There is limited evidence for the carcinogenicity in experimental animals of sulfur dioxide. There is inadequate evidence for the carcinogenicity in experimental animals of sulfites, bisulfites and metabisulfites. Overall evaluation: Sulfur dioxide, sulfites, bisulfites and metabisulfites are not classifiable as to their carcinogenicity to humans (Group 3).

A4; Not classifiable as a human carcinogen.

Sulfur dioxide

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 54: (1992) Occupational Exposures to Mists and Vapours from Strong Inorganic Acids; and Other Industrial Chemicals

The substance can be absorbed into the body by inhalation.

inhalation, skin and/or eye contact

Cough. Shortness of breath. Sore throat. Laboured breathing.

ON CONTACT WITH LIQUID: FROSTBITE.

Redness. Pain.

irritation eyes, nose, throat; rhinorrhea (discharge of thin nasal mucus); choking, cough; reflex bronchoconstriction; liquid: frostbite

Respiratory (From the Nose to the Lungs)

Eyes, skin, respiratory system

Chronic Bronchitis - Chronic bronchitis is persistent coughing and production of phlegm for at least 3 months out of the year for at least two successive years. (American Thoracic Society).

Toxic Pneumonitis - Inflammation of the lungs induced by inhalation of metal fumes or toxic gases and vapors.

Fibrogenic - Inducing tissue injury and fibrosis (scarring).

ACGIH Carcinogen - Not Classifiable.

ATSDR Final

LC50 (rat) = 2,520 ppm/1H

LC50 Rat inhalation 2420 ppm/1 hr

LC50 Mouse inhalation 3000 ppm/30 min

LC50 Mice inhalation 150 ppm/847 hr

LC50 Guinea pigs inhalation 130 ppm/154 hr

For more Non-Human Toxicity Values (Complete) data for Sulfur dioxide (6 total), please visit the HSDB record page.

Cigarette smoking (CS) and air pollution can both alter autonomic cardiac function, yet little has been reported on their combined effect on cardiovascular dysfunction. Therefore, we assessed The potential effect of cigarette smoking (CS) on the association between sulfur dioxide (SO(2)) and heart rate variability (HRV) /was examined/ in community residents. ...Evidence /was found/ that SO(2) induced short but dramatic decreases in HRV indices, the standard deviation of the NN interval (SDNN), low frequency (LF), and high frequency (HF), in smokers compared with non-smokers. /Data/ suggest that CS influences the decrease in HRV directly caused by SO(2), and the effect in susceptible groups may be more serious.

Wistar rats were exposed to intratracheally instilled with benzo(a)pyrene (B(a)P; 3 mg) or SO2 (20 ppm) inhalation alone or together. The mRNA of CYP1A1 and 1A2, c-fos, and c-jun and protein levels of c-fos and c-jun were analyzed in lungs ... and 7-ethoxyresorufin O-deethylase (EROD) and methoxyresorufin O-demethylase (MROD) activities were detected. In lungs of rats exposed to SO2 alone, the gene transcription of CYP1A1 and 1A2, the EROD and MROD activities were decreased. Meanwhile, the mRNA and protein levels of c-jun and c-fos were increased significantly. Exposure to B(a)P alone induced CYP1A1, CYP1A2 mRNA levels, the protein levels of c-jun, and the EROD and MROD activities in lungs. However, exposure to B(a)P plus inhaled SO2 neither increased nor decreased CYP1A1/2 mRNA expressions, EROD, and MROD activities in lungs, versus exposure to B(a)P alone. Nevertheless, exposure to B(a)P plus inhaled SO2 increased the mRNA and protein levels of c-jun and c-fos in lungs compared with lungs exposed to SO2 alone. Accordingly, the SO2-induced decreases of CYP1A1/2 might not influence the metabolic activation of B(a)P. However, when B(a)P and SO2 were given in the combinations, one might postulate that a synergistic effect on the expressions of c-fos and c-jun between SO2 and B(a)P, which might be one of the possible mechanisms of combination effects between B(a)P and the air pollutants.

