Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

SULFUR DIOXIDE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sulfur dioxide (an oxide of sulfur) is a colorless, nonflammable gas formed when sulfur-containing materials are burned. It is classified as an irritant gas. It is easily compressed into a liquid and condenses to a liquid at minus 10 degrees C under normal atmospheric pressure.

Specific Substances

    1) Bisulfite
    2) Fermenicide liquid
    3) Fermenicide powder
    4) Sulfur dioxide
    5) Sulfur oxide
    6) Sulfurous acid anhydride
    7) Sulfurous anhydride
    8) Sulfurous oxide
    9) Oxides of sulfur
    10) Molecular Formula: SOx
    11) Molecular Formula: SO2
    12) CAS 7446-09-5
    13) SCHWEFELDIOXYD
    14) SIARKI DWUTLENEK
    1.2.1) MOLECULAR FORMULA
    1) SO2 O2-S

Available Forms Sources

    A) FORMS
    1) PHARMACEUTICALS - Bronchodilator aerosols have been demonstrated to release 0.1 to 6 ppm of sulfur dioxide when nebulized (Koepke et al, 1983).
    2) Sulfur dioxide is a colorless, nonflammable gas that is easily compressed to a liquid; it is supplied commercially as a liquid. It possesses a sharp, irritating, pungent odor (Budavari, 2000; CHRIS , 2002; Lewis, 2001; NIOSH , 2002).
    3) Available grades include commercial, USP, technical, refrigeration, food-grade and anhydrous (99.98% minimum) (CGA, 1999; Lewis, 2001). Specifications for food-grade sulfur dioxide are as follows (CGA, 1999):
    Sulfur dioxide99.9 weight % minimum
    Arsenic (as As)3 ppm maximum
    Heavy metals (as Pb)30 ppm maximum
    Lead (as Pb)10 ppm maximum
    Nonvolatile residue0.05 weight % maximum
    Selenium (as Se)20 ppm maximum
    Water0.05 weight % maximum

    B) SOURCES
    1) Sulfur dioxide is formed when sulfur-containing materials are burned in air (Bingham et al, 2001; CGA, 1999; Lewis, 2001). It is also derived from the roasting of pyrites in a special furnace (Lewis, 2001).
    2) The gas is readily liquefied by cooling with ice and salt or at a pressure of three atm (Lewis, 2001). Selective absorption of sulfur dioxide from cleaned gas, followed by drying and liquefaction is also used for sulfur dioxide gases resulting from metallurgic and smelting operations (GCA, 1999).
    3) Sulfur dioxide is a by-product of fossil fuel combustion, petroleum refining, and paper manufacturing. It is also released during volcanic eruptions and naturally-occurring fires (Harbison, 1998). Point sources such as coal- and oil-fueled power plants and metal smelters are the main source of industrial airborne sulfur dioxide (Goldfrank, 1998).
    4) It is a common pollutant in urban areas (Baxter et al, 2000). It is one of the most frequently encountered irritant gasses (Bingham et al, 2001; CGA, 1999). Sulfur dioxide is a major contributor to acid rain (Franklin et al, 1985; (Goldfrank, 1998).
    C) USES
    1) Sulfur dioxide is used as a preservative for fruits and vegetables, as a disinfectant in breweries, granaries and food factories, for bleaching textile fibers, straw, wicker ware, gelatin, glue, beet sugars, and as a solvent (Ashford, 1994; Budavari, 2000). It is also used in the manufacture of sodium sulfate and sulfuric acid (Harbison, 1998).
    2) Sulfur dioxide is used as a dechlorination reagent (drinking water and effluent); in treating wood pulp for paper manufacturing; in ore and metal refining; extraction of lubricating oils; as a food additive (dried fruits and vegetables, meats, soups, and sauces); in refrigeration; in tanning; and as a reducing agent (AAR, 2000; ACGIH, 1991; Ashford, 1994; Budavari, 2000; CGA, 1999; Harbison, 1998; Hathaway et al, 1996).
    3) The majority of sulfur dioxide produced for captive use is employed in the sulfuric acid and wood pulp industries (ATSDR, 1998).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Sulfur dioxide (SO2) is an irritant colorless, nonflammable gas at room temperature with a characteristic pungent odor to warn of its presence. It is manufactured into sulfuric acid. It is mostly produced by the combustion of elemental sulfur, though it can also be generated by heating sulfide ores. Sulfuric dioxide is also used as a produce preservative, disinfectant, bleaching agent, and dechlorination reagent.
    B) TOXICOLOGY: Sulfur dioxide readily converts to sulfurous acid (H2SO3) upon contact with water. It also has irritant effects on the mucosa of the nasopharynx, respiratory tract, and conjunctiva, as well as causing bronchoconstriction.
    C) EPIDEMIOLOGY: Sulfur dioxide is commonly used in certain industries but significant acute exposures are rarely reported to poison centers. It is a major air pollutant from automobiles, smelters, and certain industrial plants.
    D) WITH POISONING/EXPOSURE
    1) ACUTE TOXICITY: Acute exposures may cause typical irritant gas symptoms such as burning of the eyes, nose, and throat, lacrimation, and cough. More severe symptoms include wheezing, a chemical bronchitis and laryngospasm. With severe exposures, patients may develop a chemical pneumonitis and noncardiogenic pulmonary edema. Exposures to levels of 400 to 500 ppm are considered immediately life-threatening. After exposure to high concentrations, victims who survive may develop residual obstructive or restrictive lung disease, reactive airway disease syndrome, or chronic bronchitis.
    2) DERMAL EXPOSURE: Dermal exposures from liquefied sulfur dioxide (boiling point -10 degree C or 14 degrees F) may cause serious skin (chemical burn) and frostbite injuries.
    3) OCULAR EXPOSURE: Eye exposures to sulfur dioxide may start with eye irritation from the formation of sulfurous acid. However, exposure to liquefied sulfur dioxide can cause severe corneal damage that can lead to blindness.
    0.2.20) REPRODUCTIVE
    A) Maternal toxicity and embryotoxicity have been observed.
    0.2.21) CARCINOGENICITY
    A) A higher incidence of respiratory cancer may be observed with exposure to sulfur dioxide and other agents in combination.

Laboratory Monitoring

    A) Useful laboratory studies may include arterial or venous blood gases in those with severe respiratory symptoms.
    B) Other monitoring and studies that may also be useful include chest x-ray, pulse oximetry, and spirometry/peak expiratory flow rates.
    C) Blood levels of sulfur dioxide are not available.

Treatment Overview

    0.4.3) INHALATION EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) INHALATION EXPOSURE: Move patient to fresh air. Monitor for respiratory distress. If cough or other signs of breathing difficulties develop, evaluate further with a chest x-ray, blood gases, and/or pulse oximetry. Administer oxygen and assist ventilation as needed. Treat bronchospasm with inhaled beta2 agonists. The use of steroids is controversial. Antibiotics may be useful for pulmonary infectious complications.
    2) DERMAL EXPOSURE: Remove contaminated clothing and wash exposed areas thoroughly with soap and water. Rewarm areas affected by frostbite. Frostbite can be treated by rewarming in water bath with a temperature of 40 to 42 degrees C for 15 to 30 minutes. Further wound care may be needed and treatment with analgesics such as ibuprofen or opioids.
    3) OCULAR EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature water for a least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a healthcare facility.
    B) DECONTAMINATION
    1) PREHOSPITAL OR HOSPITAL: There is no indication for the use of ipecac or activated charcoal. Their use would have no benefit and would only expose patients to further adverse effects. INHALATION: The mainstay of treatment is to remove the patient from exposure to fresh air. DERMAL: Remove contaminated clothing and decontaminate exposed skin with soap and water. OCULAR: Irrigate the eyes immediately with room temperature water.
    C) AIRWAY MANAGEMENT
    1) Monitor respiratory function closely. Airway management may be needed following a severe exposure and include early intubation and ventilation in patients exhibiting respiratory distress.
    D) ANTIDOTE
    1) There is no specific antidote for sulfur dioxide.
    E) ENHANCED ELIMINATION
    1) There is no evidence for the use of dialysis, hemoperfusion, urinary alkalinization or multiple dose activated charcoal. It is unlikely that any modes of enhanced elimination would have any direct benefit to patients poisoned with sulfur dioxide.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients may remain at home. Patients with minimal exposures and rapidly improving symptoms may also remain at home.
    2) OBSERVATION CRITERIA: Patients with a history of significant inhalation exposure or respiratory tract irritation should be admitted for at least 24 hours of observation. Patients with improving symptoms or who are asymptomatic may be discharged to home.
    3) ADMISSION CRITERIA: Patients with worsening symptoms or severe respiratory distress should be admitted to the hospital. If stable, patients may be admitted to a standard hospital ward; worsening or a new onset of symptoms (eg, respiratory insufficiency requiring intubation) may necessitate an ICU setting. Patients should remain in the hospital until they are clearly improving and stable from a respiratory standpoint.
    4) CONSULT CRITERIA: Patients with severe respiratory symptoms may benefit from a pulmonologist or intensivist consult. A toxicologist or poison center can give advice following an individual exposure and may be useful in giving public health advice in cases of mass exposure.
    G) PITFALLS
    1) The onset of acute lung injury after a toxic exposure may be delayed up to 24 to 72 hours after exposure. In cases of acute lung injury, the lowest amount of PEEP possible will minimize the development of barotrauma and other complications. In addition, crystalloid solution should be administered judiciously to keep the pulmonary wedge pressure relatively low.
    H) TOXICOKINETICS
    1) Sulfur dioxide is very soluble in water and forms sulfurous acid. Sulfur dioxide is most likely absorbed as sulfurous acid or one of its ionization products. Absorbed sulfur dioxide is almost entirely oxidized to sulfate ion and then excreted in the urine as inorganic sulfate.
    I) PREDISPOSING CONDITIONS
    1) Extremes of age and those with underlying respiratory illnesses or medical conditions such as asthma may be more sensitive and have more severe symptoms after exposure to sulfur dioxide.
    J) DIFFERENTIAL DIAGNOSIS
    1) Exposure to sulfur dioxide can look like exposure to other irritant gases such as tear gas (CS), chloroacetophenone (CN) and other irritant substances. It can also resemble other causes of respiratory distress such as an asthma exacerbation.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Rewarming and a variety of topical treatments are indicated for frostbite injury. SEE MAIN TREATMENT SECTION FOR MORE INFORMATION.

