Pend Oreille Health: January 2017

So far, Pend Oreille County officials, including health officials, have not bothered to inform residents of the extreme risks that will arise from the proposed silicon smelter operation in Usk.

This is unconscionable and a dereliction of duty. Simply put, they are not doing their jobs.

Missing from the public space and required information are the Material Safety Data Sheets, toxicity, safety, transportation, and risks assessments to county residents. These are critical disclosures every resident is allowed to see, required by law. Also missing is the environmental protection assessment, also required by law.

I have had a chemical engineer review the entire content of this blog, particularly the chemical compositions and byproducts of silicon smelting operations covered again below. He has confirmed that that statements made herein to this blog are accurate. Moreover, he has issued the following words of warning:

a) All hazardous materials are supposed to be listed, including emergency procedures, short term and long term exposure health risks, etc.

b) Plastic tanks and containers have defects and leak; caps are not properly secured; valves leak; people put stuff into wrong containers; people disobey instructions and take short cuts that save them time; and delivery vehicles crash. I've seen it all, including general managers with hose pipes, hoping to wash chemical spills away into the nearest creek before anyone notices.

c) The incompetence or graft (taking bribes) of local authority officials. In my experience with dealing with such people, they are poorly qualified and 90% of the time don't know what they are talking about. It's always about 'development' and rubber-stamping it with the minimum of inconvenience.

d) Ask local officials for a full list of all chemicals to be transported to and from the site, and for all the health and safety information relating to those materials.

e) Ask for details of the processes to be used at the processing plant and the chemical intermediates generated in the processing that are likely to leak into the general environment.

f) Material Safety Data Sheets are required for the transport of dangerous materials and for occupational safety.

Listed farther down below (because of space restrictions) are the chemicals and compounds used in the silicon smelting processing.

Each known chemical listed shows the safety and toxicity data linked to the US National Library of Medicine Biotechnology Database. Known hazards are listed.

Be advised: they all represent significant, serious and severe threats to Pend Oreille residents.

Dangerous chemicals are used in the processing step, including: Hydrochloric Acid, Trichlorosilane, Hydrogen, Silane (extremely explosive). Many of these chemicals will arrive by truck or by train (community risk).

Toxic amounts of particulate dust (to humans and wildlife) are created (even respirators are insufficient for workers). Tremendous amounts of waste are also generated and will require long-term safe storage (somewhere).

Waste products include silicon tetrachloride (extremely toxic), processed impurities (aluminum, iron, copper, selenium, etc.) and are often simply stored in open unlined pits exposed to the environment. The location is in close proximity to the Pend Oreille River and guarantees eventual leakage into the environment. Fish and wildlife are also at risk from shifting winds. Any downstream / downwind residences and communities will be exposed to dangerous air-borne particulates, chemicals and fumes. Up to 80% of the materials used in processing can be discarded as wastes.

Extremely dangerous and toxic gasses (volitiles) are also used and created during processing, including Carbon Monoxide, Hydrogen, Sulfur Hexaflouride (SF6), Silicon Tetrafluoride (SiF4), Sulfur Difluoride (SF2), Silane (SiH4), Tetrafluorosilane (SiF4), Sulfur Dioxide (SO2). Fugitive gasses can and do escape processing facilities.

The Usk location appears to be selected based on several factors, including a rural and uninformed population to the risk of silicon smelting operations.

The processing involves conversion of metallurgical grade silicon using hydrochloric acid and copper to produce a gas called trichlorosilane (HSiCl3). The trichlorosilane is then distilled to remove remaining impurities, which typically include chlorinated metals of aluminum, iron, and carbon. It is finally heated or reduced with hydrogen to produce silane (SiH4) gas.

Poisonous silicon tetrachloride liquid is a severe environmental hazard. Silicon tetrachloride makes the soil too acidic for plants, causes severe irritation to living tissues, and is highly toxic when ingested or inhaled.

The byproduct of polysilicon production - silicon tetrachloride - is a highly toxic substance that poses severe environmental hazards. When exposed to humid air, silicon tetrachloride transforms into acids and poisonous hydrogen chloride gas, which can make people who breathe the air dizzy and can make their chests contract.

Illness and disease surround these type of operations, including pulmonary fibrosis, cancers (lung, stomach, colon, prostate, liver, pancreatic, etc.) with incidents rise 1.5 to 1.7 times the normal rate.

Unfortunately, many of these new technologies use toxic, explosive, corrosive, or potentially carcinogenic materials, such as cadmium and selenium. Silicon smelting is a environmental and health hazard.

Chemicals and compounds used in the silicon smelting processing (this list is not all inclusive).

Hydrochloric Acid - Hydrochloric acid is corrosive to the eyes, skin, and mucous membranes. Acute (short-term) inhalation exposure may cause eye, nose, and respiratory tract irritation and inflammation and pulmonary edema in humans. Acute oral exposure may cause corrosion of the mucous membranes, esophagus, and stomach and dermal contact may produce severe burns, ulceration, and scarring in humans. Chronic (long-term) occupational exposure to hydrochloric acid has been reported to cause gastritis, chronic bronchitis, dermatitis, and photosensitization in workers. Prolonged exposure to low concentrations may also cause dental discoloration and erosion. EPA has not classified hydrochloric acid for carcinogenicity.

Safety and Hazards

Hazards Identification

GHS Classification

Signal: Danger (flammable, irritant, health hazard, environment)

GHS Hazard Statements
Aggregated GHS information from 9 notifications provided by 119 companies to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

H226 (100%): Flammable liquid and vapor [Warning Flammable liquids - Category 3]
H304 (79.83%): May be fatal if swallowed and enters airways [Danger Aspiration hazard - Category 1]
H315 (99.16%): Causes skin irritation [Warning Skin corrosion/irritation - Category 2]
H317 (78.99%): May cause an allergic skin reaction [Warning Sensitization, Skin - Category 1]
H319 (94.96%): Causes serious eye irritation [Warning Serious eye damage/eye irritation - Category 2A]
H335 (19.33%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation - Category 3]
H400 (77.31%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard - Category 1]
H410 (77.31%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard - Category 1]

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage values above 10% are shown.

Precautionary Statement Codes
P210, P233, P240, P241, P242, P243, P261, P264, P271, P272, P273, P280, P301+P310, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P312, P321, P331, P332+P313, P333+P313, P337+P313, P362, P363, P370+P378, P391, P403+P233, P403+P235, P405, and P501
(The corresponding statement to each P-code can be found here.)

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Trichlorosilane
Signal: Danger (flammable, corrosive, acute toxicity, irritant, health hazard)

GHS Hazard Statements
H224: Extremely flammable liquid and vapor [Danger Flammable liquids - Category 1]
H260: In contact with water releases flammable gases which may ignite spontaneously [Danger Substances And Mixtures Which, In Contact With Water, Emit Flammable Gases - Category 1]
H302: Harmful if swallowed [Warning Acute toxicity, oral - Category 4]
H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation - Category 1A, B, C]
H318: Causes serious eye damage [Danger Serious eye damage/eye irritation - Category 1]
H330: Fatal if inhaled [Danger Acute toxicity, inhalation - Category 1, 2]
H371: May cause damage to organs [Warning Specific target organ toxicity, single exposure - Category 2]

Precautionary Statement Codes
P210, P223, P231+P232, P233, P240, P241, P242, P243, P260, P264, P270, P271, P280, P284, P301+P312, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P309+P311, P310, P320, P321, P330, P335+P334, P363, P370+P378, P402+P404, P403+P233, P403+P235, P405, and P501 (The corresponding statement to each P-code can be found here.)

Toxicological Information

Exposure Routes - The substance can be absorbed into the body by inhalation of its vapour and by ingestion.

Inhalation Symptoms

Cough. Sore throat. Burning sensation. Laboured breathing. Shortness of breath. Symptoms may be delayed. See Notes.

Skin Symptoms

Redness. Pain. Blisters. Skin burns.

Eye Symptoms

Redness. Pain. Severe deep burns.

Ingestion Symptoms

Burning sensation. Abdominal pain. Shock or collapse.
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Silane

Hazards Identification

GHS Classification

Signal: Danger (corrosive, irritant, health hazard)

GHS Hazard Statements
Aggregated GHS information from 4 notifications provided by 32 companies to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

H225 (100%): Highly Flammable liquid and vapor [Danger Flammable liquids - Category 2]
H315 (12.5%): Causes skin irritation [Warning Skin corrosion/irritation - Category 2]
H319 (12.5%): Causes serious eye irritation [Warning Serious eye damage/eye irritation - Category 2A]
H335 (12.5%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation - Category 3]

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage values above 10% are shown.

Precautionary Statement Codes
P210, P233, P240, P241, P242, P243, P261, P264, P271, P280, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P370+P378, P403+P233, P403+P235, P405, and P501
(The corresponding statement to each P-code can be found here.)
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Silicon Tetrachloride - Silicon tetrachloride is a colorless, fuming liquid with a pungent odor. It is decomposed by water to hydrochloric acid with evolution of heat. It is corrosive to metals and tissue in the presence of moisture.

Hazards Identification

GHS Classification

Signal: Danger (corrosive, acute toxicity, irritant)

GHS Hazard Statements
Aggregated GHS information from 16 notifications provided by 286 companies to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

H301 (27.62%): Toxic if swallowed [Danger Acute toxicity, oral - Category 3]
H314 (19.93%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation - Category 1A, B, C]
H315 (80.07%): Causes skin irritation [Warning Skin corrosion/irritation - Category 2]
H319 (80.07%): Causes serious eye irritation [Warning Serious eye damage/eye irritation - Category 2A]
H331 (27.62%): Toxic if inhaled [Danger Acute toxicity, inhalation - Category 3]
H335 (88.81%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation - Category 3]

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage values above 10% are shown.

Precautionary Statement Codes
P260, P261, P264, P270, P271, P280, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P311, P312, P321, P330, P332+P313, P337+P313, P362, P363, P403+P233, P405, and P501
(The corresponding statement to each P-code can be found here.)

