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TITANIUM TETRACHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Titanium tetrachloride is formed through a chloride process from treatment of titanium-bearing ores in the presence of coke at high temperatures. Titanium tetrachloride decomposes to hydrochloric acid and titanium dioxide at high temperatures with pure oxygen. The toxicity appears to be due to this release of hydrochloric acid. Titanium tetrachloride is an intermediate compound in the production of titanium dioxide.

Specific Substances

    1) TITANIUM TETRACHLORIDE
    2) TETRACHLOROTITANIUM
    3) TETRACHLORURE DE TITANE
    4) TITAANTETRACHLORIDE
    5) TITANE (TETRACHLORURE DE)
    6) TITANIC CHLORIDE
    7) TITANIO (TETRACLORURO DI)
    8) TITANIUM CHLORIDE
    9) TITANTETRACHLORID
    10) STCC 4932385
    11) NIOSH/RTECS XR 1925000
    12) MOLECULAR FORMULA: Cl4-Ti
    13) CAS 7550-45-0
    14) TICKLE (SLANG FOR TITANIUM TETRACHLORIDE)
    15) TITAANTETRACHLORIDE (DUTCH)
    16) TITANOCENE
    1.2.1) MOLECULAR FORMULA
    1) Cl4-Ti TiCl4

Available Forms Sources

    A) FORMS
    1) Titanium tetrachloride (TiCl4) is an acidic, corrosive, pale yellow liquid with an acrid odor (Chitkara & McNeela, 1992; Paulsen et al, 1998).
    B) SOURCES
    1) Titanium tetrachloride is formed through a chloride process from treatment of titanium-bearing ores in the presence of coke at high temperatures (Fayerweather et al, 1992).
    C) USES
    1) It is an intermediate product in the manufacture of the white, inert pigment, titanium dioxide, which is then used in the manufacture of paints, linoleum, lacquers, leather, inks, rubber, soaps, textiles, ceramics, plastics, and other commercial and building products (Chitkara & McNeela, 1992; Paulsen et al, 1998).
    2) Titanium tetrachloride decomposes to hydrochloric acid and titanium dioxide (AAR, 1987; (NFPA, 1986; Grant & Schuman, 1993). The toxicity appears to be due to this release of hydrochloric acid and heat (Sittig, 1985). Oxidation to titanium dioxide occurs at a high temperature with pure oxygen (Fayerweather et al, 1992).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Titanium tetrachloride is a colorless, fuming liquid that is decomposed by moisture to hydrochloric acid, titanium dioxide, and heat. The toxicity of this agent is likely due to the release of hydrochloric acid. Titanium tetrachloride is corrosive to tissues.
    B) Long-term exposure, even at low concentrations results in upper respiratory tract irritation and acute or chronic bronchitis. Cough, bronchoconstriction with wheezing, chemical pneumonitis, or noncardiogenic pulmonary edema may occur following inhalation.
    C) Direct skin contact can cause irritation or corrosive dermal burns, especially if the material contacts water.
    D) Even brief, direct eye contact with the liquid material can cause severe eye injury.
    E) Ingestion of this material can cause mouth, throat, esophageal, and GI tract irritation or burns. Nausea, vomiting, diarrhea, and abdominal pain may occur. Potential complications include bleeding or perforation and late development of esophageal or gastric strictures.
    F) Exposure to chloride fumes from the decomposition of titanium tetrachloride in a fire situation would be predicted to cause respiratory tract irritation with chemical pneumonitis or noncardiogenic pulmonary edema.
    0.2.3) VITAL SIGNS
    A) Fever may develop from acute inhalation exposure.
    0.2.4) HEENT
    A) Even brief direct eye contact with the liquid material can cause severe eye injury. Severe corneal damage, conjunctivitis and keratitis have also been seen with exposure to fumes.
    B) Vapor exposure can cause irritation of the mucosa of the nose and throat. Ingestion can cause mouth and throat irritation or burns.
    0.2.6) RESPIRATORY
    A) The vapors are very irritating to the respiratory tract. Cough, bronchoconstriction with wheezing, chemical pneumonitis, or noncardiogenic pulmonary edema may occur following inhalation.
    B) Long-term inhalation of low concentrations can cause pulmonary injury. However, no chronic pulmonary conditions have occurred in titanium workers when good industrial hygiene practices have been used.
    0.2.8) GASTROINTESTINAL
    A) Ingestion of this material can cause mouth, throat, esophageal, and GI tract irritation or burns. Nausea, vomiting, diarrhea, and abdominal pain may occur.
    0.2.14) DERMATOLOGIC
    A) Direct skin contact can cause irritation or corrosive dermal burns, especially if the material contacts water or perspiration.
    B) Dermal exposures cause dry skin.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    C) No information about possible male reproductive effects was found in available references at the time of this review.
    0.2.21) CARCINOGENICITY
    A) In animal studies, squamous cell carcinomas of the lungs were demonstrated, but their significance for exposed humans cannot be evaluated.

Laboratory Monitoring

    A) No methods for measurement of titanium tetrachloride 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, pulse oximetry, chest x-ray, and pulmonary function tests.
    C) Esophagrams may be useful to assess the extent of injury after ingestion.