Range Of Toxicity

    A) TOXICITY: The minimum lethal human exposure is an airborne concentration of 400 ppm for 1 minute. The odor or taste is noticeable at airborne concentrations of 3 to 5 ppm, throat and conjunctival irritation and lacrimation start at 8 to 12 ppm, and symptoms become severe at 50 ppm. Other reported minimum lethal concentrations of sulfur dioxide include 3000 ppm for 5 minutes and 1000 ppm for 10 minutes. ELDERLY: In general, elderly patients with asthma may be more sensitive. A 76-year-old woman with asthma died following inhalation exposure to approximately 150 ppm over a period of minutes.

Clinical Effects

Summary Of Exposure

    A) USES: Sulfur dioxide (SO2) is an irritant colorless, nonflammable gas at room temperature with a characteristic pungent odor to warn of its presence. It is manufactured into sulfuric acid. It is mostly produced by the combustion of elemental sulfur, though it can also be generated by heating sulfide ores. Sulfuric dioxide is also used as a produce preservative, disinfectant, bleaching agent, and dechlorination reagent.
    B) TOXICOLOGY: Sulfur dioxide readily converts to sulfurous acid (H2SO3) upon contact with water. It also has irritant effects on the mucosa of the nasopharynx, respiratory tract, and conjunctiva, as well as causing bronchoconstriction.
    C) EPIDEMIOLOGY: Sulfur dioxide is commonly used in certain industries but significant acute exposures are rarely reported to poison centers. It is a major air pollutant from automobiles, smelters, and certain industrial plants.
    D) WITH POISONING/EXPOSURE
    1) ACUTE TOXICITY: Acute exposures may cause typical irritant gas symptoms such as burning of the eyes, nose, and throat, lacrimation, and cough. More severe symptoms include wheezing, a chemical bronchitis and laryngospasm. With severe exposures, patients may develop a chemical pneumonitis and noncardiogenic pulmonary edema. Exposures to levels of 400 to 500 ppm are considered immediately life-threatening. After exposure to high concentrations, victims who survive may develop residual obstructive or restrictive lung disease, reactive airway disease syndrome, or chronic bronchitis.
    2) DERMAL EXPOSURE: Dermal exposures from liquefied sulfur dioxide (boiling point -10 degree C or 14 degrees F) may cause serious skin (chemical burn) and frostbite injuries.
    3) OCULAR EXPOSURE: Eye exposures to sulfur dioxide may start with eye irritation from the formation of sulfurous acid. However, exposure to liquefied sulfur dioxide can cause severe corneal damage that can lead to blindness.

Heent

    3.4.3) EYES
    A) Eye irritation and lacrimation are reported with exposure to concentrations of 8 to 12 ppm and greater (Grant & Schuman, 1993).
    B) CORNEAL INJURY: Severe and irreversible corneal injury has been reported after direct eye contact with highly concentrated liquefied sulfur dioxide. The injury appears to be distinct from what would be expected from the cold exposure alone (Grant & Schuman, 1993).
    1) INDUSTRIAL EXPOSURE: In 4 cases of injuries from accidental spraying in refrigeration machine workers, immediate corneal epithelial damage with underlying stromal and endothelial injury occurred (Grant, 1974).
    3.4.4) EARS
    A) GUINEA PIGS exposed to 300 ppm sulfur dioxide over 24 hours developed reduced ciliary activity at the distal site of the middle ear and increased mucous secretion at the proximal site, which could predispose to middle ear effusion (Ohashi et al, 1989).
    3.4.5) NOSE
    A) Up to 90% or more of inhaled sulfur dioxide may be absorbed in the nasopharynx (Andersen et al, 1974). Due to its high water solubility, the nasopharynx and upper respiratory mucosa are most sensitive to the effects of sulfur dioxide. At relatively low concentrations, a majority of sulfur dioxide is deposited in the nose and oropharynx (Eberhardt, 1998). Mild nasal symptoms were noted in subjects exposed to 10 and 20 mg SO2/m(3) (Sandstrom et al, 1989).
    1) Contact of sulfur dioxide with water in the mucus forms sulfurous acid which is highly irritating (ACGIH, 1980). Irritation of the lower respiratory tract occurs after capacity of the upper respiratory tract to remove SO2 has been saturated.
    B) Ulceration and perforation of the nasal septum have been reported with chronic exposure (Plunkett, 1976; Eberhardt, 1998).
    C) Loss of the sensation of smell has been reported (Plunkett, 1976). Chronically exposed workers develop tolerance to the odor and minor irritating properties of low concentrations (Eberhardt, 1998).
    D) Human nasal ciliated cells exposed to varying concentrations of sulfur dioxide have reversible decreases in ciliary beat frequency, especially at decreased pH (Kienast et al, 1994).
    3.4.6) THROAT
    A) Irritation of the upper respiratory tract may cause severe glottic edema and airway obstruction (Eberhardt, 1998; Gosselin et al, 1984).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) Pulmonary edema may occur after inhalation (Eberhardt, 1998) (ITI, 1985) (Plunkett, 1976) and may be a cause of death (Gosselin et al, 1984).
    2) Irritation of the nasopharynx, glottis, and upper respiratory tract may produce severe edema and airway obstruction (Eberhardt, 1998; Gosselin et al, 1984).
    B) HYPOXEMIA
    1) WITH POISONING/EXPOSURE
    a) Anoxia from airway obstruction has been thought to be the cause of death in workers and experimental animals exposed to high concentrations (Eberhardt, 1998; Gosselin et al, 1984).
    b) CASE SERIES: Two nonsmoking miners exposed to high concentrations of sulfur dioxide after a mine explosion had transient injury to pulmonary parenchyma and persistent injury to the airways resulting in ventilatory limitation to exercise and hypoxemia caused by ventilation-perfusion mismatch during a 2-year follow-up period (Rabinovitch et al, 1989).
    C) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Cough, dyspnea, chest discomfort, and cyanosis may occur following inhalation exposure (ITI, 1985) (Plunkett, 1976; CDC, 1984; Savic et al, 1987; Eberhardt, 1998). Bronchial hyperactivity occurs immediately after exposure and may persist for several years (Rabinovitch et al, 1989). Damage to the pulmonary parenchyma occurs as well, but appears to be transient. Dyspnea correlated with prior sulfur dioxide exposure in silicon carbide workers exposed to an average airborne concentration of 1.5 ppm with peaks at 4 ppm (Osterman et al, 1989).
    D) COUGH
    1) WITH POISONING/EXPOSURE
    a) Coughing is the most common symptom noted following exposure to low airborne concentrations (Eberhardt, 1998; Plunkett, 1976). Coughing, sneezing, sore throat, and a sensation of choking are common with inhalation of high airborne concentrations (Eberhardt, 1998; Plunkett, 1976; CDC, 1984). Cough correlated with prior sulfur dioxide exposure in silicon carbide workers exposed to an average airborne concentration of 1.5 ppm with peaks at 4 ppm (Osterman et al, 1989).
    E) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) Pneumonia may be a complication of acute inhalation injury (Eberhardt, 1998).
    F) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Bronchoconstriction and wheezing may occur (Eberhardt, 1998; Roger et al, 1985). Asthmatic patients may have bronchoconstriction with exposure to airborne concentrations of 0.5 to 1.0 ppm, such as may occur near smelters (Roger et al, 1985). Asthmatics may have significant bronchoconstriction with 2 min or more of 1 ppm sulfur dioxide exposure or less, especially following exercise (Horstman et al, 1988; Balmes et al, 1987; Linn et al, 1987; Linn et al, 1990). This phenomenon is enhanced by prior exposure to ozone at 120 ppb (Koenig et al, 1990).
    b) Exposure to a combination of sulfur dioxide and nitrogen dioxide has been shown to enhance the airway response to inhaled allergens in asthmatics (Devalia et al, 1994). No differences were measured between asthmatic Caucasians and African-Americans when challenged with 1 ppm of sulfur dioxide. Both groups had significant increases in total respiratory resistance (Heath et al, 1994).
    G) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Some patients have developed reactive airway disease (RADS), restrictive and obstructive lung disease, or chronic bronchitis after surviving an acute inhalation exposure (Eberhardt, 1998; ACGIH, 1980; NIOSH, 1974).
    1) CASE REPORT: A bank employee, exposed acutely to sulfur dioxide when a bank bag smoke bomb exploded in a vault, developed signs of obstructive and restrictive lung disease by day 10. Two years later, some lung function impairment was still evident (Coninck et al, 1995).
    2) CASE SERIES: In a 13 year follow-up study of 9 men exposed to sulfur dioxide in a pyrite mine explosion, continued abnormalities of pulmonary function (2 obstructive, 3 mixed) and persistent bronchial reactivity to histamine was found in 4 cases. The authors indicated that these 4 cases may have developed the reactive airways dysfunction syndrome (RADS). Four individuals were said to have chronic bronchitis (Piirila et al, 1996).
    3) CASE SERIES: In 5 workers exposed to high concentrations of sulfur dioxide, 2 died, one recovered, and 2 had evidence of continued respiratory disease; one with obstructive and one mixed disease on pulmonary testing (Charan et al, 1979).
    b) ALVEOLAR MACROPHAGE ACTIVITY: An increase in lysozyme positive macrophages in bronchoalveolar lavage fluid 24 hours after controlled chamber exposure with 10 and 20 mg SO2/m(3) for 20 minutes was associated with increased alveolar macrophage activity in a study of 12 volunteer subjects. In those exposed to 20 mg SO2/m(3), an increase in total number of macrophages and lymphocytes was observed, which virtually returned to pre-exposure levels by 72 hours postexposure (Sandstrom et al, 1989). In vitro exposure to sulfur dioxide gas for 15 minutes retarded the chemotactic response of human alveolar and blood macrophages (Knorst et al, 1996).
    H) BRONCHITIS
    1) WITH POISONING/EXPOSURE
    a) Workers chronically exposed to sulfur dioxide may develop chronic bronchitis (Rosenhall & Stjernberg, 1982).
    I) ASTHMA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a study of 1730 sulphite mill workers exposed to sulfur dioxide and other irritant gases, the incidence rate for physician-diagnosed asthma was 4.4 per 1,000 person-years (n=35), compared with 1.9 per 1,000 person-years (n=15) for those classified as unexposed (HR 2.7; 95% CI 1.4 to 5.1). The risk of developing asthma increased for workers with increased peak sulfur dioxide exposure time (HR 4.0; 95% CI 2.1 to 7.7) and even greater for those reporting frequent peak exposures to sulfur dioxide (HR 6.8; 95% CI 3.1 to 15). A subgroup only exposed to sulfur dioxide and no other irritant gases also reported a high risk of developing asthma (HR 5.8; 95% CI 2.8 to 12) (Andersson et al, 2006).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY INSUFFICIENCY
    a) DECREASED MUCOCILIARY ACTIVITY: Inhalational exposures in guinea pigs produced a 56% decrease in mucociliary activity, but only minor morphological changes (with exposure to 7.5 mg/m(3) of sulfur dioxide). With higher exposure levels, epithelial sloughing, intracellular edema and mitochondrial swelling, increased intercellular space, and ciliary cytoplasmic extrusion occurred (Riechelmann et al, 1995). Sulfur dioxide exposure studies in mice produced similar findings (Min et al, 1994).
    b) Weanling ferrets exposed for 3 hours to 500 ppm of sulfur dioxide had a loss of cilia, cells developing a phenotype more similar to secretory cells, and a reformation of cilia during a recovery phase (Leigh et al, 1992).
    2) DYSPNEA
    a) GUINEA PIGS sensitized with C. albicans and repeatedly exposed to sulfur dioxide had an enhanced response on re-exposure to inhaled C. albicans compared to unexposed controls (Kitabatake et al, 1995).
    b) Chronic bronchitis developed in dogs exposed to 500 ppm of sulfur dioxide for 21 weeks; recovery occurred by 5 weeks after exposure cessation (Greene et al, 1984).
    3) RESPIRATORY TRACT MALFORMATION
    a) RATS: Increased chemokine mRNA expression within tracheal tissue with correlating increases in polymorphonuclear leukocytes were found in the rat model after acute and chronic sulfur dioxide exposure (Farone et al, 1995).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and abdominal pain may occur (Eberhardt, 1998; Plunkett, 1976).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) SULFHEMOGLOBINEMIA
    1) Sulfhemoglobin levels of 6% and 12% were found at autopsy in 2 workers who died from sulfur dioxide inhalation (Finkel, 1983).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SULFHEMOGLOBINEMIA
    a) RATS: Sulfhemoglobin levels (mean 0.6%) were significantly higher in rats exposed to 0.87 ppm of sulfur dioxide over 24 hours than in unexposed controls (mean 0.08%). Methemoglobin ratios were not significantly different (Baskurt, 1988).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) FROSTBITE
    1) WITH POISONING/EXPOSURE
    a) Dermal contact with escaping compressed gas or liquid can produce frostbite injury (ACGIH, 1980; Plunkett, 1976).
    B) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Dermal contact with sulfurous acid formed from sulfur dioxide and water (Budavari, 1996; Student, 1981) can produce a chemical burn injury.
    C) PAIN
    1) WITH POISONING/EXPOSURE
    a) A burning sensation of the skin may occur (Plunkett, 1976) (ITI, 1985) and is sometimes followed by a vesicular eruption (Ebert, 1980).
    D) URTICARIA
    1) WITH POISONING/EXPOSURE
    a) INHALATION: Urticaria and a rash similar to a drug hypersensitivity reaction have been reported after inhalation exposure (NIOSH, 1974).