The antioxidant effects of exogenous salicylic acid (SA) and vitamin C (Vit C) on the oxidative stress induced by 56 mg/cu m of sulfur dioxide (SO2) in mouse livers and brains were investigated. The exposure of SO2 caused significant elevation of thiobarbituric acid-reactive substance (TBARS) levels and reduction of enzyme activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT) in brain and liver, accompanied by a decrease in relative growth rate, when compared with controls. Application of moderate concentrations of SA and Vit C markedly reduced the SO2-induced elevation of TBARS levels, with 5.5 mg/kg SA or 200 mg/kg Vit C being most effective. In contrast to the decrease of TBARS levels, the levels of SOD, POD, and CAT in liver and brain were significantly increased in comparison with controls. The polyacrylamide gel electrophoresis (PAGE) of total liver proteins showed that the SO2 inhalation caused a 30-kD protein band disappearance compared with the control. However, the band remained unchanged in the samples treated with 5.5 and 8.25 mg/kg SA or 100, 200, and 400 mg/kg Vit C. Therefore, this protein band may serve as a marker for the damage induced by SO2 and an additional basis for drug screening and selection.

Aerosols that have produced ... potentiation of response to sulfur dioxide are soluble salts of such metals as manganese, ferrous iron, and vanadium. ... These aerosols potentiate response about three fold when present at concentration of 1 mg/cu m at 50% relative humidity.

For more Interactions (Complete) data for Sulfur dioxide (20 total), please visit the HSDB record page.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Sulfur and related compounds/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Administer activated charcoal ... . Cover skin burns with dry sterile dressings after decontamination ... . /Sulfur and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasms ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Sulfur and related compounds/

Preplacement and annual medical examinations should be done whenever TWA exposures exceed 0.25 ppm (0.65 mg/cu m). These examinations should be directed toward complaints of mucous membrane irritation, cough and shortness of breath. They should ascertain that nasal passages are open. Persons with a history of asthma or with subnormal pulmonary function should be watched closely. Simple expiratory function tests should be a part of the examination. They are useful for several purposes: (a) determining whether or not a person is a suitable candidate for using respirators; (b) identifying "reactors", ie, persons who may be most susceptible to the effects of SO2. This can be done by comparing preshift and postshift tests; (c) when done periodically, they can be used to determine whether or not a person's expiratory functions are declining at a faster than normal rate. Such determinations are much more sensitive when pooled data from a number of individuals are used. The forced expiratory volume at 1 second and the maximum mid-expiratory flow rate appear to be the most useful of the simple pulmonary function tests.

/HUMAN EXPOSURE STUDIES/ Twenty five healthy adults were tested and found to have increased airway resistance (determined in a body plethysmograph) at 5 ppm (13 mg/cu m) of sulfur dioxide and at higher levels when breathing normally for 10 min, but not at lower levels. After 25 deep breaths, as might occur in laborers doing hard physical work, the subjects had a statistically significant increase in airway resistance at 1 ppm and after 8 deep breaths at 3 ppm.

/HUMAN EXPOSURE STUDIES/ In a study comprising a series of experiments over a period of 4 yr, a small increase in specific airway flow resistance (flow resistance corrected for lung volume) was seen in response to sulfur dioxide at 1 ppm, but only if the subjects took 25 maximal breaths of the gas starting from residual volume. The procedure was designed to increase dosage to the laryngotracheobronchial airways. In one subject, there was a threefold increase in specific airway flow resistance with this procedure. As expected, sulfur dioxide at 3 ppm elicited greater changes in function than did 1 ppm. The magnitudes of these changes were proportional to the numbers of deep breaths taken.

