MOBILE VIEW  | 

SULFUR TRIOXIDE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Sulfur trioxide is an irritant/caustic most often found in industrial settings. Will produce sufluric acid when combined with water.

Specific Substances

    1) Sulfur trioxide
    2) Sulfan
    3) Sulfuric anhydride
    4) Sulfuric oxide
    5) Sulfur trioxide, inhibited
    6) Sulfur trioxide, stabilized
    7) Triosul
    8) CAS 7446-11-9
    9) References: RTECS, 1994
    1.2.1) MOLECULAR FORMULA
    1) O3-S
    2) SO3

Available Forms Sources

    A) USES
    1) Intermediate in sulfuric acid manufacture; in sulfonations for formation of addition cmpd with amines; in the manufacture of explosives (HSDB , 1994).
    2) Sulfonation of organic compounds, especially non ionic detergents; solar energy collectors (HSDB , 1994).
    3) Used for preparing sulfonated oils, and alkyl arenesulfonate detergents (HSDB , 1994).
    4) Used as a powerful, but generally indiscriminate oxidizing agent, however, it will selectively oxidize pentachlorotoluene and similar compounds to the alcohol (HSDB , 1994).
    5) Its principle applications are in production of detergents and as a raw material for chlorosulfuric acid and 65% oleum (HSDB , 1994).

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) The major toxic effects of sulfur trioxide mimic those of SULFURIC ACID.
    1) It is IRRITATING or CORROSIVE to the eyes, skin, and mucous membranes.
    2) CHEMICAL PNEUMONITIS or NONCARDIOGENIC PULMONARY EDEMA may occur following inhalation.
    B) FROSTBITE INJURY may occur with dermal exposure to liquified sulfur trioxide.
    0.2.3) VITAL SIGNS
    A) Hypotension and bradycardia may occur as premorbid events in serious overexposure.
    0.2.4) HEENT
    A) EYES - Sulfur trioxide fumes are very irritating to the eyes. It may cause severe eye injury following direct contact.
    B) NASOPHARYNGEAL - Exposure is very irritating to the upper respiratory tract and may cause burns of the mucous membranes, glottis, and nasopharynx. Edema may cause upper airway obstruction.
    0.2.5) CARDIOVASCULAR
    A) Hypotension, depressed cardiac output and bradycardia may occur.
    0.2.6) RESPIRATORY
    A) ACUTE EXPOSURE - Bronchospasm, wheezing, and noncardiogenic pulmonary edema may occur. Pulmonary hemorrhages have been seen in fatally-exposed experimental animals.
    B) CHRONIC EXPOSURE - Chronic obstructive pulmonary disease may occur. Chronic bronchitis with wheezing may be noted. Individuals with pre-existing bronchitis, bronchial asthma, or emphysema may be at greater risk.
    0.2.8) GASTROINTESTINAL
    A) Esophageal or gastrointestinal tract irritation or burns may be predicted to occur; late stricture formation could develop. Nausea, vomiting, abdominal pain, bleeding, or perforation could occur acutely.
    0.2.14) DERMATOLOGIC
    A) BURNS - Serious caustic burns may develop following direct skin contact.
    B) FROSTBITE INJURY - Direct skin contact with the liquified material may cause frostbite injury.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) No methods for measurement of sulfur trioxide in biological samples were listed in available references at the time of this review.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) DO NOT INDUCE VOMITING - or give bicarbonate to neutralize. Activated charcoal is of no value. Gastric lavage is not likely to be beneficial, and carries the risk of complications of bleeding or perforation.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) Evaluate for pharyngeal, esophageal, or gastric burns.
    D) In severe cases of gastrointestinal necrosis or perforation, surgical consultation should be obtained.
    E) Sucralfate may be useful in relieving symptomatology from acid-induced injury.
    F) Obtain a follow-up esophagogram and upper GI series to evaluate for the presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
    G) Steroid use is debatable. Dose is 1 to 2 mg/kg/day of prednisone or other equivalent steroid.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    C) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    E) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    F) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    G) Patients developing chronic obstructive pulmonary disease following severe acute overexposure or long-term exposure may benefit from bronchodilating medications and a regimen of respiratory therapy.
    H) Smoking should be highly discouraged, and further sulfur trioxide or other oxides of sulfur exposure should be avoided.
    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.
    B) Prolonged initial flushing and early ophthalmologic consultation are advisable.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.
    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.
    3) Treatment of CHEMICAL BURNS may be required. Refer to the TREATMENT/DERMAL EXPOSURE section in the main body of this document for more information.