Reproductive

    3.20.1) SUMMARY
    A) Maternal toxicity and embryotoxicity have been observed.
    3.20.2) TERATOGENICITY
    A) EMBRYOTOXICITY
    1) Minor skeletal variants were noted in the offspring of mice inhaling 25 ppm of sulfur dioxide 7 hours per day from day 6 through 15 of gestation and rabbits inhaling 70 ppm 7 hours per day from day 6 through 18 of gestation (Murray et al, 1979).
    B) CONGENITAL ANOMALY
    1) Sulfur dioxide induced toxic and delayed growth effects in rat studies. Fetotoxicity, specific developmental abnormalities of the musculoskeletal system, and behavioral and growth effects were observed in mouse studies. Specific developmental abnormalities of the musculoskeletal system were detected in rabbit studies (RTECS , 2001).
    C) BIRTH WEIGHT LOW
    1) High-level maternal sulfur dioxide exposure resulted in low birth weight mouse pups. Exposure was also associated with decreased neuromuscular coordination and functional capability, with significant increases in the time required for the righting reflex (Singh, 1989).
    D) ANIMAL STUDIES
    1) Sulfur dioxide is one of the chemicals studied by the Panel on Reproductive Hazards in the Workplace of the Council on Scientific Affairs of the American Medical Association (AMA) who concluded that while there are limited experimental animal data to suggest a slight effect on the fetus, there is no human reproductive risk from at or below the OSHA PEL (5 ppm; 10 mg/m(3)) allowable workplace exposure (Council on Scientific Affairs, 1985).
    2) Longer estrus cycles, increased pre- and post-implantation deaths, and increased resorptions and fetal malformations were produced with exposure to a concentration of 4.97 mg/m(3) in rats (Abdushelishvili, 1977). Sulfur dioxide increased the prolongation of the estrus cycle caused by exposure to carbon monoxide (Mamatsashvili, 1970).
    3) Inhalation of 70 +/- 250 ppm sulfur dioxide and 25 ppm in mice was slightly toxic to the mothers and produced so-called minor skeletal variants in the offspring, but was not teratogenic in rabbits (Murray et al, 1979). Sulfur dioxide was also not teratogenic in mice at 32, 65, 125, or 250 ppm on days 7 to 17 of pregnancy (Singh, 1982). It did produce curvature of the spine in rats when mixed with nitrogen dioxide (pp 144-147). When given to pregnant rats together with carbon monoxide at 10 ppm SO2/1,500 ppm CO or 5 ppm SO2/750 ppm CO, there were lower pregnancy rates, smaller litter sizes, and lower fetal weight (Yun, 1976). Sulfur dioxide and carbon monoxide may act synergistically to decrease the pregnancy rate in rats.
    4) No teratogenic effect was observed in mice inhaling 25 ppm of sulfur dioxide 7 hours per day from day 6 through 15 of gestation or in rabbits inhaling 70 ppm 7 hours per day from day 6 through 18 of gestation (Murray et al, 1979). Similarly, a single generation study of exposure to up to 30 ppm of sulfur dioxide from nine days prior to pregnancy through organogenesis in mice revealed no adverse effects on offspring in spite of behavioral changes in the dams (Petruzzi et al, 1996).
    5) There was no association between sulfur dioxide exposure and abortions or birth defects for working women in Finland (Hemminki & Niemi, 1982; Hemminki, 1983).
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY DISORDER
    1) There are a few reports of sulfur dioxide affecting human pregnancies, but these generally involve mixed exposures. There were increased abortions in women living near a smelter in Sweden, where lead and arsenic were also present (Nordstrom, 1978). Women workers in superphosphate production exposed to sulfur dioxide and other substances were reported to have increased gynecological disease, miscarriages, and abnormal pregnancies (Danilov et al, 1975). However, there was no association between sulfur dioxide exposure and abortions or birth defects for working women in Finland (Hemminki & Niemi, 1982; Hemminki, 1983).
    B) ANIMAL STUDIES
    1) Maternal toxicity was observed in mice inhaling 25 ppm of sulfur dioxide 7 hours per day from day 6 through 15 of gestation and in rabbits inhaling 70 ppm 7 hours per day from day 6 through 18 of gestation (Murray et al, 1979).
    2) Maternal estrous cycle disorders and parturition abnormalities were observed in rat exposed to sulfur dioxide (RTECS , 2001).
    3.20.5) FERTILITY
    A) TESTIS DISORDER
    1) RAT STUDY - Sulfur dioxide induced toxic effects on the rat testes, epididymis, and sperm ducts following a TCLo test of inhalation exposure to 30 ppm/6 hours over 21 weeks (RTECS , 2001).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7446-09-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Sulfur dioxide
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) A higher incidence of respiratory cancer may be observed with exposure to sulfur dioxide and other agents in combination.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) There is no direct evidence that sulfur dioxide is carcinogenic (ACGIH, 1980). A case-control study of chemical workers did find suggestive evidence of an association of prior exposure to heat and sulfur dioxide with an increased incidence of lung cancer (Bond et al, 1986).
    2) Sulfur dioxide may be a promoter rather than a carcinogen (ACGIH, 1980). Sulfur dioxide in combination with arsenic or benzo(a)pyrene was associated with a higher incidence of respiratory cancers (arsenic) or squamous cell carcinomas (benzo(a)pyrene) (ACGIH, 1980; NIOSH, 1974; Lee & Fraumeni, 1969).
    a) In a large retrospective cohort study involving more than 6000 copper smelter workers employed between 1946 and 1976 there appeared to be a dose-response relationship for lung cancer with exposure to arsenic and exposure to sulfur dioxide. This study can not be considered as conclusive due to the number of variables and incomplete records (Enterline et al, 1987).
    3) Sulfur dioxide has been rated as equivocal tumorigenic agent by RTECS criteria for inducing lung, thorax, or respiratory tumors (RTECS , 2001; Peacock & Spence, 1967).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Sulfur dioxide may be a promoter or co-carcinogen with inhaled BENZO(a)PYRENE (a component of cigarette smoke) in rats (Pauluhn, 1985), for DIBENZ(a,h)ANTHRACENE in unspecified rodents (Pott & Stober, 1983), and with free radicals in mice (Peacock & Spence, 1967).