/HUMAN EXPOSURE STUDIES/ The effects of sulfur dioxide and ozone alone and in combinations /were studied/ on young normal subjects under conditions of light exercise. When breathed alone, 0.37 ppm of sulfur dioxide had no effect on any measurement of lung function; 0.37 ppm of ozone produced a just significant decline of ventilatory function at the end of a 2 hr exposure. However, when the two gases were present together in eight normal young subjects who were non-smokers, the maximal mid-expiratory flow rate dropped to 67% of its initial value at the end of 2 hr; the forced expiratory volume was 78% of its initial value, and the mid-expiratory flow rate (50% vital capacity) was only 54% of the initial value. A 2 hr exposure to 0.75 ppm of sulfur dioxide alone dropped the maximal mid-expiratory flow rate to 90% of its control value. /It was/ concluded that sulfur dioxide and ozone are exceedingly corrosive when present together, that "standard" must specify the presence or absence of the other, and that there is a growing incidence of the joint presence of the two pollutants in urban environments. /Air pollution/

/HUMAN EXPOSURE STUDIES/ Bronchoalveolar lavage of 12 healthy, nonsmoking subjects 24 hr after exposure for 20 min to 4 or 8 ppm (10.5 or 21 mg/cu m) sulfur dioxide showed increased alveolar macrophage lysosomal activity; at the higher level, the numbers of macrophages and lymphocytes in the lavage fluid were increased. No effect on lung function was observed.

For more Human Toxicity Excerpts (Complete) data for Sulfur dioxide (79 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ Research investigating the effects of air contaminants on biota has been limited to date. Captive adult female American kestrels (Falco sparverius) were exposed to a mixture of benzene (0.6 ppm), toluene (1 ppm), nitrogen dioxide (NO2; 2 ppm) and sulfur dioxide (SO2; 5.6 ppm), in a whole-body inhalation chamber. Thyroid axis responses to meet metabolic demands were examined through thyroid histology, plasma thyroxine (T4), and triiodothyronine (T3), and hepatic outer ring deiodination (T4-ORD). Plasma free (F) T3 and T4 were measured at baseline, and at 9 days and 18 days of exposure, whereas total (T) T3 and TT4, thyroid histology and hepatic T4-ORD were determined at the final 18 day exposure. Inhalation of these contaminants significantly suppressed plasma FT4 and TT4, and depleted follicular colloid and increased epithelial cell height at 18 days, and significantly altered the temporal pattern of plasma FT4. Significant histological changes in the follicular colloid:epithelial cell height ratio indicated sustained T4 production and release by the thyroid glands. There was no effect on plasma FT3, TT3, or hepatic T4-ORD. We hypothesize that contaminant-related activation of the hypothalamus-pituitary-thyroid axis in the kestrels increased elimination of plasma T4 through Phase II enzymes.

/BIRDS and MAMMALS/ In the oil sands of Alberta, Canada, toxicology research has largely neglected the effects of air contaminants on biota. Captive Japanese quail (Coturnix c. japonica) and American kestrels (Falco sparverius) were exposed to mixtures of volatile organic compounds and oxidizing agents (benzene, toluene, NO2 and SO2) in a whole-body inhalation chamber, to test for toxicological responses. Hepatic biotransformation measured through 7-ethoxyresorufin-O-dealkylase (EROD) tended to be increased in exposed kestrels (p=0.06) but not in quail (p=0.15). Plasma corticosterone was increased in the low dose group for quail on the final day of exposure (p=0.0001), and midway through the exposure period in exposed kestrels (p=0.04). For both species, there was no alteration of T and B-cell responses, immune organ mass, or histology of immune organs (p>0.05).

/AQUATIC SPECIES/ ... 16 to 19 ppm of sulfur dioxide killed sunfish in 1 hr. ... Concentrations of 10 ppm of sulfur dioxide in tap water caused trout to float within 10 min and also reports that 5 ppm of sulfur dioxide killed trout in 1 hr.