Toxicity

Toxicological Information

Exposure Routes

The substance can be absorbed into the body by inhalation of its vapour and by ingestion.

Inhalation Symptoms

Cough. Sore throat. Burning sensation. Laboured breathing. Shortness of breath. Symptoms may be delayed. See Notes.

Skin Symptoms

Redness. Pain. Blisters. Skin burns.

Eye Symptoms

Redness. Pain. Severe deep burns.

Ingestion Symptoms

Burning sensation. Abdominal pain. Shock or collapse.
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Silicon Tetrafluoride - Silicon tetrafluoride is a colorless, nonflammable, corrosive and toxic gas with a pungent odor similar to that of hydrochloric acid. Very toxic by inhalation. Vapor is heavier than air. Under prolonged exposure to heat the containers may rupture violently and rocket.

Hazards Identification

GHS Classification

Signal: Danger (compressed gas, corrosive, acute toxicity)

GHS Hazard Statements
Aggregated GHS information from 5 notifications provided by 132 companies to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

H280 (67.42%): Contains gas under pressure; may explode if heated [Warning Gases under pressure - Compressed gas, Liquefied gas, Dissolved gas]
H300 (18.18%): Fatal if swallowed [Danger Acute toxicity, oral - Category 1, 2]
H310 (18.18%): Fatal in contact with skin [Danger Acute toxicity, dermal - Category 1, 2]
H314 (100%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation - Category 1A, B, C]
H330 (84.85%): Fatal if inhaled [Danger Acute toxicity, inhalation - Category 1, 2]
H331 (15.15%): Toxic if inhaled [Danger Acute toxicity, inhalation - Category 3]

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage values above 10% are shown.

Precautionary Statement Codes
P260, P261, P262, P264, P270, P271, P280, P284, P301+P310, P301+P330+P331, P302+P350, P303+P361+P353, P304+P340, P305+P351+P338, P310, P311, P320, P321, P322, P330, P361, P363, P403+P233, P405, P410+P403, and P501
(The corresponding statement to each P-code can be found here.)

Toxicity

Toxicological Information

Carcinogen

A4; Not classifiable as a human carcinogen. /Fluorides, as F/

American Conference of Governmental Industrial Hygienists TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, OH, 2008, p. 31

Exposure Routes

The substance can be absorbed into the body by inhalation.

Inhalation Symptoms

Sore throat. Cough. Burning sensation. Shortness of breath. Laboured breathing. Symptoms may be delayed. See Notes.

Skin Symptoms

Redness. ON CONTACT WITH LIQUID: FROSTBITE.

Eye Symptoms

Redness.

Human Toxicity Excerpts

All silicon tetrahalides are highly toxic by inhalation and ingestion, and extremely irritation to skin and mucous membranes owing to their corrosive nature resulting from hydrolysis in moist tissue to liberate halogen acid. /Silicon Halides/

Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3035

TOXIC BY INHALATION. STRONG IRRITANT TO MUCOUS MEMBRANES.

Hawley, G.G. The Condensed Chemical Dictionary. 10th ed. New York: Van Nostrand Reinhold Co., 1981., p. 922

Ecological Information

Probable Routes of Human Exposure

... NOT EMPLOYED IN INDUSTRY, BUT IT MAY BE DISCHARGED INTO AIR IN SMELTING OPERATIONS AS THE RESULT OF INTERACTION OF CALCIUM FLUORIDE WITH SAND OR WITH THE SILICA PRESENT IN ORES.

Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 844
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Sulfur Difluoride - Chemical Names: SULFURYL FLUORIDE; Sulfonyl fluoride; Sulfuryl difluoride; Sulphuryl fluoride; Vikane; Sulfuric oxyfluoride

Sulfuryl fluoride is a colorless odorless gas. Shipped as a liquefied gas under its own vapor pressure. Noncombustible. Heavier than air. Very toxic by inhalation. Contact with the unconfined liquid can cause frostbite. Prolonged exposure to heat can cause containers to rupture violently and rocket.

Signal: Danger (compressed gas, acute toxicity, health hazard, environmental hazard)

GHS Hazard Statements
Aggregated GHS information from 5 notifications provided by 150 companies to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

H280 (100%): Contains gas under pressure; may explode if heated [Warning Gases under pressure - Compressed gas, Liquefied gas, Dissolved gas]
H330 (31.33%): Fatal if inhaled [Danger Acute toxicity, inhalation - Category 1, 2]
H331 (68.67%): Toxic if inhaled [Danger Acute toxicity, inhalation - Category 3]
H370 (31.33%): Causes damage to organs [Danger Specific target organ toxicity, single exposure - Category 1]
H373 (100%): Causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure - Category 2]
H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard - Category 1]

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage values above 10% are shown.

Precautionary Statement Codes
P260, P261, P264, P270, P271, P273, P284, P304+P340, P307+P311, P310, P311, P314, P320, P321, P391, P403+P233, P405, P410+P403, and P501
(The corresponding statement to each P-code can be found here.)

Toxicity

Toxicological Information

Carcinogen

Cancer Classification: Not Likely to be Carcinogenic to Humans

USEPA Office of Pesticide Programs, Health Effects Division, Science Information Management Branch: "Chemicals Evaluated for Carcinogenic Potential" (April 2006)

Exposure Routes

The substance can be absorbed into the body by inhalation.

inhalation, skin and/or eye contact (liquid)

Symptoms

conjunctivitis, rhinitis, pharyngitis, paresthesia; liquid: frostbite: In Animals: narcosis, tremor, convulsions; pulmonary edema; kidney injury

Inhalation Symptoms

Cough. Sore throat. Nausea. Vomiting. Tremor.

Skin Symptoms

ON CONTACT WITH LIQUID: FROSTBITE.

Eye Symptoms

Redness.

Target Organs

Eyes, skin, respiratory system, central nervous system, kidneys

Eyes, skin, respiratory system, CNS, kidneys
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Tetrafluorosilane - Chemical Names: Tetrafluorosilane; SILICON TETRAFLUORIDE; Silane, tetrafluoro-; Perfluorosilane; Silicon fluoride; 7783-61-1

Silicon tetrafluoride is a colorless, nonflammable, corrosive and toxic gas with a pungent odor similar to that of hydrochloric acid. Very toxic by inhalation. Vapor is heavier than air. Under prolonged exposure to heat the containers may rupture violently and rocket.

Safety and Hazards

Hazards Identification

GHS Classification

Signal: Danger (compressed gas, corrosive, acute toxicity)

Toxicity

Toxicological Information

Carcinogen

A4; Not classifiable as a human carcinogen. /Fluorides, as F/

Exposure Routes

The substance can be absorbed into the body by inhalation.

Inhalation Symptoms

Sore throat. Cough. Burning sensation. Shortness of breath. Laboured breathing. Symptoms may be delayed. See Notes.

Skin Symptoms

Redness. ON CONTACT WITH LIQUID: FROSTBITE.

Eye Symptoms

Redness.

Human Toxicity Excerpts

Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3035

TOXIC BY INHALATION. STRONG IRRITANT TO MUCOUS MEMBRANES.

Hawley, G.G. The Condensed Chemical Dictionary. 10th ed. New York: Van Nostrand Reinhold Co., 1981., p. 922

Ecological Information

Probable Routes of Human Exposure

... NOT EMPLOYED IN INDUSTRY, BUT IT MAY BE DISCHARGED INTO AIR IN SMELTING OPERATIONS AS THE RESULT OF INTERACTION OF CALCIUM FLUORIDE WITH SAND OR WITH THE SILICA PRESENT IN ORES.

Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 844

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Sulfur Dioxide - Sulfur dioxide is a highly toxic, colorless, nonflammable gas. It is used as a pharmaceutical aid and antioxidant. It is also an environmental air pollutant.

Sulfur dioxide is a colorless gas with a pungent odor. It is a liquid when under pressure, and it dissolves in water very easily. Sulfur dioxide in the air comes mainly from activities such as the burning of coal and oil at power plants or from copper smelting. In nature, sulfur dioxide can be released to the air from volcanic eruptions.

Sulfur dioxide is 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.

Safety and Hazards
1. Hazards Identification
1. GHS Classification
Signal: Danger

GHS Hazard Statements
Aggregated GHS information from 24 notifications provided by 1818 companies to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

H280 (22.99%): Contains gas under pressure; may explode if heated [Warning Gases under pressure - Compressed gas, Liquefied gas, Dissolved gas]
H314 (99.94%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation - Category 1A, B, C]
H318 (25.85%): Causes serious eye damage [Danger Serious eye damage/eye irritation - Category 1]
H331 (93.45%): Toxic if inhaled [Danger Acute toxicity, inhalation - Category 3]

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage values above 10% are shown.

Precautionary Statement Codes
P260, P261, P264, P271, P280, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P310, P311, P321, P363, P403+P233, P405, P410+P403, and P501
(The corresponding statement to each P-code can be found here.)
View GHS Classification from all (5) sources.
Health Hazard

It may cause death or permanent injury after very short exposure to small quantities. 1,000 ppm causes death in from 10 minutes to several hours by respiratory depression. It is an eye and respiratory tract irritant. Persons with asthma, subnormal pulmonary functions or cardiovascular disease are at a greater risk. (EPA, 1998)

Fire Hazard

Not combustible. Heating will cause rise in pressure with risk of bursting.