Genotoxicity

    A) Genotoxic effects of sulfur dioxide have been demonstrated in occupationally exposed humans and in various animal and in-vitro systems.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Useful laboratory studies may include arterial or venous blood gases in those with severe respiratory symptoms.
    B) Other monitoring and studies that may also be useful include chest x-ray, pulse oximetry, and spirometry/peak expiratory flow rates.
    C) Blood levels of sulfur dioxide are not available.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) Baseline arterial blood gases or pulse oximetry should be obtained in cases of significant inhalation exposure or if respiratory tract irritation is present.
    B) HEMATOLOGIC
    1) Elevated sulfhemoglobin levels were noted in two fatal cases of sulfur dioxide poisoning (Finkel, 1983). Although sulfhemoglobin levels are not readily available, they might be useful as confirmation of exposure.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Increased sulfates in the urine may be seen after exposure (Plunkett, 1976), but this finding may be confounded by diet and is of undetermined utility in the clinical assessment of exposed patients.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) A baseline chest x-ray should be obtained in cases of significant inhalation exposure or respiratory tract irritation. Ventilation-perfusion lung scans may be markedly abnormal in patients with moderate to severe exposure.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Any patient with a history of significant inhalation exposure or respiratory tract irritation should be admitted for at least 24 hours of observation (Kizer, 1984).
    6.3.3.2) HOME CRITERIA/INHALATION
    A) Asymptomatic patients may remain at home. Patients with minimal exposures and rapidly improving symptoms may also remain at home.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Patients with severe respiratory symptoms may benefit from a pulmonologist or intensivist consult. A toxicologist or poison center can give advice following an individual exposure and may be useful in giving public health advice in cases of mass exposure.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Any patient with a history of significant inhalation exposure should be admitted for at least 24 hours of observation (Kizer, 1984).

Monitoring

    A) Useful laboratory studies may include arterial or venous blood gases in those with severe respiratory symptoms.
    B) Other monitoring and studies that may also be useful include chest x-ray, pulse oximetry, and spirometry/peak expiratory flow rates.
    C) Blood levels of sulfur dioxide are not available.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) There is no indication for the use of ipecac or activated charcoal. Their use would have no benefit and would only expose patients to further adverse effects. INHALATION: The mainstay of treatment is to remove the patient from exposure to fresh air. DERMAL: Remove contaminated clothing and decontaminate exposed skin with soap and water. OCULAR: Irrigate the eyes immediately with room temperature water.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) There may be minimal danger to medical personnel attending the patient that has been removed from the contaminated environment.
    B) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    C) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF TOXICITY
    a) Move victims to fresh air. Monitor for respiratory distress. If cough or other signs of breathing difficulties develop, evaluate further with a chest x-ray, blood gases, and/or pulse oximetry. Administer 100% humidified supplemental oxygen with assisted ventilation as needed. Treat bronchospasm with inhaled beta2 agonists. The use of steroids is controversial. Antibiotics may be useful for pulmonary infectious complications.
    B) AIRWAY MANAGEMENT
    1) Monitor respiratory function closely. Airway management may be needed following a severe exposure and include early intubation and ventilation in patients exhibiting respiratory distress.
    2) Endotracheal intubation, cricothyroidotomy, or tracheostomy may be required if upper airway edema produces airway obstruction.
    C) MONITORING OF PATIENT
    1) Useful laboratory studies may include arterial or venous blood gases in those with severe respiratory symptoms. Other monitoring and studies that may be useful include chest x-ray, pulse oximetry, and spirometry/peak expiratory flow rates.
    2) Blood levels of sulfur dioxide are not available.
    D) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    E) BRONCHOSPASM
    1) Inhaled sympathomimetic bronchodilators may be useful if bronchospasm is present. Avoid bronchodilators containing sulfite preservatives (i.e., isoetharine).
    a) Albuterol inhalation (90 mcg aerosol) produced significant bronchodilation and prevented sulfur dioxide induced bronchoconstriction in 10 allergic adolescent subjects (Koenig et al, 1987). Ipratropium bromide inhalation (60 mcg) caused significant bronchodilation, but did not completely protect nonallergic asthmatics from the acute effects of sulfur dioxide inhalations (McManus et al, 1989).
    F) CORTICOSTEROID
    1) The use of corticosteroids is controversial. Antibiotics may be useful to treat pulmonary infectious complications. The use of free radical scavengers such as vitamin E may be beneficial.
    G) SODIUM BICARBONATE
    1) Although inhalation of 5% sodium bicarbonate has been recommended (Gosselin et al, 1984), there is no data to support the use of this procedure (Kizer, 1984); however, it is important to monitor blood gases and acid-base balance.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) SUPPORT
    1) Treatment should include recommendations listed in the INHALATION section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) BURN
    1) Dermal injury can occur from direct contact with sulfurous acid formed from sulfur dioxide and water. This injury should be treated as any other chemical burn.
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    C) ACUTE ALLERGIC REACTION
    1) Urticaria or other hypersensitivity rashes may be treated with antihistamines and corticosteroids (Ebert, 1980; NIOSH, 1974).

Abstracts

Case Reports

    A) SPECIFIC AGENT
    1) SODIUM BISULFITE: Several shrimp fishermen were exposed when using a sodium bisulfite solution to dip fish. Two of these workers died, and were found to have levels of sulfhemoglobin of 6% and 12% percent at postmortem examination (Finkel, 1983).
    B) ACUTE EFFECTS
    1) Five paper mill workers were exposed to very high concentrations of sulfur dioxide. Two died acutely and were found to have hemorrhagic alveolar edema and extensive mucosal sloughing in the small and large airways at autopsy. The 3 survivors developed eye, nose, and throat irritation, chest tightness, and severe dyspnea. One victim developed severe airway obstruction, a second developed mild and asymptomatic restrictive and obstructive lung disease, and the third victim had normal pulmonary functions (Finkel, 1983).
    C) ADVERSE EFFECTS
    1) CASE SERIES: High concentrations of sulfur dioxide occurred in 3 individuals involved in a mine explosion. One miner died within minutes, while the other two resorted to makeshift protective breathing apparatus until rescued 3.5 hours later. Approximate airborne concentration of sulfur dioxide at the time of rescue was 40 ppm. Both survivors complained of intense irritation of mucus membranes, dyspnea, retrosternal chest pain, nausea, vomiting, and urinary incontinence. Most of the symptoms resolved, except for dyspnea. Marked ventilation perfusion abnormalities were still observed 3 weeks postexposure. Partial improvement in pulmonary function and exercise performance in both patients were noted over the following 24 months (Rabinovitch et al, 1989).
    D) ADULT
    1) In a review of 3 incidents of human exposure to sulfur dioxide gas. In the first accident, 13 men working in a ship hold were exposed when a spark ignited sulfur dust in the air. Victims developed conjunctivitis, nausea, vomiting, abdominal pain, throat pain, and bronchitis. One worker developed pneumonia and died 10 days later (Finkel, 1983).

Range Of Toxicity

Summary

    A) TOXICITY: The minimum lethal human exposure is an airborne concentration of 400 ppm for 1 minute. The odor or taste is noticeable at airborne concentrations of 3 to 5 ppm, throat and conjunctival irritation and lacrimation start at 8 to 12 ppm, and symptoms become severe at 50 ppm. Other reported minimum lethal concentrations of sulfur dioxide include 3000 ppm for 5 minutes and 1000 ppm for 10 minutes. ELDERLY: In general, elderly patients with asthma may be more sensitive. A 76-year-old woman with asthma died following inhalation exposure to approximately 150 ppm over a period of minutes.

Minimum Lethal Exposure

    A) SUMMARY
    1) The lowest reported lethal concentrations of sulfur dioxide are 3000 ppm for 5 minutes and 1000 ppm for 10 minutes (RTECS , 2002; Sittig, 1991). Concentrations of 100 ppm to 500 ppm are considered immediately dangerous to life and health (ATSDR, 1999; Bingham et al, 2001; Lewis, 2000; NIOSH , 2002).
    2) Baxter et al (2000) reported 300 to 500 ppm as the 30 minute lethal concentration for "mammals" (Baxter et al, 2000).
    3) A concentration of 150 ppm over a few-minutes may be lethal to elderly individuals with asthma (Baxter et al, 2000).
    4) CASE REPORT: A 76-year-old previously healthy woman with asthma died following an inhalation exposure to sulfur dioxide produced from a sulfite-containing derusting agent. Duplication of the derusting procedure with only 7% to 10% of the derusting agent used by the patient resulted in sulfur dioxide concentrations of 150 ppm (Huber & Loving, 1991).