Range Of Toxicity

    A) The minimum lethal human dose to this agent has not been delineated.
    B) In volunteer studies, 0.08 to 1.25 ppm lead to respiratory stimulation; 5.2 ppm, a 20% increase in airway resistance was seen; 10 ppm caused coughing and throat irritation.

Summary Of Exposure

    A) The major toxic effects of sulfur trioxide mimic those of SULFURIC ACID.
    1) It is IRRITATING or CORROSIVE to the eyes, skin, and mucous membranes.
    2) CHEMICAL PNEUMONITIS or NONCARDIOGENIC PULMONARY EDEMA may occur following inhalation.
    B) FROSTBITE INJURY may occur with dermal exposure to liquified sulfur trioxide.

Vital Signs

    3.3.1) SUMMARY
    A) Hypotension and bradycardia may occur as premorbid events in serious overexposure.
    3.3.2) RESPIRATIONS
    A) COUGH/DYSPNEA - Patients may present with severe cough and dyspnea.
    3.3.4) BLOOD PRESSURE
    A) HYPOTENSION may occur as a premorbid event in serious overexposure (Aviado & Salem, 1968).
    3.3.5) PULSE
    A) BRADYCARDIA may occur as a premorbid event in serious overexposure (Aviado & Salem, 1968).

Heent

    3.4.1) SUMMARY
    A) EYES - Sulfur trioxide fumes are very irritating to the eyes. It may cause severe eye injury following direct contact.
    B) NASOPHARYNGEAL - Exposure is very irritating to the upper respiratory tract and may cause burns of the mucous membranes, glottis, and nasopharynx. Edema may cause upper airway obstruction.
    3.4.3) EYES
    A) IRRITATION - Exposure to sulfur trioxide fumes is very irritating to the eyes (Grant, 1986).
    B) BURNS - Severe eye injury, similar to that seen with concentrated sulfuric acid, may be seen following direct eye contact with sulfur trioxide (Grant, 1986).
    3.4.5) NOSE
    A) IRRITATION - Exposure to fumes may cause irritation of the mucosa of the nose and throat (Sax & Lewis, 1989; EPA, 1985; HSDB , 1990).
    3.4.6) THROAT
    A) IRRITATION - Exposure to fumes may cause irritation of the mucosa of the nose and throat (Sax & Lewis, 1989; EPA, 1985; HSDB , 1990).

Cardiovascular

    3.5.1) SUMMARY
    A) Hypotension, depressed cardiac output and bradycardia may occur.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) Hypotension and a depressed cardiac output may occur as premorbid events in serious overexposure (Aviado & Salem, 1968).
    B) BRADYCARDIA
    1) Bradycardia may occur as a premorbid event in serious overexposure (Aviado & Salem, 1968).

Respiratory

    3.6.1) SUMMARY
    A) ACUTE EXPOSURE - Bronchospasm, wheezing, and noncardiogenic pulmonary edema may occur. Pulmonary hemorrhages have been seen in fatally-exposed experimental animals.
    B) CHRONIC EXPOSURE - Chronic obstructive pulmonary disease may occur. Chronic bronchitis with wheezing may be noted. Individuals with pre-existing bronchitis, bronchial asthma, or emphysema may be at greater risk.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Inhalation of fumes is very irritating to the respiratory tract (Sax & Lewis, 1987; Sax & Lewis, 1989; EPA, 1985; HSDB , 1990).
    B) BRONCHOSPASM
    1) Bronchospasm and wheezing may occur (ILO, 1983).
    C) ACUTE LUNG INJURY
    1) Noncardiogenic pulmonary edema may develop (Aviado & Salem, 1968). Pulmonary hemorrhages have been seen in fatally-exposed experimental animals (Aviado & Salem, 1968).