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 perforation or bleeding. Insertion of a small, flexible nasogastric tube to aspirate gastric contents after large ingestion is advocated by some, but carries the risk of perforation.
    B) There is no documentation of steroids used in human exposures to titanium tetrachloride; use of steroids is controversial and should be based on the clinician's judgement.
    1) MUCOSAL DECONTAMINATION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact 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. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
    2) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.
    C) ENDOSCOPY: Because acid ingestion may cause severe gastric burns with relatively few initial signs and symptoms, endoscopic evaluation is recommended within 24 hours in any patient with a definite history of ingesting a strong acid, even if asymptomatic. If burns are found, follow 10 to 20 days later with a barium swallow.
    D) Sucralfate may be useful in relieving symptomatology from acid-induced injury.
    E) Observe for symptoms of acute obstruction (pyloric outlet obstruction), at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestion.
    F) Obtain a follow-up esophagram and upper GI series about 2 to 4 weeks following ingestion. In severe cases of gastrointestinal necrosis or perforation, surgical consultation should be obtained.
    G) PHARMACOLOGIC TREATMENT: The use of corticosteroids is controversial. Patients with first degree burns generally do well and rarely develop strictures. Corticosteroids are generally not beneficial in these patients. Some authors have advocated the use of corticosteroids for second degree, deep-partial thickness burns within 48 hours of ingestion in patients without gastrointestinal bleeding or evidence of perforation. However, no well-controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with second degree, superficial-partial thickness burns. Some authors have recommended steroids in patients with third degree burns. 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. Antibiotics are indicated for suspected perforation or infection and in patients receiving corticosteroids.
    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) Prophylactic, early treatment with supplemental oxygen has been suggested.
    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) Patients with severe acute overexposure and individuals with long-term exposure to lower concentrations should be monitored for the possible development of chronic bronchitis or a silicosis-like lung disease.
    G) Workers developing chronic pulmonary complaints may need to be precluded from further exposure.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION - Wipe eyelids and face with a DRY CLOTH or GAUZE BEFORE WATER IRRIGATION. DO NOT USE neutralizing solutions, such as sodium bicarbonate. AFTER DRY WIPING, irrigate the eyes with copious amounts of water.
    B) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each affected eye with copious amounts of water or sterile 0.9% saline for about 30 minutes. Irrigating volumes up to 20 L or more have been used to neutralize the pH. After this initial period of irrigation, the corneal pH may be checked with litmus paper and a brief external eye exam performed. Continue direct copious irrigation with sterile 0.9% saline until the conjunctival fornices are free of particulate matter and returned to pH neutrality (pH 7.4). Once irrigation is complete, a full eye exam should be performed with careful attention to the possibility of perforation.
    C) Early ophthalmologic consultation is highly advisable.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION - Wipe exposed skin with a DRY CLOTH, COTTON WASTE, or GAUZE BEFORE WATER IRRIGATION. Rinse off remaining light yellow to white granular deposit with copious amounts of cool 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) Before applying any topical agents or bandaging burns, it is essential that all of the substance be removed from the skin.
    4) Treatment of CHEMICAL BURNS may be required. Refer to TREATMENT/DERMAL EXPOSURE section in the main body of this document for more information.

Range Of Toxicity

    A) Fatalities have occurred in workers exposed by the inhalation and dermal routes, but the concentration of material was not specified. Even low airborne concentrations result in symptoms.

Clinical Effects

Summary Of Exposure

    A) Titanium tetrachloride is a colorless, fuming liquid that is decomposed by moisture to hydrochloric acid, titanium dioxide, and heat. The toxicity of this agent is likely due to the release of hydrochloric acid. Titanium tetrachloride is corrosive to tissues.
    B) Long-term exposure, even at low concentrations results in upper respiratory tract irritation and acute or chronic bronchitis. Cough, bronchoconstriction with wheezing, chemical pneumonitis, or noncardiogenic pulmonary edema may occur following inhalation.
    C) Direct skin contact can cause irritation or corrosive dermal burns, especially if the material contacts water.
    D) Even brief, direct eye contact with the liquid material can cause severe eye injury.
    E) Ingestion of this material can cause mouth, throat, esophageal, and GI tract irritation or burns. Nausea, vomiting, diarrhea, and abdominal pain may occur. Potential complications include bleeding or perforation and late development of esophageal or gastric strictures.
    F) Exposure to chloride fumes from the decomposition of titanium tetrachloride in a fire situation would be predicted to cause respiratory tract irritation with chemical pneumonitis or noncardiogenic pulmonary edema.

Vital Signs

    3.3.1) SUMMARY
    A) Fever may develop from acute inhalation exposure.
    3.3.3) TEMPERATURE
    A) A worker with acute inhalation exposure and chemical pneumonitis developed fever (Park et al, 1984).

Heent

    3.4.1) SUMMARY
    A) Even brief direct eye contact with the liquid material can cause severe eye injury. Severe corneal damage, conjunctivitis and keratitis have also been seen with exposure to fumes.
    B) Vapor exposure can cause irritation of the mucosa of the nose and throat. Ingestion can cause mouth and throat irritation or burns.
    3.4.3) EYES
    A) BURNS/OPACITIES -
    1) Even brief, direct eye contact with the liquid material can cause severe eye injury with permanent corneal opacities (EPA, 1985; ILO, 1983; Sittig, 1985; Grant & Schuman, 1993).
    2) Chitkara & McNeela (1992) reported several cases of corneal and conjunctival burns of the eyes with severe tissue damage following splash exposures. They related the severity of the injuries to be more consistent with strong alkali burns than acid burns. Total blindness resulted in two of the victims.
    3) Severe corneal damage has also been seen with exposure to fumes (EPA, 1985; HSDB , 2000; ILO, 1983; Grant & Schuman, 1993).
    4) Severe exposures may result in corneal scarring and vascularization, raised intraocular pressure, conjunctival ischemia, anterior uveitis, opacification of the lens, corneal perforation, and blindness (Chitkara & McNeela, 1992).
    B) KERATITIS - Suppurative conjunctivitis and keratitis may be seen (ILO, 1983; Sittig, 1985).
    C) CASE REPORT - ENTROPION and trichiasis of the upper and lower eyelid was reported in a 46-year-old male worker following an accidental splash injury (Chitkara & McNeela, 1992).
    3.4.5) NOSE
    A) Vapor exposure can cause irritation of the mucosa of the nose and throat (AAR, 1987; (NFPA, 1986; CHRIS , 1991). Extensive burns of the nasopharynx resulted following an accidental chemical splash to the face (Chitkara & McNeela, 1992).
    3.4.6) THROAT
    A) Vapor exposure can cause irritation of the mucosa of the nose and throat (AAR, 1987; (NFPA, 1986; CHRIS , 1991). Extensive burns of the larynx occurred following an accidental chemical splash to the face (Chitkara & McNeela, 1992).
    B) Ingestion of this material can cause mouth and throat irritation or burns (EPA, 1985).