Maximum Tolerated Exposure

    A) ACUTE
    1) It should be noted that the toxicity of sulfur dioxide is dependent upon whether it is present in an aerosol, on the humidity, and if there is other particulate matter present. A given concentration of sulfur dioxide is reported to elicit a greater response when inhaled through the mouth than when inspired through the nose (ACGIH, 1991; Bingham et al, 2001).
    a) Asthmatics and persons with pulmonary disease are more sensitive to sulfur dioxide in ambient air than are healthy individuals (ACGIH, 1991; Bingham et al, 2001). An estimated 10 to 20% of the adult population is hypersensitive to the adverse effects of sulfur dioxide (HSDB , 2002).
    2) Sulfur dioxide is a severe irritant of the eyes, skin, and upper airways of the respiratory tract. The irritant effects of sulfur dioxide are due to the formation of sulfurous acid which quickly forms when the gas comes into contact with moist surfaces (CGA, 1999; Hathaway et al, 1996).
    3) Acute exposures to sulfur dioxide have caused severe obstructive pulmonary disease that is unresponsive to bronchodilators and may last up to 3 months after exposure (Bingham et al, 2001).
    4) One hundred ppm is the maximum concentration tolerated for exposures of 30 to 60 minutes in duration. This is also the level established by NIOSH (2002) as immediately dangerous to life and health (Bingham et al, 2001).
    5) A healthy individual can tolerate concentrations no greater than 150 ppm for a few minutes (Baxter et al, 2000).
    6) Levels of sulfur dioxide in the air of less than 0.25 ppm (0.65 mg/m(3)) do not elicit an airway response in sensitive individuals, presumably because at this concentration, the sulfur dioxide is removed by the nose and mouth ((IARC, 1992)). Healthy individuals did not respond to sulfur dioxide levels less than 1 ppm (Baxter et al, 2000).
    7) CASE SERIES: Twelve healthy, young adult males were exposed continuously to sulfur dioxide for 120 hours. No adverse pulmonary effects were reported at exposure levels of 0.3 or 1 ppm, while exposure to 3 ppm caused a slight and reversible increase in airway resistance and decrease in compliance (ACGIH, 1991). In a study where subjects breathed through the mouth, a brief exposure to 1 ppm sulfur dioxide caused no effects (Hathaway et al, 1996).
    8) Significant bronchoconstriction was seen in mild asthmatics in response to exposure of 0.5 to 1 ppm sulfur dioxide while engaged in mild exercise. These same subjects adapted to the low levels of sulfur dioxide after repeated short-term exercise in its presence, as evidenced by a decrease in the induced bronchoconstriction (Baxter et al, 2000; Bingham et al, 2001).
    9) Inhalation exposure to airborne concentrations of 10 to 50 ppm of sulfur dioxide for 5 to 15 minutes results in irritation of the nose and throat, choking, sneezing, coughing, and reflex bronchoconstriction with increased pulmonary resistance. Workers routinely exposed to sulfur dioxide adapt to irritating concentrations; repeated exposure to an airborne concentration of 10 ppm caused upper respiratory irritation and nosebleeds; these symptoms did not occur at 5 ppm (CGA, 1999; Hathaway et al, 1996; HSDB , 2002).
    10) Two miners exposed to concentrations of sulfur dioxide of at least 40 ppm suffered severe airway obstruction, hypoxemia, significantly reduced tolerance to exercise, and ventilation perfusion mismatch. They exhibited evidence of active inflammation as shown by a positive gallium lung scan (HSDB , 2002).
    11) Subjects that entered a study-chamber with a 25 ppm concentration of sulfur dioxide in the ambient air found this level to be intolerable on first contact. Those who had been gradually acclimated to this level did not find it as objectionable (HSDB , 2002).
    12) Individuals with mild asthma have demonstrated much greater sensitivity to sulfur dioxide exposure (Hathaway et al, 1996). Pulmonary function test changes from baseline have been recorded in exercising asthmatic subjects exposed to airborne concentrations as low as 0.5 to 1 ppm for 2 minutes or longer (Roger et al, 1985; Schachter et al, 1984; Horstman et al, 1988). No such changes were noted in normal subjects (Schachter et al, 1984).
    13) Injury to the eye from exposure to sulfur dioxide gas in the ambient air is very uncommon. However, several severe burns to the human eye following contact with liquid sulfur dioxide have been reported (Grant & Schuman, 1993).
    a) Liquid sulfur dioxide splashed into the eyes can cause burns and chemical trauma of the cornea and subsequent opacification and vision loss (CGA, 1999; Grant & Schuman, 1993; Hathaway et al, 1996).
    b) Liquid sulfur dioxide can cause frostbite and skin burns. Skin irritation may also result when sulfur dioxide converts to sulfurous acid in moist environments (CGA, 1999; Hathaway et al, 1996).
    B) CHRONIC
    1) British steel workers were studied for effects from chronic exposure to sulfur dioxide at mean concentrations of 0.35 ppm (0.9 mg/m(3)). No effects were seen at this level (HSDB , 2002).
    2) Workers in a United States refrigerator company were studied for the effects of occupational exposure to sulfur dioxide used as a refrigerant. While workers did complain of respiratory symptoms, colds, fatigue and shortness of breath on exertion, no injury to the tracheobronchial tree or alveoli was seen. The exposures were estimated to average from 60 to 90 mg/m(3) (29-32 ppm), with peaks as high as 290 mg/m(3) (100 ppm) (HSDB , 2002).
    3) Mortality from asthma and chronic bronchitis has been noted to increase in response to worsening air pollution with sulfur dioxide and to decrease with decreased levels of sulfur dioxide air pollution (Imai et al, 1986).
    4) Children exposed to sulfur oxides as air pollutants did not show any statistically significant difference in pulmonary functions, lung growth, or frequency of respiratory disease when compared to controls in a longitudinal study (Dodge et al, 1985).
    5) Persons with a long history of exposure to high concentrations of sulfur dioxide may have an increased incidence of chronic bronchitis accompanied by emphysema (HSDB , 2002).
    6) Although sulfur dioxide itself is not considered a human carcinogen, it is thought to act as a cancer promoter (Bingham et al, 2001).

Workplace Standards

    A) ACGIH TLV Values for CAS7446-09-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Sulfur dioxide
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL: 0.25 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Pulm func; LRT irr
    d) Molecular Weight: 64.07
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7446-09-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Sulfur dioxide
    2) REL:
    a) TWA: 2 ppm (5 mg/m(3))
    b) STEL: 5 ppm (13 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 100 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7446-09-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Sulfur dioxide
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Sulfur dioxide
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Sulfur dioxide
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7446-09-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Sulfur dioxide
    2) Table Z-1 for Sulfur dioxide:
    a) 8-hour TWA:
    1) ppm: 5
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 13
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: ACGIH, 1991 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002
    1) TCLo- (INHALATION)HUMAN:
    a) 3 ppm for 5D -- changes to the respiratory system
    b) 4 ppm (OHM/TADS, 2002)
    c) 12 ppm for 1H -- changes to the respiratory system
    2) TCLo- (INHALATION)MOUSE:
    a) female, 5 ppm at 9D prior to mating and 1-14D of pregnancy -- behavioral effects on newborn
    b) female, 32 ppm for 24H at 7-18D of pregnancy -- effect on growth statistics, behavioral effects in newborn
    c) female, 25 ppm for 7H at 6-15D of pregnancy -- fetotoxicity
    d) female, 25 ppm for 7H at 6-15D of pregnancy -- developmental abnormalities of the musculoskeletal system
    e) 500 ppm for 5M/30W - Intermittent -- equivocal tumorigenic agent by RTECS criteria, tumors of the respiratory system
    3) TCLo- (INHALATION)RAT:
    a) female, 4 mg/m(3) for 24H at 72D prior to mating -- effect on growth statistics of newborn, delayed effects on newborn
    b) female, 4 mg/m(3) for 24H -- change in menstrual cycle, parturition affected, female fertility index affected
    c) female, 4970 mcg/m(3) for 12H at 12W prior to mating -- menstrual cycle changes, effect on growth statistics of newborn
    d) male, 30 ppm for 6H at 21W prior to mating -- effects on testes, epididymis and sperm duct
    e) 10 ppm for 24H/14D - Intermittent -- food intake affected, changes to the liver, biochemical changes (lipids including transport)
    f) 400 ppm for 3H/6W - Intermittent -- structural or functional change in trachea or bronchi
    g) 100 ppm for 5H/28D - Intermittent -- changes to the respiratory system, liver and biochemical changes
    h) 500 mcg/m(3) for 96D - Intermittent -- changes in surface EEG, change in motor activity, changes to xanthine, purine or nucleotides including urate
    i) 4910 mcg/m(3) for 6H/17W - Intermittent -- pigmented or nucleated red blood cells, effects on cytochrome oxidases (including oxidative phosphorylation) and dehydrogenases

Pharmacology Toxicology

Toxicologic Mechanism

    A) IRRITATION/AIR FLOW RESISTANCE - Sulfur dioxide is readily converted to sulfurous acid on contact with tears and mucous and produces pronounced irritant effects on the mucosa of the nasopharynx, respiratory tract, and conjunctiva, as well as bronchoconstriction (Andersen, 1974; (Finkel, 1983; Kizer, 1984; Schachter et al, 1984; Grant & Schuman, 1993). The two most important effects of sulfur dioxide inhalation toxicity are an increase in airflow resistance and alteration in mucous secretion. Increased airway resistance results from reduced buffer and H+ ion absorption capacity of the airway mucous (Eberhardt, 1998; Riechelmann et al, 1995; Devalia et al, 1994) Kitabatke et al, 1995). Liquid sulfur dioxide traumatizes tissues by freezing.
    B) ENHANCED OXIDATIVE STRESS - One study reported that occupational exposure to high levels of sulfur dioxide in agricultural environment (apricot sulfurization) increases oxidative stress and lipid peroxidation may play an important role in the pathogenesis of sulfur dioxide-induced bronchoconstriction. It was found that there was more oxidative burden in the distal airways than proximal airways by sulfur dioxide (Gokirmak et al, 2003).
    C) ALTERED MUCOUS SECRETION - Inhalational exposures in guinea pigs produced a 56 percent decrease in mucociliary activity, but only minor morphological changes with exposure to 7.5 mg/m(3). With higher exposure levels, epithelial sloughing, intracellular edema and mitochondrial swelling, increased intercellular space, and ciliary cytoplasmic extrusion occurred (Riechelmann et al, 1995). Sulfur dioxide exposure studies in mice produced similar findings (Min et al, 1994).
    1) Weanling ferrets exposed for 3 hours to 500 ppm of sulfur dioxide had a loss of cilia, cells developing a phenotype more similar to secretory cells, and a reformation of cilia during a recovery phase (Leigh et al, 1992).