Gastrointestinal

    3.8.1) SUMMARY
    A) Esophageal or gastrointestinal tract irritation or burns may be predicted to occur; late stricture formation could develop. Nausea, vomiting, abdominal pain, bleeding, or perforation could occur acutely.
    3.8.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Ingestions have not been reported, but the possible development of esophageal or gastrointestinal tract irritation or burns may be predicted based on this agent's other corrosive properties.
    2) Nausea, vomiting, abdominal pain, bleeding, or perforation could occur acutely.
    B) STRICTURE OF ESOPHAGUS
    1) If serious esophageal or gastric burns occurred following ingestion, late stricture formation could develop.

Dermatologic

    3.14.1) SUMMARY
    A) BURNS - Serious caustic burns may develop following direct skin contact.
    B) FROSTBITE INJURY - Direct skin contact with the liquified material may cause frostbite injury.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Serious dermal burns may develop following direct skin contact with this material (Sax & Lewis, 1987; Sax & Lewis, 1989; EPA, 1985).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7446-11-9 (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) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of this agent.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No methods for measurement of sulfur trioxide in biological samples were listed in available references at the time of this review.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No methods for measurement of sulfur trioxide in biological samples were listed in available references at the time of this review.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Increased sulfates in the urine may be seen after exposure, but this finding may be confounded by diet and is of undetermined utility in the clinical assessment of exposed patients.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Sulfur trioxide can be measured in air samples, even when other acid gases are present or the samples are highly colored or turbid, by a technique where all oxides of sulfur are oxidized and precipitated with barium, forming barium sulfate.
    a) The barium in this precipitate is then assayed by measuring the intensity of alpha emission produced by x-ray excitation in this x-ray emission spectrometric method (Cares, 1968).
    2) A second method for air monitoring uses samples collected on perimidylammonium bromide impregnated filters in two open-faced filter holders, followed by pyrolization of the collected material to evolve sulfur dioxide, which is then measured by the West-Gaeke procedure (Thomas et al, 1976).
    a) This method has a limit of detection of 0.3 micrograms and a working range of 1 to 50 micrograms (Thomas et al, 1976).
    3) BIOLOGIC SAMPLES - No methods could be found in available references.

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 observation (Kizer, 1984).
    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 observation (Kizer, 1984).