Containers may explode in heat of fire or they may rupture and release irritating toxic sulfur dioxide. Sulfur dioxide has explosive properties when it comes in contact with sodium hydride; potassium chlorate at elevated temperatures; ethanol; ether; zinc ethylsulfurinate at very cool temperatures (-15C); fluorine; chlorine trifluoride and chlorates. It will react with water or steam to produce toxic and corrosive fumes. When the liquid is heated it may release irritating, toxic sulfur dioxide gas. Avoid ammonia, monocesium or monopotassium acetylide; dicesium monoxide; iron (II) oxide; tin oxide; lead (IV) oxide; chromium; manganese; molten sodium, powder aluminum and rubidium. Sulfur dioxide has explosive properties when it comes in contact with sodium hydride; potassium chlorate at elevated temperatures; ethanol; ether; zinc ethylsulfurinate at very cool temperatures (-15C); fluorine; chlorine trifluoride and chlorates. It will react with water or steam to produce toxic and corrosive fumes. Hazardous polymerization may not occur. (EPA, 1998)

Hazards Summary

The major hazards encountered in the use and handling of sulfur dioxide stem from its toxicologic properties. Exposure to this strong-smelling, colorless gas or liquid (compressed gas) may occur from its use as a fumigant, as an intermediate in the manufacture of sulfuric acid and other sulfur compounds, in oil, mineral, food and paper processing, and in water treatment. Effectsfrom exposure may include contact burns to the eyes, skin, and mucous membranes, frostbite, bronchoconstriction, and pulmonary edema. OSHA has established a time weighted average (TWA) limit of 2 ppm and a short term exposure limit (STEL) of 5 ppm, to become effective December 31, 1992. Engineering controls, including local exhaust ventilation, should be used to maintain sulfur dioxide at or below the permissible limit. In activities and situations where over-exposure may occur, wear chemical protective clothing and a self-contained breathing apparatus. If contact should occur, immediately remove contaminated clothing (to be left at worksite for cleaning), irrigate exposed eyes with copiousamounts of tepid water for at least 15 minutes, flush exposed skin with water, and treat for possible frostbite. Emergency eyewash facilities should be available in sulfur dioxide work areas. While sulfur dioxide does not ignite easily, it may burn, and cylinders of the compressed material can explode in the heat of a fire. For fires involving sulfur dioxide, extinguish with dry chemical, CO2, Halon, water spray, fog, or standard foam. If water is used, apply from as far a distance as possible because material will react with water to form toxic and corrosive fumes. Sulfur dioxide may be shipped domestically via air (cargo only), rail (cargo only), road, and water, in containers bearing the label, "Nonflammable gas." Sulfur dioxide should be stored in tightly closed containers, in cool, well-ventilated areas, and away from sources of physical damage. For spills of liquid sulfur dioxide, first evacuate area for 50 feet in all directions, use water spray to reduce vapor, and neutralize spilled material with limestone, soda ash, or lime. Keep material from entering water sources and sewers. Before implementing land disposal of sulfur dioxide waste, consult with environmental regulatory agencies for guidance.

Fire Potential

Not combustible.

Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 49-139

... Not flammable with air.

Seiler, H.G., H. Sigel and A. Sigel (eds.). Handbook on the Toxicity of Inorganic Compounds. New York, NY: Marcel Dekker, Inc. 1988., p. 643

Skin, Eye, and Respiratory Irritations

Vapors cause severe irritation of eyes and throat ...

U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.

Irritating to ... resp system & skin.

Commission of the European Communities. Legislation on Dangerous Substances - Classification and Labelling in the European Communities. Vol. II. London and Trotman Ltd., 1989., p. 138

Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992., p. 969

Toxicity

Toxicological Information

Carcinogen

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).

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php , p. 54 178 (1992)

A4; Not classifiable as a human carcinogen.

American Conference of Governmental Industrial Hygienists. Threshold Limit Values of Chemical Substances and Biological Exposure Indices, ACGIH, Cincinnati, OH 2009, p. 53

TLV-A4, IARC-3

Exposure Routes

The substance can be absorbed into the body by inhalation.

inhalation, skin and/or eye contact

Symptoms

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

Inhalation Symptoms

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

Skin Symptoms

ON CONTACT WITH LIQUID: FROSTBITE.

Eye Symptoms

Redness. Pain.

Target Organs

Eyes, skin, respiratory system

Immunological (Immune System), Respiratory (From the Nose to the Lungs)

Human Toxicity Excerpts

/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.

Lawther PG et al; Environ Res 10: 335 (1975) as cited in OSHA; Public Hearing on Occupational Standard for Sulfur Dioxide: Statement of Edward Baier (NIOSH) (May 1977) PB 83-182485

/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.

Ferris GB et al; Amer Rev Respir Dis 113: 475-85 (1976) as cited in National Academy of Sciences; Sulfur Oxides p.157 (1978)

/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.

Bates DV, Hazucha M; Paris Vol IV: 1977 (1974) as cited in Nat'l Research Council Canada; Sulphur and its Inorganic Derivatives in the Canadian Environment p.294 (1974) NRCC No. 15015

/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.

/HUMAN EXPOSURE STUDIES/ A transient increase in the percentage of lysosome positive macrophages was seen in the bronchoalveolar lavage fluid of healthy volunteers 24 hours after a 20-minute exposure at 4 ppm (10.48 mg/cu m) sulfur dioxide and an increase in total macrophages and lymphocytes after exposure at 8 ppm (21 mg/cu m).

American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.

/HUMAN EXPOSURE STUDIES/ 40 healthy nonsmokers and 40 subjects with mild asthma /were exposed/ to air and to sulfur dioxide at 0.5 ppm for periods of 3 hr. Forced expiratory performance, closing volume, airway flow resistance, and lung volumes were measured. As a group, the healthy subjects showed no functional changes that could be judged adverse; indeed, vital capacity, maximal volume of gas that can be forcefully exhaled in 1 second after full inspiration, and maximal mid-expiratory flow rate tended to rise with time, whether clean air or sulfur dioxide was administered. The response of the group with asthma to sulfur dioxide was interpreted as showing slight functional impairment; ie, maximal mid-expiratory flow rate was said to increase less to sulfur dioxide than during the sham exposure. The other functional tests were unaffected. Among the healthy subjects, a 13 yr old boy experienced shortness of breath and had functional evidence of bronchoconstriction. On the evening after exposure to sulfur dioxide, two of the asthmatic subjects experienced shortness of breath, which required medication.

National Academy of Sciences; Sulfur Oxides p.158 (1978)

/HUMAN EXPOSURE STUDIES/ ... /Investigators/ conducted controlled studies in 15 nose-breathing volunteers who inhaled 1, 5, or 25 ppm sulfur dioxide for 6 hr. at rest. A significant reduction in nasal mucous flow rate occurred after exposure at 5 and 25 ppm. Significantly reduced FEV1was seen only at 25 ppm (nasal breathing at rest). Irritation and complaints of discomfort were proportional to the sulfur dioxide concentration but were slight at 5 ppm and absent at 1 ppm. ... /The authors/ expressed the opinion that the TLV for sulfur dioxide should be reduced to 1 ppm (2.62mg/ cu m) or less, given that exposure at 1 ppm from 1 to 6 hours caused increased nasal resistance in young, healthy (20-28 years of age) adult males. It is important to note that the ... protocol allowed the subjects to become acclimated slowly to the higher concentrations, whereas subjects who had to enter the chamber abruptly found a distinct sulfur dioxide smell at 1 ppm, strong discomfort and cough at 5 ppm, and 25 ppm was intolerable on first contact. These individuals, however, adapted rapidly, and coughing and rhinorrhea resolved within a few minutes.

American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.

/HUMAN EXPOSURE STUDIES/ ... /Investigators/ found that short-term exposure at 1 ppm (2.62 mg/cu m) sulfur dioxide by mouth breathing at rest produced increased flow resistance in 1 of 11 (9%) of human subjects. A concentration of 5 ppm (13.1 mg/cu m) produced an average flow resistance increase of 39% compared to the control; the value for 13 ppm (34 mg/cu m) was 72% above the control. The response was related to concentration, not to total dose; extending exposure time from 10 minutes to 30 minutes failed to increase the response. Repeated exposure following a 15 min interval of clean air produced a lesser response than did the initial exposure.

American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.

/HUMAN EXPOSURE STUDIES/ ... The hypothesis that pretreatment with the cysteinyl-leukotriene inhibitor montelukast sodium protects against the inflammatory and bronchoconstrictive effects of SO(2) /was tested/ in the airways of asthmatic subjects. Asthmatic volunteers (enrolled, 12 subjects; completed study, 11 subjects) were exposed to 0.75 ppm SO(2) for 10-min periods during exercise (mean ventilation, 35 L/min) and were exposed similarly to filtered air (control condition) after double-blinded pretreatments with montelukast (10 mg/d for 3 days) and placebo. After montelukast pretreatment, specific airways resistance, FEV(1), symptoms, and eosinophil counts in induced sputum showed statistically and clinically significant improvements in preexposure measurements and/or decreased responses to SO(2) exposure or exercise. The mean FEV(1) immediately after exposure was 95% of baseline FEV(1) with montelukast pretreatment vs 82% with placebo. /It was concluded that/ montelukast significantly protects against airways eosinophilic inflammation and bronchoconstriction from SO(2) exposure during exercise. This implies a role for leukotrienes in SO(2)-induced lung effects.

Gong H et al; Chest 1119 (2): 402-8 (2001). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11171715

/SIGNS AND SYMPTOMS/ Severe injuries of human eyes by sulfur dioxide have been produced only by liquified form ... Immediately after the eye has been sprayed ... the corneal epithelium becomes gray and irregular, but remains adherent to stroma ... Several hr later lids become swollen. Conjunctival epithelium appears white and rather opaque. Vessels ... may be ... thrombosed.

Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 863

/SIGNS AND SYMPTOMS/ Inhalation produces all grades of respiratory tract irritation, sometimes with pulmonary edema. Vapor concn probably determines mode of death: eg, suffocation from reflex resp arrest (very high concn), pulmonary edema (moderate concn), or systemic acidosis (low concn). There is some indication of significant variation in individual susceptibility.

Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-96

/SIGNS AND SYMPTOMS/ With acute exposure, 5 ppm causes dryness of nose and throat and a measureable incr in resistance to bronchial air flow; 6 to 8 ppm causes a decr in tidal resp volume. Sneezing, cough, and eye irritation occur at 10 ppm; 20 ppm caused bronchospasm; 50 ppm causes extreme discomfort but no injury in less than a 30-min exposure ... 1000 ppm causes death in from 10 min to several hr by resp depression.

Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972., p. 198

/SIGNS AND SYMPTOMS/ Exposure to high concn cause reflex closure of glottis for several minutes ... Persons subject to asthmatic attacks will experience asthmatic paroxysm which may persist for several days following exposure.

Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972., p. 198

/SIGNS AND SYMPTOMS/ Depending on the degree of exposure, periodic medical examination is suggested. The symptoms of asthma often do not become manifest until a few hours have passed and they are aggravated by physical effort. Rest and medical observation are therefore essential. Anyone who has shown symptoms of asthma due to this substance should avoid all further contact.

International Program on Chemical Safety/Commission of the European Communities; International Chemical Safety Card on Sulphur dioxide (October 2006). Available from, as of November 17, 2009: http://www.inchem.org/pages/icsc.html

/SIGNS AND SYMPTOMS/ Persons who have a long history of exposure to high concn of sulfur dioxide may suffer from chronic bronchitis accompanied by emphysema ... Nervous system disorders are of a functional nature-neurotic and vegeto-asthenic-probably due to the general toxicity of sulfur dioxide on the body. Stomatological exam may reveal dental caries and peridontal and gingival disorders. Patients may complain of rapid and painless dental destruction, loss of fillings, and incr tooth sensitivity to temp changes.

International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 2122

/SIGNS AND SYMPTOMS/ Exposures of less than an hour to sulfur dioxide 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.

OSHA; Public Hearing on Occupational Standard for Sulfur Dioxide: Statement of Edward Baier (NIOSH) (May 1977) PB 83-182485

/SIGNS AND SYMPTOMS/ 6-12 ppm: May cause nasal and throat irritation. 10 ppm: Upper resp irritation, some nosebleeds. 20 ppm: Definitely irritating to eyes. Chronic resp symptoms develop at this level.

Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 874

/SIGNS AND SYMPTOMS/ Acute effects: Direct resp tract irritation, cough, burning, lacrimation, conjunctival injection, difficulty in swallowing, and oropharyngeal erythema occur after substantial exposures. Vomiting, diarrhea, abdominal pain, fever, headache, vertigo, agitation, tremor, convulsions, and peripheral neuritis also have been noted. Acute high-dose exposures may produce immediate bronchospasm and pulmonary edema with subsequent resp failure. Clinical severity usually is readily apparent. Acute high-dose sulfur dioxide exposures have resulted in severe obstructive and restrictive defects 3 mo postexposure, which failed to respond to bronchodilators. Rarely, such exposures have been associated with long-term, moderately severe, obstructive defects and persistent, productive cough.

Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 875

/SIGNS AND SYMPTOMS/ High concentrations of sulfur dioxide may cause respiratory paralysis and pulmonary edema. In addition, about 10 to 20% of the adult population is estimated to be hypersensitive to the adverse respiratory effects of sulfur dioxide; however, workers regularly exposed to compound show an adaptation effect. Even though olfactory fatigue is a reported effect of exposure, the compound is so irritating that it is considered to have good warning properties.

Environment Canada; Tech Info for Problem Spills: Sulfur Dioxide (Draft) p.74 (1985)

/SIGNS AND SYMPTOMS/ Symptomology: Inhalation: Irritation of the eyes, nose, throat, and skin; cough; sneezing and lacrimation; rhinorrhea; anosmia; reflex bronchoconstriction; increased pulmonary resistance to air flow; bronchial asthma; high pitched rales; thoracic pain and struction; nasopharyingitis; tracheitis, laryngeal edema; chemical bronchopneumonia; pulmonary edema; cyanosis; systemic acidosis; asphyxia; death. Ingestion: Irritation, lacrimation, iritis, burns, corneal damage, blindness. Skin contact: Irritation, Urticaria, lesions, burns.

Environment Canada; Tech Info for Problem Spills: Sulfur Dioxide (Draft) p.82-82 (1985)

/SIGNS AND SYMPTOMS/ A basic physiological response to inhalation of sulfur dioxide is a mild degree of bronchial constriction that is dependent on intact parasympathetic innervation. When exposed to 5 ppm of sulfur dioxide for 10 min, most human subjects show increased resistance to the flow of air. Asthmatics have an increased sensitivity to sulfur dioxide; bronchoconstriction may occur at concentrations as low as 0.25 ppm.

Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1674-5

/CASE REPORTS/ Exposures of two miners to sulfur dioxide concentrations of at least 40 ppm resulted in severe airway obstruction, hypoxemia, markedly reduced exercise tolerance, ventilation perfusion mismatch, and evidence of active inflammation as documented by a positive gallium lung scan. Serial ventilation-perfusion scans over the first 12 months showed progressive improvement without returning to normal. This status has remained for 2 years.

Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1520

/EPIDEMIOLOGY STUDIES/ Approx 10,000 workers in the British steel industry were studied for chronic effects. At mean exposures to sulfur dioxide of about 0.35 ppm (0.9 mg/cu m), no effects were found.

Lowe CR et al; Brit J Industr Med 27: 121 (1970) as cited in OSHA; Public Hearing on Occupational Standard for Sulfur Dioxide: Statement of Edward Baier (NIOSH) (May 1977) PB 83-182485

/EPIDEMIOLOGY STUDIES/ ... Laboratory studies have shown exposures to SO2 at levels as low as 0.1 ppm and lasting as little as 10 min to lead to changes in respiratory functions as well as symptoms in asthmatic individuals exposed during exercise. The present study was conducted to determine whether similar responses to short-term SO2 peaks in the ambient air can be detected in a free-living population. Tests were made for an association between days with SO2 peaks above various levels, as identified from hourly measurements obtained by the New York City Aerometric Network, and days with high numbers of emergency room visits for asthma at three inner-city municipal hospitals in New York City. No association was found. Abstract: PubMed

Goldstein IF, Weinstein AL; Environ Res 40 (2): 332-45 (1986). Available from, as of November 16, 2009:

/EPIDEMIOLOGY STUDIES/ /Investigators found no greater incidence of chronic bronchitis or other respiratory disease in 147 pulp mill workers exposed at 2 to 13 ppm (5.24 to 34 mg/cu m) sulfur dioxide when compared to 124 workers from a nearby paper mill. The high prevalence (about 30%) in both groups suggests that chronic bronchitis was a problem in both groups.

American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.

/EPIDEMIOLOGY STUDIES/ One-hundred men working in a refrigerator company in the USA where sulfur dioxide was the refrigerant /were studied/. Exposures averaged 60-90 mg/cu m (20-32 ppm) with peaks as high as 200 mg/cu m (70 ppm). These peaks had probably been higher in the past ranging up to 290 mg/cu m (100 ppm) or more. The exposed group had significantly more respiratory symptoms and colds. They also complained more of fatigue and shortness of breath on exertion. Chest X-rays of the exposed and unexposed groups showed the same distribution of abnormalities. /It was concluded that/ there was no injury to the tracheobronchial tree or alveoli.

Kehoe R et a; J Ind Hyg 14: 159-73 (1932) as cited in WHO; Environ Health Criteria: Sulfur Oxides and Suspended Particulate Matter p.64 (1979)

/EPIDEMIOLOGY STUDIES/ In a study in Norway, pulp mill workers were compared with paper mill workers using a standard questionnaire on respiration and simple tests of pulmonary function. The smoking histories of the subjects were also studied. Levels of sulfur dioxide ranged from 6-100 mg/cu m (2-36 ppm) with peaks of 290 mg/cu m (100 ppm) when the digester was blowing. The exposed group had more cough, sputum, and dyspnea than the unexposed group but the vital capacities were simliar in both groups. The expiratory peak flows, however, of the exposed men under 50 years of age were lower than those in comparable unexposed group.

Skalpe IO; Br J Ind med 21: 69-73 (1964) as cited in WHO; Environ Health Criteria: Sulfur Oxides and Suspended Particulate Matter p.65 (1979)

/EPIDEMIOLOGY STUDIES/ Two recent studies have involved persons with underlying lung disease, as well as healthy persons. Nonsmoking health subjects and smokers who demonstrated functional defects associated with early obstructive pulmonary disease /were exposed/ to sulfur dioxide at 0, 0.3, 1.0, and 3.0 ppm. The subjects resided in an environmental chamber maintained at 22 + or - 1 deg C and 50 + or - 5% relative humidity. The exposures were administered in random sequence for 120 hr continuously to the healthy subjects, and for 96 hr to the smokers. Testing was done at 24 hr intervals. Sulfur dioxide at 0.3 ppm elicited no functional changes. Sulfur dioxide at 1.0 ppm caused a significant reduction in dynamic compliance measured at 120 breaths/min after 24 and 48 hr of exposure; results of other tests of ventilation and respiratory mechanics were unaffected. The reduction in dynamic compliance was greater and more prolonged with sulfur dioxide at 3.0 ppm. A notable finding was the absence of clear cut evidence of functional changes among the subjects with underlying lung disease. Their intersubject and intrasubject variability far exceeded the variation associated with exposure to all concentrations of sulfur dioxide. A variety of symptoms were noted in both groups: headache, nasal congestion, throat soreness, cough, nosebleed, gastrointestinal discomfort, and rash.

Weir FW, Bromberg PA; Recent Advances in the Assessment of the Health Effects of Environmental Pollutants 4: 1989-2004 (1974) as cited in National Academy of Sciences; Sulfur Oxides p.157-58 (1978)

/EPIDEMIOLOGY STUDIES/ The prevalence of chronic bronchitis was significantly increased over that in controls in workers exposed to sulfur dioxide while working in a sulfite pulp factory in Sweden. During the three years before the study was performed, more than 50% of the daily mean values for sulfur dioxide in the sulfite pulp mill were above 14 mg/cu m (5 ppm), with occasional peak exposures up to 140 mg/cu m. The mean annual concentration of sulfur dioxide in the surrounding community was 6.5-40 ug/cu m.