Physicochemical

Physical Characteristics

    A) Sulfur dioxide is a colorless, irritating, nonflammable gas or liquid with a strong, suffocating odor (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000) Freeman, 1989; (Grant & Schuman, 1993; Lewis, 1998; Lewis, 2000; Lewis, 2001).

Ph

    A) Aqueous solution is slightly acidic (HSDB , 2002)

Molecular Weight

    A) 64.06

Other

    A) TASTE THRESHOLD
    1) 0.3 ppm (OHM/TADS , 2002)

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) AAR: Emergency Handling of Hazardous Materials in Surface Transportation, Bureau of Explosives, Association of American Railroads, Washington, DC, 2000.
    14) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.
    15) ACGIH: Documentation of the Threshold Limit Values, 4th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1980.
    16) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    17) ATSDR: ToxFAQs for Sulfur Dioxide, Agency for Toxic Substances and Disease Registry, US Dept of Health and Human Services, Atlanta, GA, 1999.
    18) ATSDR: Toxicological Profile for Sulfur Dioxide, TP 116, Agency for Toxic Substances and Disease Registry, US Dept of Health and Human Services, Atlanta, GA, 1998.
    19) Abdushelishvili AV: SB TR-Nauchno-Issled Inst Sanit Gig (Tiflis) 1977; 13:27-33.
    20) Ackermann-Liebrich U, Leuenberger P, & Schwartz J: Lung function and long term exposure to air pollutants in Switzerland. Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) Team. Am J Respir Crit Care Med 1997; 155:122-129.
    21) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    22) Andersen I, Lundqvist GR, & Jensen PL: Human response to controlled levels of sulfur dioxide. Arch Environ Health 1974; 28:31-39.
    23) Andersson E, Knutsson A, Hagberg S, et al: Incidence of asthma among workers exposed to sulphur dioxide and other irritant gases. Eur Respir J 2006; 27(4):720-725.
    24) Ansell-Edmont: SpecWare Chemical Application and Recommendation Guide. Ansell-Edmont. Coshocton, OH. 2001. Available from URL: http://www.ansellpro.com/specware. As accessed 10/31/2001.
    25) Anttonen S: Changes in lipids of pinus sylvestris needles exposed to industrial air pollution. Ann Botan Fenn 1992; 29:89-99.
    26) Aranyi C: J Toxicol Environ Health 1983; 12:55-71.
    27) Ariel GlobalView. Ariel Research Corporation. Bethesda, MD (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    28) Aristov VN: Gig Tr Prof Zabol 1981; 7:33-36.
    29) Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.
    30) Ashford R: Ashford's Dictionary of Industrial Chemicals, Wavelength Publications Ltd, London, England, 1994.
    31) Balmes JR, Fine JM, & Sheppard D: Symptomatic bronchoconstriction after short-term inhalation of sulfur dioxide. Am Rev Respir Dis 1987; 136:1117-1121.
    32) Baskurt OK: Acute hematologic effects of sulfur dioxide inhalation. Arch Environ Health 1988; 43:344-348.
    33) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    34) Baxter PJ, Adams PH, & Aw TC: Hunter's Diseases of Occupations, 9th ed, Oxford University Press Inc, New York, NY, 2000.
    35) Beauregard M: Modeling of the photosystem-II 33 kDa protein -- structure, functions and possible sulfate-sensitive sites derived from sequence-encoded information. Environ Exp Bot 1992; 32:411-423.
    36) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    37) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    38) Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology, Vol 3. 5th ed, John Wiley & Sons, New York, NY, 2001.
    39) Bond GG, Flores GH, & Shellenberger RJ: Nested case-control study of lung cancer among chemical workers. Am J Epidemiol 1986; 124:53-66.
    40) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    41) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
    42) Buchdahl R, Parker A, & Stebbings T: Association between air pollution and acute childhood wheezy episodes: prospective observational study. Br Med J 1996; 312:661-665.
    43) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996.
    44) Budavari S: The Merck Index, 12th ed. on CD-ROM. Version 12:3a. Chapman & Hall/CRCnetBASE. Whitehouse Station, NJ. 2000.
    45) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    46) CDC: Centers for Disease Control: Sulfur dioxide exposure in Portland cement plants. MMWR 1984; 33:195-196.
    47) CGA: Handbook of Compressed Gases, 3rd ed, Compressed Gas Association, Inc, Van Nostrand Reinhold, New York, NY, 1999.
    48) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    49) Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.
    50) Charan NB, Myers CG, & Lakshminarayan S: Pulmonary injuries associated with acute sulfur dioxide inhalation. Am Rev Respir Dis 1979; 119:555-560.
    51) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    52) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2A, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1993, pp 806-811.
    53) Comasec Safety, Inc.: Chemical Resistance to Permeation Chart. Comasec Safety, Inc.. Enfield, CT. 2003. Available from URL: http://www.comasec.com/webcomasec/english/catalogue/mtabgb.html. As accessed 4/28/2003.
    54) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    55) Council on Scientific Affairs: Effects of toxic chemicals on the reproductive system, American Medical Association, Chicago, IL, 1985.
    56) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    57) Devalia JL, Rusznak C, & Herdman MJ: Effect of nitrogen dioxide and sulphur dioxide on airway response of mild asthmatic patients to allergen inhalation. Lancet 1994; 344:1668-1671.
    58) Dodge R, Solomon P, & Moyers J: A longitudinal study of children exposed to sulfur oxides. Am J Epidemiol 1985; 121:720-736.
    59) Dragun J: The Soil Chemistry of Hazardous Materials, Hazardous Materials Control Research Institute, Silver Spring, MD, 1988.
    60) DuPont: DuPont Suit Smart: Interactive Tool for the Selection of Protective Apparel. DuPont. Wilmington, DE. 2002. Available from URL: http://personalprotection.dupont.com/protectiveapparel/suitsmart/smartsuit2/na_english.asp. As accessed 10/31/2002.
    61) DuPont: Permeation Guide for DuPont Tychem Protective Fabrics. DuPont. Wilmington, DE. 2003. Available from URL: http://personalprotection.dupont.com/en/pdf/tyvektychem/pgcomplete20030128.pdf. As accessed 4/26/2004.
    62) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    63) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    64) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    65) Eberhardt M: Sulfur compounds. In: Harbison RD (Ed): Hamilton and Hardy's Industrial Toxicology, 5th ed, Mosby, St Louis, MO, 1998.
    66) Ebert F: Solving an occupational dermatitis puzzle. Occup Health Nurs 1980; 28:13-16.
    67) Enterline PE, Marsh GM, & Esmen NA: Some effects of cigarette smoking, arsenic, and SO2 on mortality among US copper smelter workers. J Occup Med 1987; 29:831-838.
    68) Euler GL, Abbey DE, & Magie AR: Chronic obstructive pulmonary disease symptom effects of long-term cumulative exposure to ambient levels of total suspended particulates and sulfur dioxide in California Seventh-Day Adventist residents. Arch Environ Health 1987; 42:213-222.
    69) Farone A, Huang S, & Paulauskis J: Airway neutrophilia and chemokine mRNA expression in sulfur dioxide-induced bronchitis. Am J Resp Cell Mol Biol 1995; 12:345-350.
    70) Finkel AJ: Hamilton and Hardy's Industrial Toxicology, 4th ed, John Wright, PSG Inc, Boston, MA, 1983.
    71) Franklin CA, Burnett RT, & Paolini RJP: Health risks from acid rain: A Canadian perspective. Environ Health Perspect 1985; 63:155-168.
    72) Garrett S & Fuerst R: Environ Res 1974; 7:286-293.
    73) Gastaminza G, Quirce S, & Torres M: Pickled onion-induced asthma -- a model of sulfite-sensitive asthma. Clin Exp Allergy 1995; 25:698-703.
    74) Generoso WM: Mutat Res 1978; 56:363-366.
    75) Gokirmak M, Yildirim Z, Canan Hasanoglu H, et al: The role of oxidative stress in bronchoconstriction due to occupational sulfur dioxide exposure. Clinical Chimica Acta 2003; 331:119-126.
    76) Goldfrank LR: Goldgrank's Toxicological Emergencies, 6th ed, McGraw-Hill, New York, NY, 1998.
    77) Goldstein IF & Weinstein AL: Environ Res 1986; 40:332-345.
    78) Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, Williams & Wilkins, Baltimore, MD, 1984.
    79) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    80) Grant WM: Toxicology of the Eye, 2nd ed, Charles C. Thomas, Springfield, IL, 1974.
    81) Grant WM: Toxicology of the Eye, 3rd ed, Charles C Thomas, Springfield, IL, 1986.
    82) Greene SA, Wolff RK, & Hahn FF: Sulfur dioxide-induced chronic bronchitis in beagle dogs. J Toxicol Environ Health 1984; 13:945-958.
    83) Grieve AW, Davis P, Dhillon S, et al: A clinical review of the management of frostbite. J R Army Med Corps 2011; 157(1):73-78.
    84) Guardian Manufacturing Group: Guardian Gloves Test Results. Guardian Manufacturing Group. Willard, OH. 2001. Available from URL: http://www.guardian-mfg.com/guardianmfg.html. As accessed 12/11/2001.
    85) Guerra D: Experientia 1981; 37:691-693.
    86) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    87) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2004; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    88) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    89) Hallam MJ, Cubison T, Dheansa B, et al: Managing frostbite. BMJ 2010; 341:c5864-.
    90) Harbison RD: Hamilton & Hardy's Industrial Toxicology, 5th ed, Mosby-Year Books, St. Louis, MO, 1998.
    91) Harkonen H, Nordman H, & Korhonen O: Long-term effects of exposure to sulfur dioxide. Am Rev Respir Dis 1983; 128:890-893.
    92) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 4th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    93) Heath SK, Koenig JQ, & Morgan MS: Effects of sulfur dioxide exposure on African-American and caucasian asthmatics. Environ Res 1994; 66:1-11.
    94) Hemminki K & Niemi M-L: Internat Arch Occup Environ Health 1982; 51:55-64.
    95) Hemminki K: Am J Ind Med 1983; 4:293-308.
    96) Hickey RJ: Mutat Res 1974; 26:445-446.
    97) Horstman DH, Seal E, & Folinsbee LJ: The relationship between exposure duration and sulfur dioxide-induced bronchoconstriction in asthmatic subjects. Am Ind Hyg Assoc J 1988; 49:38-47.