Monitoring

    A) No methods for measurement of sulfur trioxide in biological samples were listed in available references at the time of this review.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED -
    1) Induced emesis is not indicated. Dilution with small amounts of fluids may be of some use. Patients should be evaluated for oral and esophageal burns. Do not use neutralizing solutions by mouth. Treatment is primarily symptomatic.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) ACIDS - The major toxicity of sulfur trioxide following ingestion is predicted to mimic ingestion of concentrated sulfuric acid. The following treatment recommendations are adapted from those for ACIDS.
    B) EMESIS/NOT RECOMMENDED
    1) DO NOT INDUCE VOMITING - Activated charcoal is of no value. Gastric lavage is not likely to be beneficial, and carries the risk of complications of perforation or bleeding.
    C) DILUTION
    1) Immediate dilution with milk or water might be beneficial.
    2) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    6.5.3) TREATMENT
    A) SUPPORT
    1) DO NOT INDUCE VOMITING - or give bicarbonate to neutralize. Addition of buffer to strong acid causes an exothermic reaction and an immediate rise in solution temperature (Maull et al, 1985).
    B) IRRIGATION
    1) Irrigate the mouth with copious amounts of water. Immediate dilution with small amounts of milk or water may help decontaminate the oral mucosa or dislodge particles of granular acids from the esophageal mucosa.
    2) The amount of diluent recommended by the POISINDEX editorial board for caustic alkali ingestion varied, and may be useful in establishing guidelines for acid ingestion. Suggestions ranged from 2 to 12 ounces in adults and 1 to 8 ounces in children. The majority recommended a maximum amount of 8 ounces in adults and 4 ounces in children (Consensus, 1988).
    3) Dilution of acid with water has been shown to be ineffective in altering the pH. The dilution of 50 mL of 9.5% HCl with 800 mL of water resulted in a pH change of 0.99 to 1.73 (Maull et al, 1985).
    4) DEMULCENTS - Follow dilution with appropriate demulcents - milk, cornstarch, and water.
    C) SUCRALFATE
    1) Administration of sucralfate, 1 g dissolved in 30 milliliters of water, four times a day, was used in a 25-year-old man with moderately severe gastric injury after ingestion of hydrochloric acid. No other therapy was given other than antibiotics. Within 48 hours, improvement in symptoms was noted, enabling progression to a liquid diet on the 3rd day.
    a) Similar to studies where sucralfate was used in alkali caustic injury, strictures were not prevented, although nearly complete gastric mucosal healing occurred after 2 weeks. The patient received a gastrojejunostomy for pyloric stricture 6 weeks postingestion (Mittal et al, 1989).
    2) Sucralfate may be useful in relieving symptomatology from acid-induced injury. Efficacy in accelerating healing or preventing complications has not been proven.
    D) INSERTION OF NASOGASTRIC TUBE
    1) Penner (1980) argues that following a large ingestion of strong acids, a nasogastric tube should be passed and suction performed in an attempt to remove as much acid as possible prior to cold water dilution which may result in an exothermic reaction (giving off heat) and worsen the burn.
    2) Many authorities oppose this procedure, fearing esophageal or gastric perforation. Soft nasogastric or orogastric tube should only be passed within 90 minutes following ingestion of a large amount of a strong acid.
    E) DIETARY FINDING
    1) Depends on degree of damage as assessed by early endoscopy (Dilawari et al, 1984).
    1) Mild (grade I) - may have oral feedings first day
    2) Moderate (grade II) - may have liquids after 48 to 72 hours
    3) Severe (grade III) - jejunostomy tube feedings after 48 to 72 hours
    F) BURN
    1) If severe burns occur in the mouth, then esophageal burns may exist. It is reportedly unusual to have esophageal burns. Most burns occur in the pyloric end of the stomach.
    2) However, Muhletaler et al (1980) reviewed 39 esophagograms from 27 patients with a proven history of swallowing muriatic acid (27% HCl). All esophagograms obtained 11 to 16 days postingestion showed areas of narrowing, submucosal edema, atony, and mucosal ulceration.
    a) Twenty-one esophagograms obtained at least 21 days following ingestion showed stricture formation. Edema and esophageal mucosal ulcerations radiologically appeared as blurring or contour irregularities along the esophageal margins.
    3) Dilawari et al (1984) recommend early endoscopy in order to grade severity of injury (mild, moderate, severe) and predict prognosis. All patients with severe burns developed complications such as perforation, stricture, or massive hematemesis. Endoscopy did not contribute to complications. No complications developed in the mild to moderate injury patients.
    4) In a prospective study of 41 patients who ingested 50 to 200 milliliters of 20 to 35 percent acid solutions, all were assessed for location, extent, and severity of injury within 36 hours of ingestion by endoscopy or surgery, or at autopsy. Esophageal injury was present in 87.8 percent of the patients, gastric injury in 85.4 percent, and duodenal injury in 34.1 percent.
    a) Strictures, perforation, or both developed only in patients with Grade 2b (superficial localized ulceration, friability, blisters, and circumferential ulceration) and Grade 3 (multiple and deep ulcerations and areas of extensive necrosis) burns (Zargar et al, 1989). No complications relating to the endoscopic procedure were reported in this series.
    G) OBSTRUCTION
    1) Observe for symptoms of acute obstruction (pyloric spasm), at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestions.
    a) One 3-year-old child developed esophageal stricture 2 years after the acid ingestion in a prospective study of 41 patients. This child had a normal barium study at one year after ingestion (Zargar et al, 1989).
    H) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    I) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984a).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died, while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.
    J) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) 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.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) 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) OXYGEN
    1) With severe dyspnea or hypoxemia, administer humidified 100% oxygen until symptoms subside.
    B) BURN
    1) Evaluate for nasopharyngeal burns.
    C) EXPERIMENTAL THERAPY
    1) In rabbits, isoproterenol and aminophylline significantly reduced the increased pulmonary artery pressure, vascular permeability, and fluid-flux associated with hydrochloric acid lung injury (Mizus et al, 1985).
    D) AIRWAY MANAGEMENT
    1) Endotracheal intubation or tracheostomy may be required if upper airway edema produces airway obstruction.
    E) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents. Avoid bronchodilators containing sulfite preservatives (ie, isoetharine).
    F) 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).
    G) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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) OPHTHALMIC EXAMINATION AND EVALUATION
    1) CONSULTATION - Because of the potential for severe eye injury following direct contact with this material, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE 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) BURN
    1) Dermal injury can occur from direct contact with sulfurous acid formed from sulfur trioxide and water. This injury should be treated as any other chemical burn. Treat burns prophylactically for infection.
    2) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    3) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    4) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    5) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) ACUTE ALLERGIC REACTION
    1) URTICARIA - Urticaria or other hypersensitivity rashes may be treated with antihistamines and corticosteroids (Ebert, 1980; NIOSH, 1974).
    C) 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).
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Case Reports