/PLANTS/ Nitrogen dioxide (NO2) and sulfur dioxide (SO2) generated by excessive coal combustion and motor vehicle emissions are major air pollutants in the large cities of China. The objective of our study was to determine the effects of the exposure of oak pollens (Quercusmongolica) to several concentrations of NO2 or SO2. Pollen grains were exposed to 0.5 ppm to 5.0 ppm NO2 or SO2 for 4 hours and assessed for morphological damage by field emission scanning electron microscopy and for viability using the trypan blue stain. Morphological changes in pollen grains were also examined after contact with acid solutions at pH 4.0 to pH 7.0. Exposure to NO2 or SO2 significantly damaged pollen grains at all concentrations investigated, compared to exposure to air; with exposure to concentrations of 0.5 ppm to 2 ppm resulting in fissures or complete breaks in the exine and a concentration of 5 ppm resulting in complete breakdown and release of pollen cytoplasmic granules. Significantly greater amounts of pollen grain were damaged after exposure to SO2 (15.5-20.4%) than after exposure to NO2 (7.1-14.7%). Similarly, exposure to NO2 or SO2 significantly decreased the viability of pollen grains, compared with exposure to air; with SO2 being slightly more detrimental than NO2. Exposure to acid solutions also induced pollen damage, which appeared to be pH-dependent (from 24.6% at pH 6.0 to 55.8% at pH 4.0; compared to 3.8% at pH 7.0). Short-term exposure of oak pollen to high concentrations of SO2 or NO2 significantly increases their fragility and disruption, leading to subsequent release of pollen cytoplasmic granules into the atmosphere. These results suggest that heightened air pollution during the oak pollen season may possibly increase the incidence of allergic airway disease in sensitized individuals by facilitating the bioavailability of airborne pollen allergens.

For more Ecotoxicity Excerpts (Complete) data for Sulfur dioxide (18 total), please visit the HSDB record page.

The substance is harmful to aquatic organisms.

Sulfur dioxide's production from fuel combustion will result in its direct release to the environment. On a global basis, fossil fuel combustion accounts for 75 to 85% of man-made sulfur dioxide emissions, and industrial processes such as refining and smelting account for the remainder. The global sulfur cycle involves an atmospheric flux of about (140-350)X10+6 tons/annum, with (40-60)X10+6 tons as anthropogenic sulfur, in the form of sulfur dioxide, sulfuric acid, and sulfate. Sulfur dioxide can react with other compounds in the atmosphere and form fine particles that result in haze that reduces visibility. Particulate matter pollution is the major cause of haze in parts of the US. Sulfur dioxide's production and use in preserving fruits, vegetables; disinfectant in breweries and food factories; bleaching textile fibers, straw, wicker ware, gelatin, glue, beet sugars, solvent and reagent in organic synthesis may result in its release to the environment through various waste streams. It's use as a fungicide and acaricide in the wine industry will result in its direct release to the environment. Sulfur dioxide is released to the air from volcanic activity and eruptions. If released to air, a vapor pressure of 3.0X10+3 mm Hg at 25 °C indicates sulfur dioxide will exist solely as a gas in the atmosphere. Gas-phase sulfur dioxide is oxidized rapidly by homogeneous and heterogeneous reactions. The oxidation of sulfur dioxide to sulfuric acid and sulfates in the atmosphere is an important contributor to air pollution, specifically producing acid rain. Sulfur dioxide dissolves in water, forming a weak acid solution of sulfurous acid. This acid rain effects sensitive forest, soil and aquatic ecosystems. The atmospheric lifetime of sulfur dioxide is about 10 days. Sulfur dioxide may be photochemically or catalytically oxidized to SO3 and sulfate in air. If released to soil, sulfur dioxide is expected to absorb to soil. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 8.10X10-4 atm-cu m/mole. Sulfur dioxide is expected to volatilize from dry soil surfaces based upon its vapor pressure. Sulfur dioxide has been shown to be reduced to H2S using heat- and alkali-treated sewage sludge by certain sulfate reducing bacteria. If released into water, sulfur dioxide is not expected to adsorb to suspended solids and sediment based upon its rapid reaction with water to form sulfuric acid. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's reactivity with water. Occupational exposure to sulfur dioxide may occur through inhalation and dermal contact with this compound at workplaces where sulfur dioxide is produced or used. Monitoring data indicate that the general population may be exposed to sulfur dioxide via inhalation of ambient air, smoking cigarettes, ingestion of food, and dermal contact with consumer products containing sulfur dioxide. (SRC)

Volcanoes and volcanic vent activity contribute to the levels of atmospheric sulfur dioxide(1,2). Natural sources of sulfur dioxide also include decaying organic matter, and the action of the sun on seawater(2). Oceans may be a source of sulfur dioxide under times of barometric imbalance(1). Sulfur dioxide is believed to be the main sulfur compound produced by oxidation of dimethyl sulfide that is emitted from the ocean(2). Sea salt can also contribute to atmospheric levels of sulfate(1). Sulfur dioxide is a component of marihuana and cotton(3).