    98) Huber AL & Loving TJ: Fatal asthma attack after inhaling sulfur fumes (letter). JAMA 1991; 266:2225.
    99) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    100) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    101) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    102) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    103) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    104) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    105) IARC: Monographs on the Evaluation of Carcinogenicity of Chemicals to Humans. Sulfur Dioxide and Some Sulfites, Bisulfites and Metabolites (Group 3). 1972-PRESENT (Multivolume work). 54. International Agency for Research on Cancer, World Health Organization. Geneva, Switzerland. 1992. Available from URL: http://193.51.164.11/htdocs/Monographs/Vol45/ /02-Sulfur-dioxide.htm. As accessed Accessed March 5, 2002.
    106) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    107) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    108) ILO: Encyclopaedia of Occupational Health and Safety, 3rd ed, Vols 1 & 2, International Labour Organization, Geneva, Switzerland, 1983.
    109) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1988.
    110) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1995.
    111) Imai M, Yoshida K, & Kitabatake M: Mortality from asthma and chronic bronchitis associated with changes in sulfur oxides air pollution. Arch Environ Health 1986; 41:29-35.
    112) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    113) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    114) Jappinen P & Tola S: Cardiovascular mortality among pulp mill workers. Br J Ind Med 1990; 47:259-262.
    115) Kappler, Inc.: Suit Smart. Kappler, Inc.. Guntersville, AL. 2001. Available from URL: http://www.kappler.com/suitsmart/smartsuit2/na_english.asp?select=1. As accessed 7/10/2001.
    116) Katsouyanni K, Touloumi G, & Spix C: Short-term effects of ambient sulphur dioxide and particulate matter on mortality in 12 European cities: results from time series data from the APHEA project. Air Pollution and Health: a European Approach. Br Med J 1997; 314:1658-1663.
    117) Kienast K, Riechelmann H, & Knorst M: An experimental model for the exposure of human ciliated cells to sulfur dioxide at different concentrations. Clin Invest 1994; 72:215-219.
    118) Kimberly-Clark, Inc.: Chemical Test Results. Kimberly-Clark, Inc.. Atlanta, GA. 2002. Available from URL: http://www.kc-safety.com/tech_cres.html. As accessed 10/4/2002.
    119) Kitabatake M, Yamamoto H, & Yuan PF: Effects of exposure to NO2 or SO2 on bronchopulmonary reaction induced by Candida albicans in guinea pigs. J Toxicol Environ Health 1995; 45:75-82.
    120) Kizer KW: Toxic inhalations. Emerg Med Clin North Am 1984; 2:649-666.
    121) Knorst MM, Kienast K, & Gross S: Chemotactic response of human alveolar macrophages and blood monocytes elicited by exposure to sulfur dioxide. Res Exp Med (Berl) 1996; 196:127-135.
    122) Koenig JQ, Covert DS, & Hanley QS: Prior exposure to ozone potentiates subsequent response to sulfur dioxide in adolescent asthmatic subjects. Am Rev Respir Dis 1990; 141:377-380.
    123) Koenig JQ, Marshall SG, & Horike M: The effects of albuterol on sulfur dioxide-induced bronchoconstriction in allergic adolescents. J Allergy Clin Immunol 1987; 79:54-58.
    124) Koenig JQ: CRISP/85/ES02366-05--USPHS Crisp Data Base, 1985.
    125) Koepke JW, Selner JC, & Dunhill AC: Presence of sulfur dioxide in commonly used bronchodilator solutions. J Allergy Clin Immunol 1983; 72:504.
    126) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    127) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    128) Lee AM & Fraumeni JF Jr: J Natl Cancer Inst 1969; 42:1045-1052.
    129) Leigh MW, Carson JL, & Gambling TM: Loss of cilia and altered phenotypic expression of ciliated cells after acute sulfur dioxide exposure. Chest 1992; 101(3 suppl):16s.
    130) Lewis RA: Lewis' Dictionary of of Toxicology, Lewis Publishers, Boca Raton, FL, 1998.
    131) Lewis RJ: Hawley's Condensed Chemical Dictionary, 12th ed, Van Nostrand Reinhold Company, New York, NY, 1993.
    132) Lewis RJ: Hawley's Condensed Chemical Dictionary, 14th ed, John Wiley & Sons, Inc, New York, NY, 2001.
    133) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 10th ed, Van Nostrand Reinhold Company, New York, NY, 2000.
    134) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 8th ed, Van Nostrand Reinhold Company, New York, NY, 1992.
    135) Linn WS, Avol EL, & Peng RC: Replicated dose-response study of sulfur dioxide effects in normal, atopic, and asthmatic volunteers. Am Rev Respir Dis 1987; 136:1127-1134.
    136) Linn WS, Shamoo DA, & Peng RC: Responses to sulfur dioxide and excercise by medication-dependent asthmatics: effect of varying medication levels. Arch Environ Health 1990; 45:24-30.
    137) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2003. Available from URL: http://www.mapaglove.com/pro/ChemicalSearch.asp. As accessed 4/21/2003.
    138) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2004. Available from URL: http://www.mapaglove.com/ProductSearch.cfm?id=1. As accessed 6/10/2004.
    139) Mallon RG & Rossman TG: Mutat Res 1981; 88:125-133.
    140) Mamatsashvili MI: Gig Sanit 1970; 35:100-101.
    141) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    142) Marigold Industrial: US Chemical Resistance Chart, on-line version. Marigold Industrial. Norcross, GA. 2003. Available from URL: www.marigoldindustrial.com/charts/uschart/uschart.html. As accessed 4/14/2003.
    143) McManus MS, Koenig JQ, & Altman LC: Pulmonary effects of sulfur dioxide exposure and ipratropium bromide pretreatment in adults with nonallergic asthma. J Allergy Clin Immunol 1989; 83:619-626.
    144) Memphis Glove Company: Permeation Guide. Memphis Glove Company. Memphis, TN. 2001. Available from URL: http://www.memphisglove.com/permeation.html. As accessed 7/2/2001.
    145) Meng Z & Bai W: Oxidation damage of sulfur dioxide on testicles of mice. Environ Res 2004; 96(3):298-304.
    146) Min YG, Rhee CS, & Choo MJ: Histopathologic changes in the olfactory epithelium in mice after exposure to sulfur dioxide. ACTA Otolaryngol 1994; 114:447-452.
    147) Mohren GM, Jorritsma IT, & Vermetten AW: Quantifying the direct effects of SO2 and O3 on forest growth. Forest Ecol Manage 1992; 51:137-150.
    148) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    149) Moolgavkar SH, Luebeck EG, & Anderson EL: Air pollution and hospital admissions for respiratory causes in Minneapolis-St. Paul and Birmingham. Epidemiology 1997; 8:364-370.
    150) Murphy JV, Banwell PE, & Roberts AHN: Frostbite: pathogenesis and treatment. J Trauma 2000; 48:171-178.
    151) Murray FJ, Schwetz BA, & Crawford AA: Embryotoxicity of inhaled sulfur dioxide and carbon monoxide in mice and rabbits. J Environ Sci Health 1979; 13:233-250.
    152) NFPA: Fire Protection Guide to Hazardous Materials, 12th ed, National Fire Protection Association, Quincy, MA, 1997.
    153) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    154) NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.
    155) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    156) NIOSH: Criteria for a Recommended Standard: Occupational Exposure to Sulfur Dioxide, National Institute for Occupational Safety and Health, Washington, DC, 1974, pp 18-82.
    157) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    158) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    159) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    160) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    161) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    162) Nat-Wear: Protective Clothing, Hazards Chart. Nat-Wear. Miora, NY. 2001. Available from URL: http://www.natwear.com/hazchart1.htm. As accessed 7/12/2001.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    185) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    186) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    187) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    188) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    189) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    190) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    191) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    192) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    193) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    194) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    195) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    196) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    197) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    198) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    199) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    200) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    201) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    202) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    203) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    204) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    205) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    206) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    207) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    208) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    209) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    210) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    211) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    212) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    213) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    214) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    215) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    216) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    217) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    218) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    219) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    220) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    221) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    222) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    223) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    224) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    225) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    226) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    227) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    228) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    229) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    230) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    231) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    232) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    233) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    234) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    235) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    236) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    237) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    238) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    239) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    240) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    241) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    242) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    243) Neese Industries, Inc.: Fabric Properties Rating Chart. Neese Industries, Inc.. Gonzales, LA. 2003. Available from URL: http://www.neeseind.com/new/TechGroup.asp?Group=Fabric+Properties&Family=Technical. As accessed 4/15/2003.