    A) ROUTE OF EXPOSURE
    1) INHALATION
    a) SULFURIC ACID ANALOGUE - A group of 20 workers exposed to sulfuric acid in the manufacture of storage batteries and a comparable control group of unexposed workers from the same factory were studied.
    b) The concentrations of sulfuric acid, measured in the environment, were substantially higher than currently accepted standards; however, the size of the acid droplets and the proportion which would be sufficiently small to enter nasal passages were not given.
    2) The increased prevalence of abnormal respiratory function tests were not statistically significant. The prevalence of discolored or eroded teeth was significantly higher in the exposed group, and varied directly with years of exposure (El-Sadik, 1977).

Summary

    A) The minimum lethal human dose to this agent has not been delineated.
    B) In volunteer studies, 0.08 to 1.25 ppm lead to respiratory stimulation; 5.2 ppm, a 20% increase in airway resistance was seen; 10 ppm caused coughing and throat irritation.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    2) Published values (EPA, 1985; RTECS , 1990) -
    1) TCLo (INHL) HUMAN - 30 mg/m(3)
    2) LCLo (INHL) GUINEA PIG - 30 mg/m(3)/6h
    3) LCLo (INHL) GUINEA PIG - 0.03 mg/L/6h

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.

Workplace Standards

    A) ACGIH TLV Values for CAS7446-11-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7446-11-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7446-11-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    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 CAS7446-11-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: EPA, 1985 RTECS, 1990
    1) TCLo- (INHALATION)HUMAN:
    a) 30 mg/m(3)

Toxicologic Mechanism

    A) Sulfur trioxide is readily converted to sulfuric acid on contact with tears, tissue, and mucous membranes, and produces acid burns and irritation (Finkel, 1983; Kizer, 1984; Grant, 1986).

Physical Characteristics

    A) A fuming, colorless to white crystalline solid which exists in three solid modifications (ITI, 1988):
    1) an alpha form which consists of asbestos-like needles
    2) a beta form which consists of asbestos-like needles
    3) a gamma form which exist in an ice-like mass or a liquid
    B) The solid materials easily sublime (ITI, 1988).
    C) Absolutely dry sulfur trioxide is not corrosive to metals and shows no acidic reaction (ITI, 1988).
    D) In air, absorbs moisture rapidly, emitting dense white fumes which is a mist of sulfuric acid (ILO, 1983).
    1) Forms sulfuric acid in moist air or in water solution (ITI, 1988).

Molecular Weight

    A) 80.06 (Budavari, 1989)

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