/EPIDEMIOLOGY STUDIES/ The 0.75 second forced expiratory vol of school children in Cincinnati, Chattanooga, and New York City, was studied, and examined differences by race, sex, socioeconomic levels, and exposure to total particulates, suspended sulfates, and sulfur dioxide. These authors were able to demonstrate differences in forced expiratory volume to support a relationship between suspended sulfates, other particulates and impaired function; the difference was apparent only after matching for age, sex, race, and socioeconomic status and when no overt clinical manifestations were present. The most dramatic difference occurred in Cincinnati, where children in "clean" neighborhoods had similar levels of sulfur dioxide but different levels of total particulates (61-85 ug/cu m in the clean area vs 96-133 ug/cu m polluted areas) and in suspended sulfates (7.7-9.1 ug/cu m vs. 8.9-10.1 ug/cu m).

Shy CM et al; Arch Environ Health 27: 124 (1973) as cited in Nat'l Research Council Canada; Sulphur and its Inorganic Derivatives in the Canadian Environment p.297 (1977) NRCC No. 15015

/EPIDEMIOLOGY STUDIES/ The effects of sulfur dioxide on 190 workers employed in a broom manufacturing factory where sulfur dioxide was used for bleaching broom corn were studied. Concentrations of sulfur dioxide in the air, sulfates in the urine, methemoglobin and sulfhemoglobin in the blood, and irritant effects on the workers were analyzed. Measurements were made in summer when open windows provided natural ventilation and in winter when the building was closed. Sulfur dioxide in air averaged 45.7 mg/cu m in winter and 0.2 mg/cu m in summer. When compared to control groups not exposed to sulfur dioxide in the workplace (43 workers checked for methemoglobin and 39 for sulfates), differences in all parameters were statistically significant. In winter the mean values were: total urinary sulfates 21.2 umol/L (p < 0.01), organic urinary sulfates 4.1 umol/L (p < 0.01), methemoglobin 1.6% (p < 0.01), and sulfhemoglobin 0.7% (p < 0.05). In summer the mean values were: total urinary sulfates 19.3 umol/L (p< 0.05), organic urinary sulfates 3.7 umol/L (p < 0.01), methemoglobin 0.7% (p < 0.05), and sulfhemoglobin 0.5% (p< 0.05). Corresponding values for controls were 16.7 umol/L, 1.8 umol/L, 0.5%, and <0.5%, respectively. Interviews with 190 workers revealed the following discomforts: coughing (94.2%), difficulty in breathing (91.0%), burning sensation in throat (83.7%), burning sensation in eyes (80.0%), sub-sternal pain (75.3%), burning sensation in throat (74.7%), sore throat (65.8%), tearing (64.7%), hoarseness (56.3%), pain in nose (49.5%), pain in eyes (39.5%), red eyelids (35.5%), red eyes (16.3%), nose bleeding (3.7%), and sneezing (3.2%). Abstract: PubMed

Savic M et al; Int Arch Occup Environ Health 59 (5): 513-8 (1987)

/EPIDEMIOLOGY STUDIES/ ... This study is an extension of an ecologic study that found an increased rate of hospitalizations for respiratory conditions among children living near petroleum refineries in Montreal (Canada). ... A time-stratified case-crossover design /was used/ to assess the risk of asthma episodes in relation to short-term variations in sulfur dioxide levels among children 2-4 years of age living within 0.5-7.5 km of the refinery stacks. Health data used to measure asthma episodes included emergency department (ED) visits and hospital admissions from 1996 to 2004. ... Daily levels of SO2 at the residence of children /were estimated/ using a) two fixed-site SO2 monitors located near the refineries and b) the AERMOD (American Meteorological Society/Environmental Protection Agency Regulatory Model) atmospheric dispersion model. ... Conditional logistic regression /was used/ to estimate odds ratios associated with an increase in the interquartile range of daily SO2 mean and peak exposures (31.2 ppb for AERMOD peaks). ... /Results were adjusted for/ temperature, relative humidity, and regional/urban background air pollutant levels. ... The risks of asthma ED visits and hospitalizations were more pronounced for same-day (lag 0) SO2 peak levels than for mean levels on the same day, or for other lags: the adjusted odds ratios estimated for same-day SO2 peak levels from AERMOD were 1.10 [95% confidence interval (CI), 1.00-1.22] and 1.42 (95% CI, 1.10-1.82), over the interquartile range, for ED visits and hospital admissions, respectively. /It was concluded that/ short-term episodes of increased SO2 exposures from refinery stack emissions were associated with a higher number of asthma episodes in nearby children.

Smargiassi A et al; Env Health Perspect 117 (4): 653-9 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19440507

/EPIDEMIOLOGY STUDIES/ This retrospective cohort study investigated whether the risk of delivering full term (37-44 completed weeks of gestation) low birth weight (LBW) infants is associated with differences in exposure to air pollutants in different trimesters. Full-term infants (37 completed weeks of gestation) with a birth weight below 2500 g were classified as term LBW infants. The study infants comprised 92,288 full-term live singletons identified from the Taiwan birth registry and born in the city of Taipei or Kaoshiung in Taiwan between 1995 and 1997. Maternal exposures to various air pollutants including CO, SO2, O3, NO2, and PM10 in each trimester of pregnancy was estimated as the arithmetic means of all daily measurements taken by the air quality monitoring station nearest to the district of residence of the mother at birth. The multivariable logistic regression model with adjustment for potential confounders was used to assess the independent effect of specific air pollutants on the risk of term LBW. This study suggested a 26% increase in term LBW risk given maternal ambient exposure to SO2 concentration exceeding 11.4 ppb during pregnancy compared to low exposure (<7.1 ppb) (OR=1.26, 95% CI=1.04-1.53). Since the relative risk of term LBW was reassessed according to exposure level in each trimester, mothers exposed to >12.4 ppb of SO2 in the last trimester showed 20% higher risk (OR=1.20, 95% CI=1.01-1.41) of term LBW delivery than mothers with lower exposure (<6.8 ppb). No significant elevation ORs was observed for other air pollutants.

Lin C-M et al; Environ Res 96 (1): 44-50 (2004). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15261783

/EPIDEMIOLOGY STUDIES/ The prevalence of recent (previous 12 months) symptoms of allergic diseases was obtained by means of the questionnaire of the International Study of Asthma and Allergies in Childhood (ISAAC), Spain, with the participation of 7 centers (Asturias, Barcelona, Bilbao, Cartagena, La Coruna, Madrid, and Valencia) and 20,455 schoolchildren aged between 6 and 7 years, from 2002 to 2003. The pollutant detection systems of the aforementioned centers provided the mean annual concentrations of sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and total suspended particulate matter. The annual average concentration of SO2 showed a significant association with a higher prevalence of recent severe asthma (adjusted odds ratio [aOR] between level-1 and level-3 pollution, 1.32; 95% confidence interval [CI], 1.01-1.73), rhinitis (aOR, 1.56; 95% CI, 1.39-1.75), and rhinoconjunctivitis (aOR, 1.70; 95% CI, 1.45-2.00). The annual average concentration of CO was associated with a higher prevalence of rhinitis (aOR, 1.65; 95% CI, 1.34-2.04), rhinoconjunctivitis (aOR, 1.76; 95% CI, 1.31-2.37), and eczema (aOR, 1.55; 95% CI, 1.17-2.04). The annual average concentration for NO2 and total suspended particulate matter showed inverse associations with the prevalence of nocturnal dry cough. /The authors concluded that these/ findings suggest that air pollutants such as SO2 and CO increase the risk of recent symptoms of asthma and allergic rhinitis in schoolchildren aged between 6 and 7 years in Spain.

Arnedo-Pena A et al; Archivos de bronconeumologia 45 (5): 224-9 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19371994

/EPIDEMIOLOGY STUDIES/ ... The Kilauea Volcano is the largest point source for sulfur dioxide in the United States, releasing air pollution on nearby communities since 1983. The objectives of this study were to provide the first population-based epidemiological estimates and qualitative descriptions of cardiorespiratory health effects associated with volcanic air pollution. An environmental-epidemiological design was used. Exposure levels of Kilauea's air pollutants were determined by environmental sampling. Prevalence estimates of cardiorespiratory health effects in adults were measured (N = 335) and compared between an exposed and nonexposed reference community. Descriptions of the human-environment interaction with the long-standing eruption were recorded from informants in the natural setting. Ambient and indoor concentrations of volcanic air pollution were above the World Health Organization's recommended exposure levels. There were statistically significant increased odds associated with exposure for self-reported cough, phlegm, rhinorrhea, sore and dry throat, sinus congestion, wheezing, eye irritation, and diagnosed bronchitis. Thirty-five percent of the informants perceived that their health was affected by the eruption, mainly current and former smokers and those with chronic respiratory disease...

Longo BM Nursing Res 58 (1): 23-31 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19092552

/EPIDEMIOLOGY STUDIES/ Infants are known to be susceptible to the adverse health effects of ambient air pollution. The authors examined the relationship between air pollution and postneonatal mortality from all causes among firstborn infants in Seoul, Korea, during 1999-2003, using both case-crossover and time-series analyses. Using a bidirectional control-sampling approach, the authors compared the effects of various types of air pollution on postneonatal mortality. The relative risk of postneonatal mortality from all causes was 1.000 (95% confidence interval [CI] = 0.998-1.002) for particulate matter with a diameter <10 um, 1.002 (95% CI = 0.994-1.009) for nitrogen dioxide, 1.015 (95% CI = 0.973-1.058) for sulfur dioxide, 1.029 (95% CI = 0.833-1.271) for carbon monoxide, and 0.984 (95% CI = 0.977-0.992) for ozone for each 1-unit increase of air pollution level in the 1:6 control selection scheme. The authors observed a positive association between air pollution and infant daily mortality except for the studied particulate matter and ozone, although it was not statistically significant. They obtained similar results in the time-series analysis. The risk of postneonatal infant death from all causes was positively associated with all studied air pollutants except ozone...