Respiratory

    3.6.1) SUMMARY
    A) The vapors are very irritating to the respiratory tract. Cough, bronchoconstriction with wheezing, chemical pneumonitis, or noncardiogenic pulmonary edema may occur following inhalation.
    B) Long-term inhalation of low concentrations can cause pulmonary injury. However, no chronic pulmonary conditions have occurred in titanium workers when good industrial hygiene practices have been used.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) The vapors are very irritating to the respiratory tract (NFPA, 1986; Budavari, 1996; Sax & Lewis, 1987; Lewis, 1996; EPA, 1985; HSDB , 2000).
    B) PNEUMONITIS
    1) Cough, bronchoconstriction with wheezing, chemical pneumonitis, or noncardiogenic pulmonary edema may occur following inhalation (EPA, 1985; Lawson, 1961). Chitkara & McNeela (1992) reported a fatal case of splash and acute inhalation exposure resulting in progressive deterioration of pulmonary function compliance, to the degree that it became impossible to maintain adequate oxygenation.
    C) EDEMA
    1) In inhalation exposures, edema of the pharynx, vocal cords, and trachea were noted; sequelae were stenosis of the larynx, trachea, and upper bronchi (HSDB , 2000; Finkel, 1983; Park et al, 1984).
    D) SEQUELA
    1) Diffuse endobronchial polyposis, diffuse endobronchial erythema, and suspected bronchiolitis obliterans have also been noted as late sequelae of acute inhalation injury (Park et al, 1984).
    E) RESPIRATORY FINDING
    1) Titanium tetrachloride is corrosive to tissues; long-term inhalation of low concentrations can cause pulmonary injury with reduced ventilatory capacity (AAR, 1987; (Sittig, 1985).
    a) However, no chronic pulmonary conditions have occurred in titanium workers when good industrial hygiene practices have been used (HSDB , 2000).
    b) In a small study of titanium tetrachloride workers, only one was identified with possible chronic pulmonary complications (Lawson, 1961).
    c) In a study of 209 workers with exposure to titanium tetrachloride and titanium dioxide, reduced ventilatory capacity and a 17 percent incidence of pleural thickening and plaques were noted, although asbestos exposure could have been all or partly responsible for the pleural disease noted (Garabrant et al, 1987).
    F) BRONCHITIS
    1) Workers with long-term exposure to titanium dust (particularly titanium dioxide) have a high incidence of chronic bronchitis and restrictive pulmonary changes (ILO, 1983; Anon, 1980). Those with long-term exposure to titanium tetrachloride may complain of upper respiratory tract irritation and acute or chronic bronchitis (ILO, 1983; Sittig, 1985).

Gastrointestinal

    3.8.1) SUMMARY
    A) Ingestion of this material can cause mouth, throat, esophageal, and GI tract irritation or burns. Nausea, vomiting, diarrhea, and abdominal pain may occur.
    3.8.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Ingestion of this material can cause mouth, throat, esophageal, and gastrointestinal tract irritation or burns (EPA, 1985).
    B) VOMITING
    1) Nausea, vomiting, diarrhea, and abdominal pain may occur (EPA, 1985).
    C) GASTROINTESTINAL HEMORRHAGE
    1) Potential complications of ingestions may include early bleeding or perforation and late development of esophageal or gastric strictures.

Dermatologic

    3.14.1) SUMMARY
    A) Direct skin contact can cause irritation or corrosive dermal burns, especially if the material contacts water or perspiration.
    B) Dermal exposures cause dry skin.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Direct skin contact can cause irritation or corrosive dermal burns, especially if the material contacts water or perspiration (Lewis, 1996; EPA, 1985; HSDB , 2000; ILO, 1983; Sittig, 1985; Lawson, 1961; Paulsen et al, 1998). In many cases dermal burns are severe enough to require grafting.
    a) Workers with dermal exposure who washed with water before dry wiping off the material developed severe burns; those who dry-wiped the skin before flushing with water had a much less severe injury (Lawson, 1961).
    2) CASE REPORTS - Paulsen et al (1998) reported two cases of accidental spraying with liquid TiCl4 resulting in 18% to 20% total body surface area burns as a result of the combined sequence of hydrochloric acid and the heat generated in dermal areas where TiCl4 was mixed with perspiration. Wound biopsies taken on post-burn days 3 and 6 indicated that TiCl4 did not retard wound healing. Surgery was required to excise the full-thickness burned areas of involved skin and to place split-thickness skin grafts.
    B) DRY SKIN
    1) Laboratory workers have had direct dermal contact with the pure material, yet developed only a tendency to have dry skin (Lawson, 1961).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    C) No information about possible male reproductive effects was found in available references at the time of this review.
    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.
    2) No information about possible male reproductive effects was found in available references at the time of this review.
    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 CAS7550-45-0 (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) In animal studies, squamous cell carcinomas of the lungs were demonstrated, but their significance for exposed humans cannot be evaluated.
    3.21.3) HUMAN STUDIES
    A) PULMONARY CARCINOMA
    1) A study of 398 employees exposed to titanium tetrachloride observed from 1956 through 1983 found that the risk of lung cancer was not statistically significantly higher for exposed workers than for a referent group (Fayerweather et al, 1992).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) In a two-year rat study of inhalation of titanium tetrachloride hydrolysis products, 5 of 143 animals developed squamous cell carcinomas of the lung (Lee et al, 1986).
    a) The authors of this study concluded that these tumors were an exaggerated extension of squamous metaplasia seen in the animals exposed to the highest concentration (10 mg/m(3)), and that their significance for exposed humans could not be evaluated (Lee et al, 1986).

Genotoxicity

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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No methods for measurement of titanium tetrachloride 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, pulse oximetry, chest x-ray, and pulmonary function tests.
    C) Esophagrams may be useful to assess the extent of injury after ingestion.

Radiographic Studies

    A) RADIOGRAPHIC-OTHER
    1) Esophagrams in the acute and subacute phase demonstrate edema, hemorrhage, ulcerations, atony, and dilation. Strictures of the esophagus may be present in the chronic phase. These radiographic findings are not different from those found in alkaline corrosive esophagitis (Muhletaler, 1980).
    B) CHEST RADIOGRAPH
    1) Obtain an upright chest x-ray to evaluate for perforation, mediastinitis and aspiration in severely symptomatic patients.