Hydrogen sulfide, from the natural decay of vegetation on land, marsh lands and in the oceans, is probably oxidized to sulfur dioxide within hours.

Sulfur accounts for 15% of the inner core of the earth and 0.052% of its crust. The total sulfur content of the earth is estimated to be approximately 18.2X10+145 tons. The global sulfur cycle involves an atmospheric flux of about (140-350)X10+6 tons/annum, with (100-290)X10+6 tons involving biological decay, sea spray and volcanic activity. Sulfur also particiaptes in microbial cycles. /Sulfur/

Sulfur dioxide's production from fuel combustion will result in its direct release to the environment(1). Sulfur dioxide in the atmosphere is formed as a by-product of fuel combustion from power generation and industrial processes, and by the oxidation of reduced gases in the air(2). Sulfur dioxide can react with other compounds in the atmosphere and form fine particles that result in haze that reduces visibility. Particulate matter pollution is the major cause of haze in parts of the world(3). Sulfur dioxide's production and use for preserving fruits, vegetables; disinfectant in breweries and food factories; bleaching textile fibers, straw, wicker ware, gelatin, glue, beet sugars, solvent and reagent in organic synthesis(4) may result in its release to the environment through various waste streams. It's use as a fungicide and acaricide in the wine industry will result in its direct release to the environment(5). Sulfur dioxide is a constituent of tobacco smoke(6).

The oxidation of sulfur dioxide to sulfuric acid and sulfates in the atmosphere is an important contributor to air pollution, specifically producing acid rain. Sulfur dioxide dissolves in water, forming a weak acid solution of sulfurous acid. This acid rain effects sensitive forest, soil and aquatic ecosystems. Sulfur in precipitation is, up to a point, beneficial to plant growth as sulfur is an essential element. At low levels, sulfur dioxide in the atmosphere is not harmful to crops but damage can occur at high levels. The 1990 Clean Air Act Amendments were designed to cut annual sulfur dioxide emissions 40% from 1980 levels, and thereby decrease the effects of acid rain, which can cause damage at great distances from the source of emission. Estimated emissions in the USA declined from 25.7X10+6 tons in 1980 to approximately 20X10+6 tons in 2006; approximately 65% of emissions is attributable to electric utilities. Regulatory action to limit sulfur emissions is applicable to power generation, the selection of fuel and the coal mining, gas and petroleum industries. A large part of the amount of sulfur dioxide in the atmosphere is attributed to burning sulfur-containing fuel, notably coal, and smelting sulfide ores(1).

On a global basis, fossil fuel combustion accounts for 75 to 85% of man-made sulfur dioxide emissions, and industrial processes such as refining and smelting account for the remainder.

It is estimated that 93.5% of sulfur dioxide pollution is produced in the Northern Hemisphere, and the remaining 6.5% in the Southern Hemisphere.

For more Artificial Pollution Sources (Complete) data for Sulfur dioxide (7 total), please visit the HSDB record page.