Son J-Y et al; Arch Environ Occup Health 63 (3): 108-13 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18980873

/EPIDEMIOLOGY STUDIES/ The objective of this study is to assess the short-term effect of sulfur dioxide (SO(2)) air pollution levels on hospital admissions for cardiovascular diseases. Daily mean hospital admissions for cardiovascular diseases, ischemic heart diseases (IHDs), and stroke in seven European areas (the cities of Birmingham, London, Milan, Paris, Rome, and Stockholm, and in The Netherlands) participating in the multicenter European study of air pollution (Aphea-II), were measured. Time series analysis of daily hospital admission counts was performed using poison autoregressive models. A summary regression coefficient for all cities was provided. Daily numbers of all cardiovascular admissions except stroke, and particularly IHDs, rose significantly with an increase of daily SO(2)levels of the same day and day before. After adjusting for PM(10)(i.e. particles with size <10 um), the association of SO(2) with IHD admissions remained significant (i.e. an increase of 0.7%; 95% confidence interval=0.1-1.3, per each 10 ug/cu m increase of SO(2)) among subjects younger than 65 years, but not among subjects older than 65. In the older group the increase was only significant for particles (1.3%; CI 0.7-1.8, per each increase in 10 ug/cu m of PM(10)). This study provides new evidence for the effects of urban air pollution on cardiac diseases in Europe, and suggests that SO(2) pollution may play an independent role in triggering ischemic cardiac events...

Sunver J et al; Europ Heart J 24 (8): 752-60 (2003). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12713769

/EPIDEMIOLOGY STUDIES/ To investigate the relationship between air pollution and risk of death from bladder cancer, the authors conducted a matched case-control study using deaths that occurred in Taiwan from 1995 through 2005. Data on all eligible bladder cancer deaths were obtained from the Bureau of Vital Statistics of the Taiwan Provincial Department of Health. The control group consisted of people who died from causes other than cancer or diseases associated with genitourinary problems. The controls were pair matched to the cases by sex, year of birth, and year of death. Each matched control was selected randomly from the set of possible controls for each case. Classification of exposure to municipality air pollution was based on the measured levels of nitrogen dioxide and sulfur dioxide. The results ... show that there is a significant positive association between the levels of air pollution and bladder cancer mortality. The adjusted odds ratios (95% confidence interval) were 1.37 (1.03-1.82) for the group with medium air pollution level and 1.98 (1.36-2.88) for the group with high air pollution level when compared to the group with the low air pollution level. Trend analyses showed statistically significant trend in risk of death from bladder cancer with increasing air pollution level...

Liu C-C et al; Inhal Toxicol 21 (1): 48-54 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18923949

/EPIDEMIOLOGY STUDIES/ The EMECAM study is a collaborative effort to evaluate the impact of air pollution on mortality in Spain. In this paper the combined results are presented for the short term effects of particulates and sulfur dioxide on both daily mortality for all and for specific causes. The relation between daily mortality for all causes, cardiovascular diseases, and respiratory diseases, and air pollution for particulates (daily concentrations) and SO(2) (24 and 1 hour concentrations) was assessed in 13 Spanish cities for the period 1990-6. With a standardised method, magnitude of association in each city was estimated by Poisson regression in a generalised additive model. Local estimates were obtained from both single and two pollutant analyses. Lastly, combined estimates for each cause and pollutant were obtained. For combined results, in single pollutant models a 10 ug/cu m increase in the concentration of the mean of the concurrent and one day lag for black smoke was associated with a 0.8% (95% confidence interval (95% CI) 0.4 to 1.1%) increase in total mortality. The estimates for total suspended particles (TSPs) and particulate matter of aerodynamic diameter <10 um (PM(10)) and total mortality were slightly lower. The same increase in concentrations of SO(2) was associated with a 0.5% increase in daily deaths. For groups of specific causes, higher estimations were found, especially for respiratory conditions. Peak concentrations of SO(2) showed significant associations with the three groups of mortality. When two pollutant analyses were performed, estimates for particulates, especially for black smoke, did not substantially change. The estimates for daily concentrations of SO(2) were greatly reduced, but, on the contrary, the association with peak concentrations of SO(2) did not show any change...

Ballester F et al; Occup Environ Med 59 (5): 300-8 (2002). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11983845

/EPIDEMIOLOGY STUDIES/ /The/ objective in this study was to evaluate the mortality of workers exposed to sulfur dioxide in the pulp and paper industry. The cohort included 57,613 workers employed for at least 1 year in the pulp and paper industry in 12 countries. ... Exposure to SO(2) /was assessed/ at the level of mill and department, using industrial hygiene measurement data and information from company questionnaires; 40,704 workers were classified as exposed to SO(2). ... The standardized mortality ratio (SMR) analysis analysis showed a moderate deficit of all causes of death [SMR = 0.89; 95% confidence interval (CI), 0.87-0.96] among exposed workers. Lung cancer mortality was marginally increased among exposed workers (SMR = 1.08; 95% CI, 0.98-1.18). After adjustment for occupational coexposures, the lung cancer risk was increased compared with unexposed workers (rate ratio = 1.49; 95% CI, 1.14-1.96). There was a suggestion of a positive relationship between weighted cumulative SO(2) exposure and lung cancer mortality (p-value of test for linear trend = 0.009 among all exposed workers; p = 0.3 among workers with high exposure). Neither duration of exposure nor time since first exposure was associated with lung cancer mortality. Mortality from non-Hodgkin lymphoma and from leukemia was increased among workers with high SO(2) exposure; a dose-response relationship with cumulative SO(2) exposure was suggested for non-Hodgkin lymphoma. For the other causes of death, there was no evidence of increased mortality associated with exposure to SO(2). Although residual confounding may have occurred,/the/ results suggest that occupational exposure to SO(2) in the pulp and paper industry may be associated with an increased risk of lung cancer.

Lee WJ et al; Environ Health Perspect 110 (10): 991-5 (2002). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12361923

/EPIDEMIOLOGY STUDIES/ ... A time-series analysis /was conducted/ to examine the specific effects of major air pollutants [particulate matter less than 10 microns in diameter (PM(10)), sulfur dioxide (SO(2)), and nitrogen dioxides (NO(2))] on daily mortality in Shanghai, China, using both single-pollutant and multiple-pollutant models. In the single-pollutant models, PM(10), SO(2), and NO(2) were found to be associated with mortality from both all non-accidental causes and from cardiopulmonary diseases. Unlike some prior studies in North America, we found a significant effect of gaseous pollutants (SO(2) and NO(2)) on daily mortality even after adjustment for PM(10) in the multiple-pollutant models...

Chen G et al; J Occup Health 50 (1): 41-7 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18285643

/EPIDEMIOLOGY STUDIES/ ... Using time-stratified case-crossover study design, an association was examined between stroke mortality and particulate matter with aerodynamic diameter of < 10 um (PM10) of 2002 - 2004 in Hangzhou city. Meanwhile, the acute health effect of other gaseous pollutants (sulfur dioxide, SO2 and nitrogen dioxide, NO2) was also analyzed. A total of 9906 deaths from stroke were included. The crude stroke mortality was 83.54 per 100 000. After being adjusted for meteorological factors, when an increase of 10 ug/cu m in PM10, SO2 and NO2 in three days was noticed, it appeared that the increases of mortality of stroke were 0.56% (95% CI: 0.14%-0.99%), 1.62% (95% CI: 0.26% - 3.01%) and 2.07% (95% CI: 0.54% - 3.62%) respectively. There was no distinct association in multi-pollutant models. In sensitivity analysis, the associations were found in all single-pollutant models but not statistically significant in multi-pollutant models after replacing the missing values. ... It is suggested that the short-term elevation in PM10 as well as SO2 and NO2 daily concentrations were related to the increase of stroke mortality in Hangzhou city. .

Ren Y-J et al; Zhonghua liu xing bing xue za zhi 29 (9): 878-81 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19173848

/EPIDEMIOLOGY STUDIES/ /The relationship between/ maternal exposure to particulate matter with aerodynamic diameter < 10, < 2.5 um (PM(10), PM(2.5)), sulfur dioxide, nitrogen dioxide, and carbon monoxide and birth weight /were analyzed/ for 358,504 births in Massachusetts and Connecticut from 1999 to 2002. Analysis included logistic models for low birth weight (< 2,500 g) and linear models with birth weight as a continuous variable. ... An interquartile increase in gestational exposure to NO(2), CO, PM(10), and PM(2.5) lowered birth weight by 8.9 g [95% confidence interval (CI), 7.0-10.8], 16.2 g (95% CI, 12.6-19.7), 8.2 g (95% CI, 5.3-11.1), and 14.7 g (95% CI, 12.3-17.1), respectively. Lower birth weight was associated with exposure in the third trimester for PM(10), the first and third trimesters for CO, the first trimester for NO(2) and SO(2), and the second and third trimesters for PM(2.5). Effect estimates for PM(2.5) were higher for infants of black mothers than those of white mothers...

Bell ML et al; Environ Health Perspect 115 (7): 1118-24 (2007). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17637932

/EPIDEMIOLOGY STUDIES/ ...A time-series analysis /was conducted/ to examine the modifying effect of season, sex, age, and education on the association between outdoor air pollutants [particulate matter < 10 microm in aerodynamic diameter (PM(10)), sulfur dioxide, nitrogen dioxide, and ozone] and daily mortality in Shanghai, China, using 4 years of daily data (2001-2004). ... Outdoor air pollution was associated with mortality from all causes and from cardiorespiratory diseases in Shanghai. An increase of 10 ug/cu m in a 2-day average concentration of PM(10), SO(2), NO(2), and O(3) corresponds to increases in all-cause mortality of 0.25% [95% confidence interval (CI), 0.14-0.37), 0.95% (95% CI, 0.62-1.28), 0.97% (95% CI, 0.66-1.27), and 0.31% (95% CI, 0.04-0.58), respectively]. The effects of air pollutants were more evident in the cool season than in the warm season, and females and the elderly were more vulnerable to outdoor air pollution. Effects of air pollution were generally greater in residents with low educational attainment (illiterate or primary school) compared with those with high educational attainment (middle school or above)...