Methods

    A) OTHER
    1) No methods for measurement of titanium tetrachloride in biological or environmental samples were listed in available references at the time of this review.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No methods for measurement of titanium tetrachloride 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, pulse oximetry, chest x-ray, and pulmonary function tests.
    C) Esophagrams may be useful to assess the extent of injury after ingestion.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY -
    1) Do NOT induce emesis nor administer activated charcoal as this substance causes primarily corrosive injury.
    B) DILUTION -
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact 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).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    6.5.2) PREVENTION OF ABSORPTION
    A) HYDROCHLORIC ACID
    1) The major toxicity of titanium tetrachloride following ingestion is its decomposition to HYDROCHLORIC ACID. The following treatment recommendations are adapted from those for ACIDS.
    B) EMESIS
    1) Do NOT INDUCE VOMITING.
    C) NASOGASTRIC SUCTION
    1) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    D) ACTIVATED CHARCOAL
    1) Activated charcoal is of no value.
    E) DILUTION
    1) 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) CONTRAINDICATED TREATMENT
    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 milliliters of 9.5 percent HCl with 800 milliliters of water resulted in a pH change of 0.99 to 1.73 (Maull et al, 1985).
    C) ENDOSCOPIC PROCEDURE
    1) The following recommendations are extrapolated from experience with ingestions of acids and/or alkaline corrosives.
    2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    3) 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.
    4) 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)
    5) 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).
    6) 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.
    7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    D) CORTICOSTEROID
    1) The use of steroids for the treatment of caustic ingestion is controversial. The following recommendations are extrapolated from experience with ingestions of acids and/or alkaline corrosives. No specific cases were found in the literature where corticosteroids were used to treat titanium tetrachloride ingestions.
    a) 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.
    b) 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).
    c) 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).
    d) 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).
    e) 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).
    f) 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).
    g) 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).
    h) STUDIES
    1) ANIMAL
    a) 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).
    b) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    c) 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).
    2) HUMAN
    a) 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).
    b) META ANALYSIS
    1) 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).
    2) 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).
    3) 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).
    c) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    d) 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).
    e) 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).
    1) 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).
    2) 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).
    3) 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).
    4) 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).
    5) 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).
    f) ADVERSE EFFECTS
    1) 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).
    E) SUCRALFATE
    1) Administration of sucralfate, 1 gram 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 antibiotic. 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.
    F) 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) Use of nasogastric suction is controversial. There are no studies to evaluate its efficacy and safety following titanium tetrachloride ingestions. If used, soft nasogastric or orogastric tube should only be passed within 90 minutes following the large ingestion of a strong acid.
    G) 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
    H) BURN
    1) If severe burns occur in the mouth then esophageal burns may exist. It is reportedly unusual for acid ingestion to result in 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 percent 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 (1984) recommends 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.
    I) OBSTRUCTION
    1) Observe for symptoms of acute obstruction (pyloric outlet obstruction), at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestion.
    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).
    J) FOLLOW-UP VISIT
    1) Obtain a follow-up esophagram and upper GI series to evaluate presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
    K) 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.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) GENERAL CONSIDERATIONS -
    1) 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.
    2) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    3) 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.
    B) PROPHYLACTIC OXYGEN -
    1) Prophylactic, early treatment with supplemental oxygen has been said to minimize the possibility of developing noncardiogenic pulmonary edema following inhalation exposure (Lawson, 1961).
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    B) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    C) 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).
    D) MONITORING OF PATIENT
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    2) Patients with severe acute overexposure and individuals with long-term exposure to lower concentrations should be monitored for the possible development of chronic bronchitis or a silicosis-like lung disease (ILO, 1983; Lawson, 1961).
    a) Workers developing chronic pulmonary complaints may need to be precluded from further exposure (ILO, 1983).
    E) CORTICOSTEROID
    1) Diffuse endobronchial polyposis, erythema of the bronchial mucosa, and suspected bronchiolitis obliterans have been described following inhalation injury (Park et al, 1984).
    a) Treatment of several weeks duration with high-dose corticosteroids apparently resulted in resolution of the polyposis and improvement in pulmonary function (Park et al, 1984), although the value of steroids for treating the polyposis component has been questioned (Glassroth, 1984).
    F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) DRY WIPING -
    1) Because titanium tetrachloride reacts with water to release highly corrosive hydrochloric acid, the eyelids and face should FIRST be WIPED with a DRY CLOTH or GAUZE BEFORE WATER IRRIGATION is begun to PREVENT serious facial or eyelid BURNS (Grant, 1986; Lawson, 1961).
    a) Neutralizing solutions, such as sodium bicarbonate, should NEVER BE USED as they generate heat which may cause further burns.
    B) WATER RINSE -
    1) AFTER DRY WIPING, the eyes should rapidly be copiously irrigated with water.
    2) 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).
    C) The pH of the conjunctival sac should be tested after irrigation and irrigation continued until it is no longer acidic.
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) Because of the potential for severe and permanent eye damage following either vapor exposure or direct contact with the liquid material, prolonged initial flushing, AFTER DRY WIPING, and early ophthalmologic consultation are highly advisable.
    B) SUPPORT
    1) SUMMARY
    a) If ocular damage is minor, artificial tears/lubricants, topical cycloplegics, and antibiotics may be all that are needed.
    2) ARTIFICIAL TEARS
    a) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    3) TOPICAL CYCLOPLEGIC
    a) Use to guard against development of posterior synechiae and ciliary spasm (Brodovsky et al, 2000a; Grant & Schuman, 1993a). Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    4) TOPICAL ANTIBIOTICS
    a) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000a; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008).
    5) PAIN CONTROL