Sulfur dioxide (SO2) is an atmospheric pollutant that is moderately persistent in the atmosphere and highly water soluble. When applied as a pesticide, SO2 may be transported, deposited, or transformed in various chemical reactions. SO2 participates in the sulfur biogeochemical cycle, which involves complex reactions of sulfur-containing compounds between abiotic and biotic components of ecosystems. The main degradation route of SO2 is atmospheric oxidation, and sulfur oxides may undergo long-distance transport prior to removal from the atmosphere by wet or dry deposition. According to the Pesticide Use Reporting (PUR) database maintained by the California Department of Pesticide Regulation (DPR), SO2 use in California from 2010 to 2015 was primarily for fumigations (96%), including treatments of postharvest grape products and winery equipment sterilizations. Other site uses contributed less than 5% of reported statewide SO2 use from 2010 to 2015. A slight increasing trend in use of SO2 as a pesticide was observed from 2010 to 2015, with the highest reported uses of SO2 within California counties during the months of July-November. Although the primary sources of SO2 in the environment are anthropogenic emissions from the combustion of fossil fuels, emissions of SO2 from pesticide uses have the potential to contribute to the environmental and public welfare impacts of SO2 pollution. Oxidation of atmospheric SO2 may contribute to the negative environmental and public welfare impacts of acid rain, which include toxicity to aquatic organisms, fish, and terrestrial vegetation, and corrosion of man-made materials.

TERRESTRIAL FATE: Sulfur dioxide may be absorbed by soil(1). Volatilization of sulfur dioxide from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 8.10X10-4 atm-cu m/mole(2). However, reaction with water to sulfuric acid is expected to attenuate volatilization(SRC). Sulfur dioxide is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.0X10+3 mm Hg at 25 °C(3). Biodegradation data in soil were not available(SRC, 2018). However, a sulfate-reducing bacteria isolated from sewage sludge was shown to biodegrade sulfur dioxide to hydrogen sulfide(1).

TERRESTRIAL FATE: Although snow covered surfaces are inefficient receptors of gaseous and particulate sulfur cmpd, the spring melt of the accumulated winter snowpack can result in rapid, short term inputs of high sulfate, low pH water to freshwater systems with resulting disastrous effects on fish.

AQUATIC FATE: Sulfur dioxide may be absorbed by water and snow covers. Melting snowpacks in spring can result in short-term high input of sulfate into freshwater(1). Volatilization from water surfaces is(2) based upon a Henry's Law constant of 8.10X10-4 atm-cu m/mole(3). However, reaction in water is expected to attenuate this process(SRC). Biodegradation data in water were not available(SRC, 2018). However, a sulfate-reducing bacteria isolated from sewage slduge was shown to biodegrade sulfur dioxide to hydrogen sulfide(1).

For more Environmental Fate (Complete) data for Sulfur dioxide (10 total), please visit the HSDB record page.

PURE CULTURE: Sulfur dioxide has been shown to be reduced to H2S (hydrogen sulfide) using heat- and alkali-treated sewage sludge by the sulfate reducing bacteria, Desulfovbrio desulfuricans or Desuotomaculum orientis(1).

The oxidation of sulfur dioxide to sulfuric acid and sulfates in the atmosphere is important with regard to air pollution studies. Radicals, e.g. hydrogen monoxide, water, and carboxcylic acid, appear to be the principal species responsible for the homogeneous oxidation of sulfur dioxide in the atmosphere, which occurs at rates as high as 4.0%/hr(1). Sulfur dioxide is oxidized rapidly by homogeneous and heterogeneous reactions and is removed from the atmosphere by precipitation and by dry deposition on surfaces, mainly as sulfuric acid(2). Sulfur dioxide in air can be oxidized to sulfate by cloud or rain droplets and thus form "acid rain"(1). Meteorologic conditions resulted in high acidic pollution during the summer months in Ohio, Pennsylvania, Virginia, West Virginia, Tennessee and Kentucky. The EPA Acid Rain Program projected a 40% reduction in sulfur dioxide yearly emissions in the US between 1980 and 2010, which would also contribute to less sulfate haze(2). Sulfur dioxide may be photochemically or catalytically oxidized to SO3 and sulfate in air. The atmospheric lifetime of sulfur dioxide is about 10 days(2). .

Suggested values of reaction rates for gas phase oxidation of sulfur dioxide to sulfate for the western European summer range from 0.5 to 5%/hr in sunlight, depending on the degree of pollution of the atmosphere, with the lower figure relating to clean air. This oxidation involves other short lived pollutants which have been photochemically generated, therefore, the direct photo-oxidation of sulfur dioxide is not important. Because these reactions are dependent on solar radiation, their importance decreases significantly in winter time and at night.