Kan H et al; Environ Health Perspect 116 (9): 1183-88 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18795161

/EPIDEMIOLOGY STUDIES/ This study was /undertaken/ to determine the acute mortality effects of the gaseous pollutants in Wuhan, a city with 7.5 million permanent residents during the period from 2000 to 2004. There are approximately 4.5 million residents in Wuhan who live in the city's core area of 201 km2, where air pollution levels are highest, and pollution ranges are wider than the majority of the cities in the published literature. ... Consistent NO2 effects on mortality /were found/ with the strongest effects on the same day. Every 10-ug/cu m increase in NO2 daily concentration on the same day was associated with an increase in nonaccidental (1.43%; 95% confidence interval [CI]: 0.87-1.99%), cardiovascular (1.65%; 95% CI: 0.87-2.45%), stroke (1.49%; 95% CI: 0.56-2.43%), cardiac (1.77%; 95% CI: 0.44-3.12%), respiratory (2.23%; 95% CI: 0.52-3.96%), and cardiopulmonary mortality (1.60%; 95% CI: 0.85-2.35%). These effects were stronger among the elderly than among the young. Formal examination of exposure-response curves suggests no-threshold linear relationships between daily mortality and NO2, where the NO2 concentrations ranged from 19.2 to 127.4 ug/cu m. SO2 and O3 were not associated with daily mortality...

Qian Z et al; J Air Waste Management Assoc 57 (7): 785-93 (2007). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17687993

/EPIDEMIOLOGY STUDIES/ ... For the approximately 70,000 children from the 1999-2005 National Health Interview Survey eligible for this study, ... between 40,000 and 60,000 ambient pollution monitoring data from the U.S. Environmental Protection Agency /were assigned/, depending on the pollutant. ... Monitors within 20 miles of the child's residential block group /were used/ . ... Logistic regression models, fit with methods for complex surveys, /were used/ to examine the associations between the reporting of respiratory allergy or hay fever and annual average exposure to particulate matter < or = 2.5 um in diameter (PM2.5), PM < or = 10 um in diameter, sulfur dioxide, and nitrogen dioxide and summer exposure to ozone, controlling for demographic and geographic factors. Increased respiratory allergy/hay fever was associated with increased summer O3 levels [adjusted odds ratio (AOR) per 10 ppb = 1.20; 95% confidence interval (CI), 1.15-1.26] and increased PM2.5 (AOR per 10 ug/cu m = 1.23; 95% CI, 1.10-1.38). These associations persisted after stratification by urban-rural status, inclusion of multiple pollutants, and definition of exposures by differing exposure radii. No associations between the other pollutants and the reporting respiratory allergy/hay fever were apparent...

Parker JD et al; Environ Health Perspect 117 (1): 140-7 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19165401

/EPIDEMIOLOGY STUDIES/ Eruption at Kilauea Volcano, Hawai'i, has continued since 1983, emitting sulfurous air pollution into nearby communities. The purpose of this cohort study was to estimate the relative risk (RR) of acute bronchitis over a period from January 2004 to December 2006 in communities exposed to the volcanic air pollution. A community-based case review was conducted using medical records from clinics and emergency rooms in exposed and unexposed study areas. Initial visits by local residents for diagnosed acute bronchitis were clinically reviewed. The cumulative incidence rate for the 3-yr period was 117.74 per 1000 in unexposed communities and 184.63 per 1000 in exposed communities. RR estimates were standardized for age and gender, revealing an elevated cumulative incidence ratio (CIR) of 1.57 (95% CI = 1.36-1.81) for acute bronchitis in the exposed communities. Highest risk [CIR: 6.56 (95% CI = 3.16-13.6)] was observed in children aged 0-14 yr who resided in the exposed communities. Exposed middle-aged females aged 45-64 yr had double the risk for acute bronchitis than their unexposed counterparts. These findings suggest that communities continuously exposed to sulfurous volcanic air pollution may have a higher risk of acute bronchitis across the life span.

Longo BM, Yang W; J Toxicol Environ Health 71 (24): 1565-71 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18850456

/EPIDEMIOLOGY STUDIES/ To determine the influence of gaseous air pollutants on neonatal respiratory morbidity, ... the association between daily respiratory hospitalizations and daily concentrations of ambient air pollution gases: ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide, /were tested/ in 11 large Canadian cities. ... The percent increases in hospitalization associated with an increase in air pollution equivalent to its interquartile range were 3.35 [95% confidence interval (CI), 1.73-4.77] for O3, 2.85 (95% CI, 1.68-4.02) for NO2, 1.66 (95% CI, 0.63-2.69) for SO2, and 1.75 (95% CI, 0.48-3.02) for CO. The independent effect of all pollutants combined was 9.61% (95% CI, 4.52-14.7%)...

Dales RE et al; Environ Health Perspect 114 (11): 1751-4 (2006). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17107863

/EPIDEMIOLOGY STUDIES/ ...The aim of this study is to investigate the association between exposure to black smoke (BS; particulate matter with aerodynamic diameter < 4 ug/cu m) and sulfur dioxide (SO(2)) during the first trimester of pregnancy and risk of congenital anomalies ... A case-control study design /was used/ among deliveries to mothers resident in the UK Northern health region during 1985-1990. Case data were ascertained from the population-based Northern Congenital Abnormality Survey and control data from national data on all births. Data on BS and SO(2) from ambient air monitoring stations were used to average the total pollutant exposure during the first trimester of pregnancy over the daily readings from all monitors within 10 km of the mother's residence. Logistic regression models estimated the association via odds ratios. A significant but weak positive association was found between nervous system anomalies and BS (OR = 1.10 per increase of 1000 ug/cu m total BS; 95% CI: 1.03, 1.18), but not with other anomaly subtypes. For SO(2), a significant negative association was found with congenital heart disease combined and patent ductus arteriosus: OR significantly < 1 for all quartiles relative to the first quartile. The relationship between SO(2) levels and other anomaly subtypes was less clear cut: there were either no significant associations or a suggestion of a U-shaped relationship (OR significantly <1 for moderate compared to lowest levels, but not with high SO(2) levels). Overall, maternal exposure to BS and SO(2) in the Northern region had limited impact on congenital anomaly risk ...

Rankin J et al; Environ Res 109 (2): 181-7 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19135190

/EPIDEMIOLOGY STUDIES/ ... The authors investigated short-term relations between ambient air pollution estimated in small geographic areas (French census blocks) and asthma attacks in Strasbourg, France, in 2000-2005--in the general population and in populations with contrasting levels of socioeconomic deprivation. Emergency health-care networks provided data on 4,683 telephone calls made for asthma attacks. Deprivation was estimated using a block-level index constructed from census data. Hourly concentrations of particulate matter less than 10 um in aerodynamic diameter (PM(10)), sulfur dioxide, nitrogen dioxide, and ozone were modeled by block with ADMS-Urban software. Adjusted case-crossover analyses showed that asthma calls were positively but not significantly associated with PM(10) (for a 10-ug/cu m increase, odds ratio (OR) = 1.035, 95% confidence interval (CI): 0.997, 1.075), sulfur dioxide (OR = 1.056, 95% CI: 0.979, 1.139), and nitrogen dioxide (OR = 1.025, 95% CI: 0.990, 1.062). No association was observed for ozone (OR = 0.998, 95% CI: 0.965, 1.032). Socioeconomic deprivation had no significant influence on these relations.

Laurent O et al; Am J Epidemiol 168 (1): 58-65 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18467319

/EPIDEMIOLOGY STUDIES/ To evaluate the relationship between exposure to gaseous air pollutants (ozone [O3], carbon monoxide [CO], nitrogen dioxide [NO2], and sulfur dioxide [SO2]) socioeconomic status and the prevalence of symptoms of asthma, rhinitis and atopic eczema in adolescents...16,209 adolescents from Sao Paulo West (SPW), Sao Paulo South (SPS), Santo Andre (SA), Curitiba (CR), and Porto Alegre (PoA) were enrolled. Data on air pollutants and socioeconomic status were compared to prevalence of symptoms with the Spearman correlation coefficient. Socioeconomic status was quite similar in all cities. The levels of O3 in SPW, SPS, and SA, and of CO in SA were higher than the acceptable ones. In relation to O3 and CO exposures, adolescents from SPW and SA had a significant risk of current wheezing, whereas living in SPW was associated with a high risk of rhinoconjunctivitis, eczema, and flexural eczema and living in CR to rhinitis. Exposure to NO2 was associated with a high risk of current wheezing in SPW and SA, and of severe asthma in SPW and PoA. Exposure to SO2 was associated with a high risk of current wheezing in SPW and SA, severe asthma in SPW and PoA, and nighttime cough, eczema, flexural eczema and severe eczema in SPW. Living in SPW, CR, or PoA was associated with a high risk of rhinitis, rhinoconjunctivitis, and severe rhinitis...

Sole D et al; J Invest Allerogology Clin Immunol 17 (1): 6-13 (2007). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17323857

/EPIDEMIOLOGY STUDIES/ ... The impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics /were examined/. ... 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada /were identified/. ... Residential exposures by month of pregnancy /were estimated/ using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) um in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth. Residence within 50 m of highways was associated with a 22% (95% CI, 0.81-1.87) [corrected] increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00-1.04; IDW: OR = 1.05; 95% CI, 1.03-1.08 per 10-microg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance...

Brauer M et al; Environ Health Perspect 116 (5): 680-6 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18470315

/EPIDEMIOLOGY STUDIES/ ... The Public Health and Air Pollution in Asia (PAPA) project assessed the effects of short-term exposure to air pollution on daily mortality in Bangkok, Thailand, and in three cities in China: Hong Kong, Shanghai, and Wuhan. ... In individual cities, associations were detected between most of the pollutants [nitrogen dioxide, sulfur dioxide, particulate matter < or = 10 microm in aerodynamic diameter (PM(10)), and ozone] and most health outcomes under study (i.e., all natural-cause, cardiovascular, and respiratory mortality). The city-combined effects of the four pollutants tended to be equal or greater than those identified in studies conducted in Western industrial nations. In addition, residents of Asian cities are likely to have higher exposures to air pollution than those in Western industrial nations because they spend more time outdoors and less time in air conditioning...