    a) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    6) Begin irrigation immediately with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available. Lactated Ringer's solution may also be effective. Once irrigation has begun, instill a drop of local anesthetic (eg, 0.5% proparacaine) for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Singh et al, 2013; Spector & Fernandez, 2008; Ernst et al, 1998; Grant & Schuman, 1993a). In one study, isotonic saline, lactated Ringer's solution, normal saline with bicarbonate, and balanced saline plus (BSS Plus) were compared and no difference in normalization of pH were found; however, BSS Plus was better tolerated and more comfortable (Fish & Davidson, 2010).
    a) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000b). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993a). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
    b) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993a).
    c) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).
    7) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000).
    8) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000; Singh et al, 2013):
    a) GRADE 1 (prognosis good): Corneal epithelial damage; no limbal ischemia.
    b) GRADE 2 (prognosis good): Cornea hazy; iris details visible, ischemia less than one-third of limbus.
    c) GRADE 3 (prognosis guarded): Total loss of corneal epithelium; stromal haze obscures iris details; ischemia of one-third to one-half of limbus.
    d) GRADE 4 (prognosis poor): Cornea opaque; iris and pupil obscured, ischemia affects more than one-half of limbus.
    9) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):
    a) GRADE 1 (prognosis very good): 0 clock hour of limbal involvement and 0% conjunctival involvement.
    b) GRADE 2 (prognosis good): Less than 3 clock hour of limbal involvement and less than 30% conjunctival involvement.
    c) GRADE 3 (prognosis good): Greater than 3 and up to 6 clock hour of limbal involvement and greater than 30% to 50% conjunctival involvement.
    d) GRADE 4 (prognosis good to guarded): Greater than 6 and up to 9 clock hour of limbal involvement and greater than 50% to 75% conjunctival involvement.
    e) GRADE 5 (prognosis guarded to poor): Greater than 9 and less than 12 clock hour of limbal involvement and greater than 75% and less than 100% conjunctival involvement.
    f) GRADE 6 (very poor): Total limbus (12 clock hour) involved and 100% conjunctival involvement.
    10) SUMMARY
    a) If the damage is minor, the above may be all that is needed. For grade 3 or 4 injuries, one or more of the following may be used, only with ophthalmologic consultation: acetazolamide, topical timolol, topical steroids, citrate, ascorbate, EDTA, cysteine, NAC, penicillamine, tetracycline, or soft contact lenses.
    11) ARTIFICIAL TEARS
    a) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    12) PAIN CONTROL
    a) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    13) CARBONIC ANHYDRASE INHIBITOR
    a) Acetazolamide (250 mg orally 4 times daily) may be given to control increased intraocular pressure (Singh et al, 2013; Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    14) TOPICAL STEROIDS
    a) DOSE: Dexamethasone 0.1% ointment 4 times daily to reduce inflammation. If persistent epithelial defect is present, discontinue dexamethasone by day 14 to reduce the risk of stromal melt (Tuft & Shortt, 2009). Other sources suggest that corticosteroids should be stopped if the epithelium has not covered surface defects by 5 to 7 days (Grant & Schuman, 1993b).
    b) Topical prednisolone 0.5% has also been used. A further increase in corneoscleral melt may occur if topical steroids are used alone. In one study, topical prednisolone 0.5% was used in combination with topical ascorbate 10%; no increase in corneoscleral melt was observed when topical steroids were used until re-epithelization (Singh et al, 2013; Fish & Davidson, 2010).
    c) In one retrospective study, fluorometholone 1% drops were administered every 2 hours initially, then decreased to four times daily when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete (Brodovsky et al, 2000b).
    1) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000b).
    15) ASCORBATE
    a) Oral or topical ascorbate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    b) DOSE: Ascorbate 10% 4 times daily topically or 1 g orally (2 g/day) (Singh et al, 2013; Tuft & Shortt, 2009).
    c) Ascorbate is needed for the formation of collagen and the concentration of ascorbate in the anterior chamber is decreased when the ciliary body is damaged by alkali burns (Tuft & Shortt, 2009; Grant & Schuman, 1993b). In one retrospective study, ascorbate drops (10%) were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received 500 mg of oral ascorbate 4 times daily, until discharge from the hospital (Brodovsky et al, 2000b).
    1) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000b).
    16) CITRATE
    a) Topical citrate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    b) DOSE: Potassium citrate 10% 4 times daily topically (Tuft & Shortt, 2009).
    c) Citrate chelates calcium, and thereby interferes with the harmful effects of neutrophil accumulation, such as release of proteolytic enzymes and superoxide free radicals, phagocytosis and ulceration (Grant & Schuman, 1993b). In one retrospective study, 10% citrate drops were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received a urinary alkalinizer containing 720 mg of citric acid anhydrous and 630 mg of sodium citrate anhydrous 3 times daily, until discharge from the hospital (Brodovsky et al, 2000b).
    1) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000b).
    17) COLLAGENASE INHIBITORS
    a) Inhibitors of collagenase can inhibit collagenolytic activity, prevent stromal ulceration, and promote wound healing. Several effective agents, such as cysteine, n-acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, and citrate, have been recommended (Singh et al, 2013; Tuft & Shortt, 2009; Perry et al, 1993; Seedor et al, 1987).
    b) TETRACYCLINE: Has been found to have an anticollagenolytic effect. Systemic tetracycline 50 mg/kg/day reduced the incidence of alkali-induced corneal ulcerations in rabbits (Seedor et al, 1987).
    c) DOXYCYCLINE: Decreased epithelial defects and collagenase activity in a rabbit model of alkali burns to the eye (Perry et al, 1993). DOSE: 100 mg twice daily (Tuft & Shortt, 2009).
    18) ANTIBIOTICS
    a) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000a; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008). In patients with severe burns, a topical fluoroquinolone antibiotic drop 4 times daily may also be used (Tuft & Shortt, 2009). A topical fourth generation fluoroquinolone has been recommended as an antimicrobial prophylaxis in patients with large epithelial defect (Fish & Davidson, 2010).
    19) TOPICAL CYCLOPLEGIC
    a) Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    20) SOFT CONTACT LENSES
    a) A bandage contact lens (eg, silicone hydrogel) may make the patient more comfortable and protect the surface (Fish & Davidson, 2010; Tuft & Shortt, 2009). Hydrophilic high oxygen permeability lenses are preferred (Singh et al, 2013). Soft lenses with intermediate water content and inherent rigidity may facilitate reepithelialization. The use of 0.5 normal sodium chloride drops hourly and artificial tears or lubricant eyedrops instilled 4 times a day may help maintain adequate hydration and lens mobility.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DRY WIPING -
    a) Because titanium tetrachloride reacts with water to release highly corrosive hydrochloric acid, exposed skin should FIRST be WIPED with a DRY CLOTH, COTTON WASTE, or GAUZE BEFORE WATER IRRIGATION is begun to PREVENT serious dermal BURNS (Lawson, 1961; Paulsen et al, 1998).
    2) WATER RINSE -
    a) Dry wiping leaves a tenacious light yellow to white granular deposit on the skin, which can be rinsed off with copious amounts of cool water (Lawson, 1961; Paulsen et al, 1998).
    b) Wash the exposed area with copious amounts of water. A physician may need to examine the area if irritation or pain persists.
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) BURN
    1) Before applying any topical agents or bandaging titanium tetrachloride burns, it is essential to ensure that all of the material has been removed from the skin (Lawson, 1961; Paulsen et al, 1998).
    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.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Fatalities have occurred in workers exposed by the inhalation and dermal routes, but the concentration of material was not specified. Even low airborne concentrations result in symptoms.