Catalyzed, liquid phase, oxidation /of sulfur dioxide/ in the presence of metals (e.g. iron, manganese) is important in urban plumes and perhaps urban fogs where their concentrations are sufficiently high, but probably not in cleaner, rural air.

Liquid phase oxidation involving the strong oxidizing agents ozone and hydrogen peroxide may also be very important (e.g. hydrogen sulfide and other organic sulfides oxidized to sulfur dioxide); however, reaction rates and atmospheric concentrations, respectively, for these two substances are not sufficiently well known.

For more Environmental Abiotic Degradation (Complete) data for Sulfur dioxide (6 total), please visit the HSDB record page.

Sulfur dioxide can be absorbed by soil. In the form of acid rain it is the leading cause of an increase in heavy metal mobility in soil(1).

Sulfur dioxide uptake is dependent upon soil pH and moisture content.

The Henry's Law constant for sulfur dioxide is 8.10X10-4 atm-cu m/mole(1). This Henry's Law constant indicates that sulfur dioxide is expected to volatilize from water surfaces(2). Sulfur dioxide's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). However volatilization may be attenuated by reaction with water to form sulfuric acid(SRC). Sulfur dioxide is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.0X10+3 mm Hg(3).

RAIN/SNOW/FOG: It has been estimated that 70% of the sulfate that is present in rainwater comes from the washout of sulfur dioxide from the atmosphere(1).

Fossil fuel accounts for 75-85% of man-made sulfur dioxide emissions; 93.5% of these emissions originate in the Northern Hemisphere. Fuel combustion for electrical utilities accounted for the greatest portion of total sulfur dioxide emissions in the US, with Ohio and Indiana ranked the highest for emissions. Sulfur dioxide emissions have exhibited a steady decrease in the US since the 1970s(1). Sulfur dioxide was reported at 383 ppm in plume emissions from a coal-burning industrial power plant near Dayton, OH(2). Sulfur dioxide concentration of 23.61 kg/yr was reported for diesel exhaust from vehicles on a very large dairy operation in the Po Valley, northern Italy(3).

Trend in world-wide sulfur dioxide emissions(1).

Table: Global SO2 Emission Trends [Table#861]

Sulfur dioxide emissions from Connecticut sources in 2008 amounted to 20,000 tons. 3000 tons were attributed to mobile sources and 17,000 tons from stationary/area sources. 96% of stationary/area source sulfur dioxide emissions were generated by the combustion of residential and commercial heating oil and electricity generation. New York State requires the use of ultra-low sulfur heating oil (less than or equal to 15 ppm). Rhode Island adopted a sulfur rule in 2013. Maine, Massachusetts, New Jersey, Pennsylvania and Vermont have rules requiring low-sulfur fuels by 2018(1).[Table#862]

This study aims to estimate the emissions of carbon dioxide (CO2), sulfur dioxide (SO2), and nitric oxide (NO) for coal combustion in thermal power plants in India using plant-specific emission factors during the period of 2001/02 to 2009/10. The mass emission factors have been theoretically calculated using the basic principles of combustion under representative prevailing operating conditions in the plants and fuel composition. The results show that from 2001/02 to 2009/10 period, total CO2 emissions have increased from 324 to 499 Mt/year; SO2 emissions have increased from 2,519 to 3,840 kt/year; and NO emissions have increased from 948 to 1,539 kt/year from the Indian coal-fired power plants. National average emissions per unit of electricity from the power plants do not show a noticeable improvement during this period. Emission efficiencies for new plants that use improved technology are found to be better than those of old plants. As per these estimates, the national average of CO2 emissions per unit of electricity varies between 0.91 and 0.95 kg/kWh while SO2 and NO emissions vary in the range of 6.9 to 7.3 and 2.8 to 2.9 g/kWh, respectively. Yamunagar plant in Haryana state showed the highest emission efficiencies with CO2 emissions as 0.58 kg/kWh, SO2 emissions as 3.87 g/kWh, and NO emissions as 1.78 g/kWh, while the Faridabad plant has the lowest emission efficiencies with CO2 emissions as 1.5 kg/kWh, SO2 emissions as 10.56 g/kWh, and NO emissions as 4.85 g/kWh. Emission values at other plants vary between the values of these two plants.