Wong C-M et al; Environ Health Perspect 116 (9): 1195-202 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18795163

/EPIDEMIOLOGY STUDIES/ ...The association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort /was examined using/ data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter < or = 2.5 um (PM(2.5)), as well as various exposure variables related to traffic, were estimated at the home address. ... Traffic intensity on the nearest road was independently associated with mortality. Relative risks (95% confidence intervals) for a 10-ug/cu m increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00-1.11) for natural cause, 1.04 (0.95-1.13) for cardiovascular, 1.22 (0.99-1.50) for respiratory, 1.03 (0.88-1.20) for lung cancer, and 1.04 (0.97-1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO(2) and PM(2.5), but no associations were found for SO(2). CONCLUSIONS: Traffic-related air pollution and several traffic exposure variables were associated with mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO(2) and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.

Beelen R et al; Environ Health Persp 116 (2): 196-202 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18288318

/SURVEILLANCE/ ...Data from 861 children with persistent asthma in 7 US urban communities who performed 2-week periods of twice-daily pulmonary function testing every 6 months for 2 years /were analyzed/. Asthma symptom data were collected every 2 months. Daily pollution measurements were obtained from the Aerometric Information Retrieval System. The relationship of lung function and symptoms to fluctuations in pollutant concentrations was examined by using mixed models. Almost all pollutant concentrations measured were below the National Ambient Air Quality Standards. In single-pollutant models, higher 5-day average concentrations of NO2, sulfur dioxide, and particles smaller than 2.5 um were associated with significantly lower pulmonary function. Higher pollutant levels were independently associated with reduced lung function in a 3-pollutant model. Higher concentrations of NO2 and particles smaller than 2.5 um were associated with asthma-related missed school days, and higher NO2 concentrations were associated with asthma symptoms...

O'Connor GT et al; J Allergy Clin Immunol 121 (5): 1133-9 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18405952

/SURVEILLANCE/ A questionnaire survey was administered to pupils (11-15 years of age) in 10 schools in urban Taiyuan, collecting data on respiratory health and selected home environmental factors. Indoor and outdoor school air pollutants and climate factors were measured in winter. A total of 1,993 pupils (90.2%) participated; 1.8% had cumulative asthma, 8.4% wheezing, 29.8% had daytime attacks of breathlessness. The indoor average concentrations of sulfur dioxide, nitrogen dioxide, ozone, and formaldehyde by class were 264.8, 39.4, 10.1, and 2.3 ug/cu m, respectively. Outdoor levels were two to three times higher. Controlling for possible confounders, either wheeze or daytime or nocturnal attacks of breathlessness were positively associated with SO2, NO2, or formaldehyde. In addition, environmental tobacco smoke and new furniture at home were risk factors for wheeze, daytime breathlessness, and respiratory infections... CONCLUSIONS: Indoor chemical air pollutants of mainly outdoor origin could be risk factors

Zhao Z et al; Environ Health Perspect 116 (1): 90-7 (2008). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18197305

/SURVEILLANCE/ ... 182 children with asthma, 9-14 years of age, /were studied/ for 4 weeks. Daily ambient concentrations of sulfur dioxide, nitrogen dioxide, ozone, and particulate matter < or = 2.5 um in aerodynamic diameter (PM(2.5)) were monitored from two stations. Once a week ... spirometry and fractional exhaled nitric oxide (FeNO) /were measured/ ... and thiobarbituric acid reactive substances (TBARS) and 8-isoprostane--two oxidative stress markers--and interleukin-6 (IL-6) in breath condensate /were estimated/. ... Interquartile-range increases in 3-day average SO2 (5.4 ppb), NO2 (6.8 ppb), and PM(2.5) (5.4 ug/cu m) were associated with decreases in forced expiratory flow between 25% and 75% of forced vital capacity, with changes being -3.1% [95% confidence interval (CI), -5.8 to -0.3], -2.8% (95% CI, -4.8 to -0.8), and -3.0% (95% CI, -4.7 to -1.2), respectively. SO2, NO2, and PM(2.5) were associated with increases in TBARS, with changes being 36.2% (95% CI, 15.7 to 57.2), 21.8% (95% CI, 8.2 to 36.0), and 24.8% (95% CI, 10.8 to 39.4), respectively. Risk estimates appear to be larger in children not taking corticosteroids than in children taking corticosteroids. O3 (5.3 ppb) was not associated with health end points. FeNO, 8-isoprostane, and IL-6 were not associated with air pollutants...

Liu L et al; Environ Health Persp 117 (4): 668-74 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19440509

/SURVEILLANCE/ This study investigated the acute effect of air pollution on the respiratory health of children living in the industrial area of Puchuncavi, in Region V of Chile. The 114 children studied were from 6 to 12 years old; 57 of them had chronic respiratory symptoms and 57 did not. Each day for 66 days the air was checked for levels of sulfur dioxide (SO2) and of breathable particles that were < 10 microns (PM10). The children were selected and classified according to their susceptibility to chronic respiratory disease by means of a questionnaire used with 882 children living within the area of the emissions from a copper foundry and a thermoelectric plant. Each day, each studied child's peak expiratory flow (PEF) and incidence of respiratory symptoms were checked and recorded. Using regression models (generalized estimation equations), estimates were made of the association of SO2 and PM10 levels with PEF and the incidence of cough, expectoration, episodes of wheezing, dyspnea, and use of bronchodilators. Among the children who were initially symptomatic, an increase of 50 ug/cu m in the daily mean level of SO2 caused a reduction of -1.42 L/min (95% confidence interval (95% CI): -2.84 to -0.71) in the PEF of the following day. An increase of 30 ug/cu m in the cumulative concentration of PM10 over three days produced a PEF reduction of -2.84 L/min (95% CI: -4.26 to 0.00). With respect to symptoms, an increase of 30 ug/cu m in the weekly mean level of PM10 was related with a 26% increase (odds ratio (OR) = 1.26; 95% CI: 1.01 to 1.57) in the incidence of cough and of 23% (OR = 1.23; 95% CI: 1.00 to 1.50) in the incidence of expectoration. An increase of 50 ug/cu m in the mean level of SO2 for three days was associated with a 5% increase (OR = 1.05; 95% CI: 1.00 to 1.10) in the incidence of expectoration. An increase of 30 micrograms/m3 in the daily average of PM10 increased the use of bronchodilators two days later by 10% (OR = 1.10; 95% CI: 1.03 to 1.18). Among the initially asymptomatic children, a significant effect from PM10 exposure was found after an increase of 30 ug/cu m in the mean daily PM10 level, with a reduction of -1.34 L/min (95% CI: -2.68 to -0.67) in the PEF of the following day. A similar increase in the cumulative exposure over three days was associated with an increase of 9% in the incidence of episodes of wheezing (OR = 1.09; 95% CI: 1.01 to 1.31). It is concluded that high levels of PM10 and SO2 affect the respiratory health of children living in the industrial area of Puchuncavi.

Sanchez J et al; Revista panamericana de salud publica 6 (6); 384-91 (1999). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10659669

/SURVEILLANCE/ ... The relationship between measures of lung function (forced expiratory volume in 1 s (FEV(1)) and FEV(1) as a percentage of forced vital capacity (FVC)) and average exposure to particulate matter <10 um in diameter, nitrogen dioxide, sulfur dioxide and ozone was examined in four representative cross-sectional surveys of the English population aged > or =16 in 1995, 1996, 1997 and 2001. Year-specific estimates were pooled using fixed effects meta-analysis. Greater exposure to particulate matter <10 um in diameter, nitrogen dioxide and sulfur dioxide was associated with lower adult FEV(1). The size of the effect on population mean FEV(1) was about 3% for particulate matter <10 um, and 0.7% for nitrogen dioxide and sulfur dioxide, for a 10 ug/cu m increase in pollutant concentration. The effects were most marked in men, older adults and ex-smokers. FEV(1) was not associated with ozone concentration. No associations were found between the pollutants and FEV(1) as a percentage of FVC...

Forbes LJL et al; Thorax 64 (8): 657-63 (2009). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19359266

/SURVEILLANCE/ ... Apricot sulfurization workers (ASW) are exposed to high concentrations of SO(2), resulting in an asthma-like syndrome. The aim of this study was to evaluate whether oxidative stress plays a role in the pathogenesis of asthma-like syndrome due to the high concentrations of SO(2) exposure in agricultural environment. Serum antioxidant enzyme activities and malondialdehyde (MDA) concentrations, which are markers of lipid peroxidation, and pulmonary function tests (PFT) were measured in 40 volunteer ASW and compared to 20 healthy control subjects. The superoxide dismutase (SOD, 2.2+/-0.6 vs. 3.2+/-0.7 U/mL), glutathione peroxidase (GSH-Px, 0.6+/-0.3 vs. 1.1+/-0.3 U/mL) and catalase (107.6+/-27.4 vs. 152.6+/-14.3 k/L) activities in ASW were significantly (p<0.0001) lower than controls, whereas the malondialdehyde concentration (4.1+/-0.9 vs. 1.9+/-5.3 nmol/L) was higher in ASW (p<0.0001). ASW had significant decreases in pulmonary function parameters after exposure. These results show that occupational exposure to high concentrations of SO(2) enhances oxidative stress and lipid peroxidation may be considered as a new mechanism of SO(2)-induced bronchoconstriction.

Gokirmak M et al; Clin Chim Acta 331 (1-2): 119-26 (2003). Available from; as of November 28, 2009: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12691872

There are MANY more results that can be viewed on the US National Library Of Medicine Biotechnology Database. I've simply run out of space to list them all.

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