Minimum Lethal Exposure

    A) OCCUPATIONAL
    1) Fatalities have occurred in workers exposed by the inhalation and dermal routes, but the concentration of material was not specified (Lawson, 1961).
    B) ANIMAL DATA
    1) Published Values (ITI, 1988) -
    1) LDLo (IM) RAT - 50 mg/kg
    2) LCLo (INHL) MOUSE - 10 mg/m(3)/2h
    3) LDLo (IM) HAMSTER - 83 mg/kg

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Even low airborne concentrations are intolerable (CHRIS , 1991).
    2) Direct eye and skin splashes of the liquid material can cause severe burn injuries (Grant & Schuman, 1993; Lawson, 1961).
    3) A two-minute inhalation exposure to the fumes resulted in Adult Respiratory Distress Syndrome, chemical pneumonitis, diffuse endobronchial polyposis, diffuse endobronchial erythema, suspected bronchiolitis obliterans, and tracheal stenosis requiring stenting in one case (Park et al, 1984).
    B) ANIMAL DATA
    1) Rats exposed to titanium tetrachloride hydrolysis products at concentrations of 0.1 to 10 milligrams/cubic meter, 6 hours daily, 5 days per week for two years had a pulmonary response similar to that seen with nuisance dust (Lee et al, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS7550-45-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7550-45-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7550-45-0 :
    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 CAS7550-45-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES

Physicochemical

Physical Characteristics

    A) Titanium tetrachloride is a colorless, fuming liquid, with an acrid odor, that is decomposed by moisture to hydrochloric acid and titanium dioxide with liberation of heat (AAR, 1987; (NFPA, 1986; Budavari, 1996; Lewis, 1996; EPA, 1985; HSDB , 2000; OHM/TADS , 1991; Grant & Schuman, 1993; CHRIS , 1991).

Molecular Weight

    A) 189.73 (Budavari, 1996)