For more Effluent Concentrations (Complete) data for Sulfur dioxide (8 total), please visit the HSDB record page.

URBAN/SUBURBAN: The sulfur dioxide mean 8-hr max concentration was 4.6 ppb in a high traffic area of Los Angeles County, CA, measured November 1999 through January 2000(1). Sulfur dioxide levels of 76.2 and 55.2 ug/cu m were reported in urban and suburban areas, respectively, measured in Eskisehir, Turkey. A concentration of 57.5 ug/cu m was reported for an urban traffic area. Testing was conducted in winter, February 27-March 13, 2009(2). Average sulfur dioxide concentrations of 2.8 and 3.2 ug/cu m were measured in urban and suburban environments, respectively, in Mallorca (Balearic Islands) measured from 2000 to 2012. The regional background concentration was 2.3 ug/cu m. Levels are influenced by power generation and an increased maritime traffic(3). Concentration ranges were: 2.55-17.43 ppb (winter); 1.48-15.55 ppb (summer); 1.24-6.37 ppb (monsoon) during 2008 in New Delhi, India(4). Sulfur dioxide concentrations were observed to fluctuate from 0 to 150 ug/cu m in a study of urban pollution and haze clouds over Beijing, China during the dusty season in March 2013(5). The arithmetic mean concentration for the years 2004 to 2010 for sulfur dioxide, based on 85 major city regions of China, was 19.87 ug/cu m (5.78 ug/cu m, min; 118 ug/cu m max)(6).

RURAL/REMOTE: Sulfur dioxide exhibited a yearly average of 1.1 ppb following a 15-year (1997-2011) term assessment of air quality from a background station at Jeranut, Pahang on the Malaysian Peninsula(1).

RURAL/REMOTE: A mean sulfur dioxide level of 2.6 ppbw was reported for a relatively pristine region in western Maryland that is >50 km downwind of power plants in Ohio, Pennsylvania and West Virginia; sampling was conducted from 2006 to 2014(1).[Table#849]

SOURCE DOMINATED: Sulfur dioxide Combustion Emissions(1).[Table#850]

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: Dispose of as unused product.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

If ... THERE IS NO FIRE, go directly to the Table of Initial Isolation and Protective Action Distances /(see table below)/ ... to obtain initial isolation and protective action distances. IF THERE IS A FIRE, or IF A FIRE IS INVOLVED, go directly to the appropriate guide /(see guide(s) below)/ and use the evacuation information shown under PUBLIC SAFETY.

Table: Table of Initial Isolation and Protective Action Distances for Sulfur dioxide; Sulphur dioxide ID: 1079 [Table#859]

Table: Table of Initial Isolation and Protective Action Distances For Different Quantities in Sulfur dioxide/Sulphur dioxide: Large Spills ID:1079 [Table#860]

/GUIDE 125 GASES - CORROSIVE/ Fire or Explosion: 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. . For UN1005: Anhydrous ammonia, at high concentrations in confined spaces, presents a flammability risk if a source of ignition is introduced

/GUIDE 125 GASES - CORROSIVE/ Health: 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.

For more DOT Emergency Guidelines (Complete) data for Sulfur dioxide (10 total), please visit the HSDB record page.

UN 1079; Sulfur dioxide

IMO 2.3; Sulfur dioxide

49 042 90; Sulfur dioxide

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials. Sulfur dioxide is included on the dangerous goods list.

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. Sulfur dioxide is included on the dangerous goods list.

Poison Gas Corrosive

Symbol: T; R: 23-34; S: (1/2)-9-26-36/37/39-45

UN Hazard Class: 2.3; UN Subsidiary Risks: 8