    244) Nordenson I: Hereditas 1980; 93:161-164.
    245) Nordstrom S: Hereditas 1978; 88:51-54.
    246) North: Chemical Resistance Comparison Chart - Protective Footwear . North Safety. Cranston, RI. 2002. Available from URL: http://www.linkpath.com/index2gisufrm.php?t=N-USA1. As accessed April 30, 2004.
    247) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    248) OHM/TADS : Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    249) OHM/TADS: Oil and Hazardous Materials Technical Assistance Data System. US Environmental Protection Agency. Washington, D.C. (Internet Version). Edition expires 2004; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    250) OSHA: 29 CFR 1910.101. Compressed gases (general requirements). Final rules effective through January 1, 2002, Occupational Safety and Health Administration, Washington, DC, 2002c.
    251) Ohashi Y, Nakai Y, & Koshimo H: Acute effects of sulfur dioxide exposure on the middle ear mucosa. Ann Otol Rhinol Laryngol 1989; 98:301-307.
    252) Ostapovich IK: Gig Sanit 1975; 2:9-13.
    253) Osterman JW, Greaves IA, & Smith TJ: Respiratory symptoms associated with low level sulphur dioxide exposure in silicon carbide production workers. Br J Ind Med 1989; 46:629-635.
    254) Pauluhn J: Exp Pathol (JENA) 1985; 28:31.
    255) Peacock PR & Spence JB: Br J Cancer 1967; 21:606-618.
    256) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    257) Peters A, Goldstein IF, & Beyer U: Acute health effects of exposure to high levels of air pollution in eastern Europe. Am J Epidemiol 1996; 144:570-581.
    258) Petruzzi S, Dell'Omo G, & Fiore M: Behavioural disturbances in adult CD-1 mice and absence of effects on their offspring upon SO2 exposure. Arch Toxicol 1996; 70:757-766.
    259) Piirila PL, Nordman H, & Korhonen OS: A thirteen-year follow-up of respiratory effects of acute exposure to sulfur dioxide. Scand J Work Environ Health 1996; 22:191-196.
    260) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    261) Plunkett ER: Handbook of Industrial Toxicology, Chemical Publishing Co, Inc, New York, NY, 1976.
    262) Pohanish RP & Greene SA: Rapid Guide to Chemical Incompatibilities, Van Nostrand Reinhold Company, New York, NY, 1997.
    263) Ponka A & Virtanen M: Asthma and ambient air pollution in Helsinki. J Epidemiol Community Health 1996; 50 (Suppl 1):s59-62.
    264) Ponka A: Absenteeism and respiratory disease among children and adults in Helsinki in relation to low-level air pollution and temperature. Environ Res 1990; 52:34-46.
    265) Pott F & Stober W: Environ Health Perspect 1983; 47:293-303.
    266) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    267) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 5/31/2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    268) Rabinovitch S, Greyson ND, & Weiser W: Clinical and laboratory features of acute sulfur dioxide inhalation poisoning: two-year follow-up. Am Rev Respir Dis 1989; 139:556-558.
    269) Rahlenbeck SI & Kahl H: Air pollution and mortality in East Berlin during the winters of 1981-1989. Internat J Epidemiol 1996; 25:1220-1226.
    270) Riechelmann H, Maurer J, & Kienast K: Respiratory epithelium exposed to sulfur dioxide -- functional and ultrastructural alterations. Laryngoscope 1995; 105:295-299.
    271) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    272) Roger LJ, Kehrl HR, & Hazucha M: Bronchoconstriction in asthmatics exposed to sulfur dioxide during repeated exercise. J Appl Physiol 1985; 59:784-791.
    273) Rom WN, Wood SD, & White GL: Longitudinal evaluation of pulmonary function in copper smelter workers exposed to sulfur dioxide. Am Rev Respir Dis 1986; 133:830-833.
    274) Romieu I, Meneses F, & Sienra-Monge JJ: Effects of urban air pollutants on emergency visits for childhood asthma in Mexico City. Am J Epidemiol 1995; 141:546-553.
    275) Ronneberg A: Mortality and cancer morbidity in workers from an aluminium smelter with prebaked carbon anodes. 1. Exposure assessment. Occup Environ Med 1995a; 52:242-249.
    276) Ronneberg A: Mortality and cancer morbidity in workers from an aluminium smelter with prebaked carbon anodes. 3. Mortality from circulatory and respiratory diseases. Occup Environ Med 1995b; 52:255-261.
    277) Rosenhall L & Stjernberg N: Sulphur dioxide and bronchitis. Eur J Respir Dis 1982; 118(Suppl):91-94.
    278) Safety 4: North Safety Products: Chemical Protection Guide. North Safety. Cranston, RI. 2002. Available from URL: http://www.safety4.com/guide/set_guide.htm. As accessed 8/14/2002.
    279) Sandstrom T, Stjernberg N, & Andersson MC: Is the short term limit value for sulphur dioxide exposure safe? Effects of controlled chamber exposure investigated with bronchoalveolar lavage. Br J Ind Med 1989; 46:200-203.
    280) Savic M, Siriski-Sasic J, & Djulizibaric D: Discomforts and laboratory findings in workers exposed to sulfur dioxide. Internat Arch Occup Environ Health 1987; 59:513-518.
    281) Schachter EN, Witek TJ, & Beck GJ: Airway effects of low concentrations of sulfur dioxide: Dose-response characteristics. Arch Environ Health 1984; 39:34-42.
    282) Schneider LK & Calkins CA: Environ Res 1970; 3:473-483.
    283) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    284) Shalamberidze OP & Tsereteli NT: Gig Sanit 1971; 36:178-182.
    285) Shapiro R: Mutat Res 1977; 39:149-175.
    286) Sheppard D: Am Rev Respir Dis 1981; 123:486.
    287) Singh J: Neonatal development altered by maternal sulfur dioxide exposure. Neurotoxicology 1989; 10:523-528.
    288) Singh J: Proc Inst Environ Sci 1982; 28:144-145.
    289) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.
    290) Smith TJ, Peters JM, & Reading JC: Pulmonary impairment from chronic exposure to sulfur dioxide in a smelter. Am Rev Resp Dis 1977; 116:31-39.
    291) Sorsa M et al: Hereditas, 1982.
    292) Soyseth V, Kongerud J, & Haarr D: Relation of exposure to airway irritants in infancy to prevalence of bronchial hyper-responsiveness in schoolchildren. Lancet 1995; 345:217-220.
    293) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    294) Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.
    295) Student PJ: Emergency Handling of Hazardous Materials in Surface Transportation, Bureau of Explosives, Association of American Railroads, Washington, DC, 1981, pp 486.
    296) Sunyer J, Castellsague J, & Saez M: Air pollution and mortality in Barcelona. J Epidemiol Community Health 1996; 50(Suppl 1):s76-80.
    297) Sunyer J, Spix C, & Quenel P: Urban air pollution and emergency admissions for asthma in four European cities: the APHEA Project. Thorax 1997; 52:760-765.
    298) Thomas FM & Runge M: Proton neutralization in the leaves of english oak (quercus robur L) exposed to sulphur dioxide. J Exp Botany 1992; 43:803-809.
    299) Tingley: Chemical Degradation for Footwear and Clothing. Tingley. South Plainfield, NJ. 2002. Available from URL: http://www.tingleyrubber.com/tingley/Guide_ChemDeg.pdf. As accessed 10/16/2002.
    300) Trelleborg-Viking, Inc.: Chemical and Biological Tests (database). Trelleborg-Viking, Inc.. Portsmouth, NH. 2002. Available from URL: http://www.trelleborg.com/protective/. As accessed 10/18/2002.
    301) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    302) Tsereteli NT: Aktual Vopr Gig Naselennykh Mest, Mater Vses Konf Molodykh Uchenykh, 1971.
    303) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    304) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    305) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    306) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    307) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    308) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    309) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    310) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    311) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    312) US DHHS: Occupational Health Guidelines for Sulfur Dioxide. DHHS (NIOSH) Publication No 81-123, 1981.
    313) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    314) Urben PG: Bretherick's Reactive Chemical Hazards Database, Version 3.0, Butterworth-Heinemann Ltd, Oxford, UK, 1999.
    315) Vigotti MA, Rossi G, & Bisanti L: Short term effects of urban air pollution on respiratory health in Milan, Italy, 1980-89. J Epidemiol Community Health 1996; 50(Suppl 1):s71-75.
    316) Wells Lamont Industrial: Chemical Resistant Glove Application Chart. Wells Lamont Industrial. Morton Grove, IL. 2002. Available from URL: http://www.wellslamontindustry.com. As accessed 10/31/2002.
    317) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    318) Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.
    319) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.
    320) Yoon JS: Genetics 1981; 97:S117.
    321) Yun DR: Seoul J Med 1976; 16:242-246.
    322) Zarkower A: Arch Environ Health 1972; 25:45-50.
    323) von Mutius E, Sherrill DL, & Fritsch C: Air pollution and upper respiratory symptoms in children from East Germany. Eur Respir J 1995; 8:723-728.