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) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    14) Aceto T Jr, Terplan K, & Fiore RR: Chemical burns of the esophagus in children and glucocorticoid therapy. J Med 1970; 1:101-109.
    15) Adam JS & Brick HG: Pediatric caustic ingestion. Ann Otol Laryngol 1982; 91:656-658.
    16) 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.
    17) Anderson KD, Touse TM, & Randolph JG: A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990; 323:637-640.
    18) Anon: Health Hazard Evaluation Report Number HHE-79-17-751 at RMI Metals Reduction Plant, Ashtabula, Ohio, Hazard Evaluations and Technical Assistance Branch, Division of Surveillance, Hazard Evaluations, and Field Studies, NIOSH, Cincinnati, OH, 1980.
    19) 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.
    20) 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.
    21) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    22) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    23) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    24) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    25) Boukthir S, Fetni I, Mrad SM, et al: [High doses of steroids in the management of caustic esophageal burns in children]. Arch Pediatr 2004; 11(1):13-17.
    26) Boysen PG & Modell JH: Pulmonary edema, in: Textbook of Critical Care Medicine, 2nd ed. Shoemaker WC, Ayres S, Grenvik A et al (Eds), WB Saunders Company, Philadelphia, PA, 1989, pp 515-518.
    27) Brodovsky SC, McCarty AC, & Snibson G: Management of alkali burns an 11-year retrospective review. Ophthalmology 2000; 107:1829-1835.
    28) Brodovsky SC, McCarty CA, & Snibson G: Management of alkali burns an 11-year retrospective review. Ophthalmology 2000b; 107:1829-1835.
    29) Brodovsky SC, McCarty CA, & Snibson G: Management of alkali burns an 11-year review. Ophthalmology 2000a; 107:1829-1835.
    30) 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.
    31) Budavari S: The Merck Index, 11th ed, Merck & Co, Inc, Rahway, NJ, 1989, pp 1493.
    32) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996.
    33) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 1990; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    34) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 1991; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    35) Caravati EM: Alkali. In: Dart RC, ed. Medical Toxicology, Lippincott Williams & Wilkins, Philadelphia, PA, 2004.
    36) Carvajal HF & Stewart CE: Emergency management of burn patients: the first few hours. Emerg Med Reports 1987; 8:129-136.
    37) 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.
    38) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    39) Chitkara DK & McNeela BJ: Titanium tetrachloride burns to the eye. Br J Ophthalmol 1992; 76:380-382.
    40) Chodak GW & Passaro E: Acid ingestion: need for gastric resection. JAMA 1978; 239:229-226.
    41) Chudnofsky CR & Otten EJ: Acute pulmonary toxicity to nitrofurantoin. J Emerg Med 1989; 7:15-19.
    42) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2A. Toxicology, 3rd ed, John Wiley & Sons, New York, NY, 1981.
    43) Cleveland WW, Chandler JR, & Lawson RB: Treatment of caustic burns of the esophagus. JAMA 1963; 186:182-183.
    44) 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.
    45) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    46) Consensus: POISINDEX(R) Editorial Board Consensus opinion poll, Irritants/Caustics Specialty Board, Micromedex, Inc, Greenwood Village, CO, 1988.
    47) 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.
    48) Dilawari JB, Singh S, & Rao PN: Corrosive acid ingestion in man, a clinical and endoscopic study. Gut 1984a; 25:183-187.
    49) Dilawari JB, Singh S, & Rao PN: Corrosive acid ingestion in man: a clinical and endoscopic study. GUT 1984; 25:183-187.
    50) 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.
    51) 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.
    52) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    53) EPA: EPA chemical profile on titanium tetrachloride, Environmental Protection Agency, Washington, DC, 1985.
    54) 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/.
    55) 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.
    56) Ernst AA, Thomson T, & Haynes ML: Warmed versus room temperature saline solution for ocular irrigation: a randomized clinical trial. Ann Emerg Med 1998; 32:676-679.
    57) Estrera A, Taylor W, & Mills LJ: Corrosive burns of the esophagus and stomach: a recommendation of an aggressive surgical approach. Ann Thorac Surg 1986; 41:276-283.
    58) Fayerweather WE, Karns ME, & Gilby PG: Epidemiologic study of lung cancer mortality in workers exposed to titanium tetrachloride. J Occup Med 1992; 34:164-169.
    59) Ferguson MK, Migliore M, & Staszak VM: Early evaluation and therapy for caustic esophageal injury. Am J Surg 1989; 157:116-120.
    60) Finkel AJ: Hamilton and Hardy's Industrial Toxicology, 4th ed, John Wright, PSG Inc, Boston, MA, 1983, pp 136-137.
    61) Fish R & Davidson RS: Management of ocular thermal and chemical injuries, including amniotic membrane therapy. Curr Opin Ophthalmol 2010; 21(4):317-321.
    62) Garabrant DH, Fine LJ, & Oliver C: Abnormalities of pulmonary function and pleural disease among titanium metal production workers. Scand J Work Environ Health 1987; 13:47-51.
    63) Glassroth J: Diffuse endobronchial polyposis following a titanium tetrachloride inhalation injury (Letter). Am Rev Resp Dis 1984; 130:1189.
    64) Gorman RL, Khin-Maung-Gyi MT, & Klein-Schwartz W: Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestions. Am J Emerg Med 1992; 10:89-94.
    65) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    66) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993a.
    67) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993b.
    68) Grant WM: Toxicology of the Eye, 3rd ed, Charles C Thomas, Springfield, IL, 1986, pp 919.
    69) 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.
    70) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1993; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    71) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    72) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    73) Haller JA & Bachman K: The comparative effect of current therapy on experimental caustic burns of the esophagus. Pediatrics 1964; 236-245.
    74) Haller JA, Andrews HG, & White JJ: Pathophysiology and management of acute corrosive burns of the esophagus. J Pediatr Surg 1971; 6:578-584.
    75) Hawkins DB, Demeter MJ, & Barnett TE: Caustic ingestion: controversies in management. A review of 214 cases. Laryngoscope 1980; 90:98-109.
    76) Haynes BW Jr: Emergency department management of minor burns. Top Emerg Med 1981; 3:35-40.
    77) Homan CS, Maitra SR, & Lane BP: Effective treatment of acute alkali injury of the esopahgus with early saline dilution therapy. Ann Emerg Med 1993; 22:178-182.
    78) Homan CS, Maitra SR, & Lane BP: Histopathologic evaluation of the therapeutic efficacy of water and mild dilution for esophageal acid injury. Acad Emerg Med 1995; 2:587-591.
    79) Homan CS, Maitra SR, & Lane BP: Therapeutic effects of water and milk for acute alkali injury of the esophagus. Ann Emerg Med 1994; 24:14-19.
    80) Hovarth OP, Olah T, & Zentai G: Emergency esophagogastrectomy for the treatment of hydrochloric acid injury. Ann Thorac Surg 1991; 52:98-101.
    81) Howell JM, Dalsey WC, & Hartsell FW: Steroids for the treatment of corrosive esophageal injury: a statistical analysis of past studies. Am J Emerg Med 1992; 10:421-425.
    82) Howell JM: Alkaline ingestions. Ann Emerg Med 1987; 15:820-825.
    83) 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.
    84) 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.
    85) 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.
    86) 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.
    87) 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.
    88) 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.
    89) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    90) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    91) ILO: Encyclopaedia of Occupational Health and Safety, 3rd ed, Vol 2, International Labour Organization, Geneva, Switzerland, 1983, pp 2179-2181.
    92) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1988, pp 523-524.
    93) 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.
    94) 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.
    95) Ip M, Wong K-L, & Wong K-F: Lung injury in dimethyl sulfate poisoning. J Occup Med 1989; 31:141-143.
    96) 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.
    97) 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.
    98) Knox WG, Scott JR, & Zintel HA: Bouginage and steroids used singly or in combination in experimental corrosive esophagitis. Ann Surg 1967; 166:930-941.
    99) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    100) Kuckelkorn R, Kottek A, & Schrage N: Poor prognosis of severe chemical and thermal eye burns: the need for adequate emergency care and primary prevention. Int Arch Occup Environ Health 1995; 281-284.
    101) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    102) Lawson JL: The toxicity of titanium tetrachloride. J Occup Med 1961; 3:7-12.
    103) Lee KP, Kelly DP, & Schneider PW: Inhalation toxicity study on rats exposed to titanium tetrachloride atmospheric hydrolysis products for two years. Toxicol Appl Pharmacol 1986; 83:30-45.
    104) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 9th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    105) LoVecchio F, Hamilton R, & Sturman K: A meta-analysis of the use of steroids in the prevention of stricture formation from second degree caustic burns of the esophagus (abstract). J Toxicol-Clin Toxicol 1996; 35:579-580.
    106) 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.
    107) 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.
    108) Maggart M & Stewart S: The mechanisms and management of noncardiogenic pulmonary edema following cardiopulmonary bypass. Ann Thorac Surg 1987; 43:231-236.
    109) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    110) 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.
    111) Marshall F II: Caustic burns of the esophagus: ten year results of aggressive care. South Med J 1979; 72:1236-1237.
    112) Maull KI, Osman AP, & Maull CD: Liquid caustic ingestions: an in vitro study of the effects of buffer, neutralization, and dilution. Ann Emerg Med 1985a; 4:1160-1162.
    113) Maull KI, Osmand AP, & Maull CD: Liquid caustic ingestions: an in vitro study of the effects of buffer, neutralization, and dilation. Ann Emerg Med 1985; 14:1160-1162.
    114) 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.
    115) Meredith JW, Kon ND, & Thompson JN: Management of injuries from liquid lye ingestion. J Trauma 1988; 28:1173-1180.
    116) Mittal PK, Gulati R, & Sibia SS: Sucralfate therapy for acid-induced upper gastrointestinal tract injury (Letter). Am J Gastroenterol 1989; 84:204-205.
    117) Moazam F, Talbert JL, & Miller D: Caustic ingestion and its sequelae in children. South Med J 1987; 80:187-188.
    118) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    119) Moylan JA: Burn care after thermal injury. Top Emerg Med 1980; 2:39-52.
    120) NFPA: Fire Protection Guide on Hazardous Materials, 9th ed, National Fire Protection Association, Boston, MA, 1986, pp 49(87-88),491M-170,491M-213.
    121) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    122) 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.
    123) 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.
    124) 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.
    125) 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.
    126) 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.
    127) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    128) 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.
    129) 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.
    130) 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.
    131) 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.
    132) 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.
    133) 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.
    134) 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.
    135) 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.
    136) 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.
    137) 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.
    138) 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.
    139) 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.
    140) 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.
    141) 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.
    142) 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.
    143) 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.
    144) 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.
    145) 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.
    146) 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.
    147) 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.
    148) 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.
    149) 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.
    150) 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.
    151) 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.
    152) 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.
    153) 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.
    154) 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.
    155) 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.
    156) 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.
    157) 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.
    158) 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.
    159) 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.
    160) 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.
    161) 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.
    162) 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.
    163) 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.
    164) 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.
    165) 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.
    166) 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.
    167) 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.
    168) 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.
    169) 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.
    170) 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.
    171) 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.
    172) 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.
    173) 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.
    174) 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.
    175) 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.
    176) 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.
    177) 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.
    178) 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.
    179) 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.
    180) 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.
    181) 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.
    182) 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.
    183) 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.
    184) 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.
    185) 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.
    186) 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.
    187) 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.
    188) 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.
    189) 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.
    190) 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.
    191) 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.
    192) 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.
    193) 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.
    194) 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.
    195) 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.
    196) 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.
    197) 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.
    198) 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.
    199) 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.
    200) 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.
    201) 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.
    202) 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.
    203) 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.
    204) 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.
    205) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    206) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    207) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    208) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    209) 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.
    210) 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.
    211) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    212) Nuutinen M, Uhari M, & Karvali T: Consequences of caustic ingestions in children. Acta Paediatr 1994; 83:1200-1205.
    213) OHM/TADS : Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 1990; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    214) OHM/TADS : Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 1991; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    215) Oakes DD, Sherck JP, & Mark JBD: Lye ingestion. J Thorac Cardiovasc Surg 1982; 83:194-204.
    216) Park T, DiBenedetto R, & Morgan K: Diffuse endobronchial polyposis following a titanium tetrachloride inhalation injury. Am Rev Resp Dis 1984; 130:315-317.
    217) Paulsen SM, Nanney LB, & Lynch JB: Titanium tetrachloride: an unusual agent with the potential to create severe burns. J Burn Care Rehabil 1998; 19:377-381.
    218) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    219) Pelclova D & Navratil T: Do corticosteroids prevent oesophageal stricture after corrosive ingestion?. Toxicol Rev 2005; 24(2):125-129.
    220) Perry HD, Hodes LW, & Seedor JA: Effect of doxycycline hyclate on corneal epithelial wound healing in the rabbit alkali-burn model. Preliminary observations. Cornea 1993; 12:379-82.
    221) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    222) Previtera C, Giusti F, & Gugliemi M: Predictive value of visible lesions (cheeks, lips, oropharynx) in suspected caustic ingestion: may endoscopy reasonably be omitted in completely negative pediatric patients?. Pediatr Emerg Care 1990; 6:176-178.
    223) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1991; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    224) Rao RB & Hoffman RS: Caustics and Batteries, in Goldfrank LR, Flomenbaum NE, Lewin NA et al (eds): Goldfrank's Toxicologic Emergencies, 7th ed, McGraw-Hill, New York, NY, 2002.
    225) Reyes HM, Lin CY, & Schluhk FF: Experimental treatment of corrosive esophageal burns. J Pediatr Surg 1974; 9:317-327.
    226) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    227) Roberts JR: Minor burns (Pt II). Emerg Med Ambulatory Care News 1988; 10:4-5.
    228) Rosenberg N, Kunderman PJ, & Vroman L: Prevention of experimental esophageal stricture by cortisone II. Arch Surg 1953; 66:593-598.
    229) Rumack BH & Burrington JD: Caustic ingestions: a rational look at diluents. J Toxicol Clin Toxicol 1977; 11:27-34.
    230) Saari KM, Leinonen J, & Aine E: Management of chemical eye injuries with prolonged irrigation. Acta Ophthalmol Suppl 1984; 52-59.
    231) Saedi S, Nyhus LM, & Gabrys BF: Pharmacological prevention of esophageal stricture: an experimental study in the cat. Am Surg 1973a; 39:465-469.
    232) Saedi S, Nyhust LM, & Gabrys BF: Pharmacological prevention of esophageal stricture: an experimental study in the cat. Am Surg 1973; 39:465-469.
    233) 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.
    234) Sax NI & Lewis RJ: Dangerous Properties of Industrial Materials, 7th ed, Van Nostrand Reinhold Company, New York, NY, 1989, pp 3280.
    235) Sax NI & Lewis RJ: Hawley's Condensed Chemical Dictionary, 11th ed, Van Nostrand Reinhold Company, New York, NY, 1987, pp 1160.
    236) Schild JA: Caustic ingestion in adult patients. Laryngoscope 1985; 95:1199-1201.
    237) Seedor JA, Perry HD, & McNamara TF: Systemic tetracycline treatment of alkali-induced corneal ulceration in rabbits. Arch Ophthalmol 1987; 105:268-271.
    238) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    239) Singh P, Tyagi M, Kumar Y, et al: Ocular chemical injuries and their management. Oman J Ophthalmol 2013; 6(2):83-86.
    240) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2nd ed, Noyes Publications, Park Ridge, NJ, 1985, pp 865-866.
    241) Smilkstein MJ & Fraunfelder F: Ophthalmic Principles, In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed., McGraw-Hill, New York, NY, 2002.
    242) Spector J & Fernandez WG: Chemical, thermal, and biological ocular exposures. Emerg Med Clin North Am 2008; 26(1):125-136.
    243) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    244) Stentoft J: The toxicity of cytarabine. Drug Saf 1990; 5:7-27.
    245) 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.
    246) Sugawa C & Lucas CE: Caustic injury of the upper gastrointestinal tract in adults: a clinical and endoscopic study. Surgery 1989; 106:802-807.
    247) 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.
    248) 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.
    249) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    250) Tuft SJ & Shortt AJ: Surgical rehabilitation following severe ocular burns. Eye (Lond) 2009; 23(10):1966-1971.
    251) 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.
    252) 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.
    253) 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-.
    254) 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.
    255) 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.
    256) 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.
    257) 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.
    258) 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-.
    259) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    260) 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.
    261) Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.
    262) Vergauwen P, Moulin D, & Buts JP: Caustic burns of the upper digestive and respiratory tracts. Eur J Pediatr 1991; 150:700-703.
    263) 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.
    264) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    265) 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.
    266) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.
    267) Wu MH & Lai WW: Surgical management of extensive corrosive injuries of the alimentary tract. Surg Gynecol Obstetr 1993; 177:12-16.
    268) Yarington CT & Heatly CA: Steroids, antibiotics, and early esophagoscopy in caustic esophageal trauma. N Y State J Med 1963; 63:2960-2963.
    269) Zargar SA, Kochhar R, & Mehta S: The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 1991; 37:165-169.
    270) Zargar SA, Kochhar R, & Nagi B: Ingestion of corrosive acids: spectrum of injury to upper gastrointestinal tract and natural history. Gastroenterology 1989; 97:702-707.
    271) Zitnik RJ & Cooper JA: Pulmonary disease due to antirheumatic agents. Clin Chest Med 1990; 11:139-150.