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BENZOTRICHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Benzotrichloride is a colorless to yellow, oily, unstable, fuming liquid with a penetrating, pungent odor.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C7-H5-Cl3 C6H5CCl3

Available Forms Sources

    A) FORMS
    1) Benzotrichloride is a colorless to yellow, oily, unstable, fuming liquid with a penetrating, pungent odor (Budavari, 1996; Lewis, 1998). Commercial grades of this compound can contain the following impurities: chlorotoluenes; chlorobenzyl chlorides; benzyl chloride; chlorobenzal chlorides; chlorobenzotrichlorides; benzylidene chloride; and hydrochloric acid (HSDB , 2000; Lewis, 1998).
    B) SOURCES
    1) Benzotrichloride is produced by the chlorination of boiling toluene (100 to 140 degrees C) in the presence of ultraviolet light and 2% phosphorus trichloride and purified by rectification (Budavari, 1996; IARC, 1982; Lewis, 1997).
    C) USES
    1) Benzotrichloride is used as a raw material in synthetic dyes (Malachite Green, Rosamine, Quinoline Red, and Alizarin Yellow A) and in organic synthesis (ITI, 1995; Lewis, 1997; Lewis, 1998; Sittig, 1991). It is also used as an intermediate in the synthesis of ethyl benzoate and benzenyl groups (Budavari, 1996; Lewis, 1998).
    2) Benzotrichloride is used in the production of benzotrifluoride, an important additive in herbicide, pharmaceutical, and antimicrobial agents. This compound is also used in the production of hydroxybenzophenone ultra-violet stabilizers which are used in the prevention of discoloration of a variety of plastics (IARC, 1982).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Benzotrichloride is used as a raw material in synthetic dyes, as an intermediate in the synthesis of ethyl benzoate and benzenyl groups, and in the production of benzotrifluoride, which is an important additive in herbicide, pharmaceutical, and antimicrobial agents. This compound is also used in the production of hydroxybenzophenone ultra-violet stabilizers which are used to prevent discoloration of plastics.
    B) TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars. Benzotrichloride is a possible human carcinogen and may be associated with lung tumors from occupational exposure.
    C) EPIDEMIOLOGY: Exposure is rare. Benzotrichloride is typically available for industrial purposes.
    D) In experimental animals, signs and symptoms of exposure have included slowed respiration; hyperemia of extremities; motor automatism; twitching of peripheral muscles; leukopenia; mild anemia; decreased renal function; and mild histological changes in the liver, kidney, and thyroid.
    E) WITH POISONING/EXPOSURE
    1) Benzotrichloride exposure is unusual; limited data regarding specific toxicity following exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    2) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or Grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop Grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation, particularly gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema. Exposure to large doses may cause CNS depression.
    3) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Other rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because acidic products available in the home are generally of low concentration.
    a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.
    4) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported. Exposure to large doses may cause CNS depression.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    6) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis, and systemic toxicity.
    0.2.4) HEENT
    A) Irritation of the eyes, nose, throat, and mucous membranes may occur from contact with the fumes. Direct contact with the liquid may cause serious burns.
    0.2.5) CARDIOVASCULAR
    A) Degenerative changes were seen in the myocardium of animals exposed to lethal doses of benzyl chloride, a closely related compound.
    0.2.6) RESPIRATORY
    A) The fumes of benzotrichloride are highly irritating. Severe respiratory tract irritation with possible pulmonary edema or lung injury may develop.
    0.2.7) NEUROLOGIC
    A) CNS depression and excitation has occurred in experimental animals exposed to large doses of benzotrichloride.
    0.2.8) GASTROINTESTINAL
    A) Irritation or burns of the esophagus or gastrointestinal tract may occur. Anorexia, nausea, vomiting, diarrhea, and abdominal cramping or pain may be noted.
    0.2.9) HEPATIC
    A) Degenerative changes were seen in animals fatally poisoned with benzyl chloride.
    0.2.10) GENITOURINARY
    A) Degenerative changes were found in animals lethally poisoned with benzyl chloride.
    0.2.11) ACID-BASE
    A) Because benzotrichloride liberates hydrochloric acid upon contact with moisture, significant exposures would be expected to result in acidosis.
    0.2.14) DERMATOLOGIC
    A) Benzotrichloride is corrosive to skin. It produced depigmentation of the hair in mice. Skin irritation or burns may be seen.
    0.2.20) REPRODUCTIVE
    A) Teratogenic effects have been reported in rats.
    0.2.21) CARCINOGENICITY
    A) Lung cancer deaths were elevated in workers exposed to benzotrichloride and other substances. Benzotrichloride has induced lung tumors in animals by various routes of exposure. Skin tumors, leukemias, and lymphomas have also occurred in animal studies.
    0.2.22) OTHER
    A) Benzotrichloride may be hazardous by inhalation or ingestion. It was rapidly absorbed from the gastrointestinal tract, and was eliminated primarily in the urine of rats.

Laboratory Monitoring

    A) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. Serum lactate and base deficit may also be useful in these patients.
    C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings does NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade 2 or 3 burns, to evaluate for strictures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is very little information available regarding the treatment of benzotrichloride-induced injury; the following data is derived from experience with other acids.
    B) MILD TO MODERATE ORAL TOXICITY
    1) Within the first 12 hours of exposure, if burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.
    C) SEVERE ORAL TOXICITY
    1) Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.
    D) DILUTION
    1) Dilute with 4 to 8 ounces of water may be useful if it can be performed shortly after ingestion in patients who are able to swallow, with no vomiting or respiratory distress; then the patient should be NPO until assessed for the need for endoscopy. Neutralization, activated charcoal, and gastric lavage are all contraindicated.
    E) AIRWAY MANAGEMENT
    1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury. Severe edema may make intubation difficult; be prepared for surgical airway management (cricothyroidotomy) in patients with severe upper airway edema.
    F) ENDOSCOPY
    1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with acid ingestion. The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns.
    G) BRONCHOSPASM
    1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids
    H) CORTICOSTEROIDS
    1) The use of corticosteroids to prevent stricture formation is controversial. Corticosteroids should not be used in patients with grade I or grade III injury, as there is no evidence that it is effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use, so routine use is not recommended.
    I) STRICTURE
    1) A barium swallow or repeat endoscopy should be performed several weeks after ingestion in any patient with grade II or III burns or with difficulty swallowing to evaluate for stricture formation. Recurrent dilation may be required. Some authors advocate early stent placement in these patients to prevent stricture formation.
    J) SURGICAL MANAGEMENT
    1) Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns on endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, early resection and repair in these patients is associated with improved outcome.
    K) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: Patients with an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged to home.
    2) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, or extensive grade II burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    L) PITFALLS
    1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns.
    2) Patients may have severe tissue necrosis and impending perforation requiring early surgical intervention without having severe hypotension, rigid abdomen, or radiographic evidence of intraperitoneal air.
    3) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses.
    4) The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn. All patients with acidic eye injury should be evaluated by an ophthalmologist.
    M) DIFFERENTIAL DIAGNOSIS
    1) Alkaline corrosive ingestion, gastrointestinal hemorrhage, or perforated viscus.
    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) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) 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.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) Severe eye irritation may occur, and early ophthalmologic consultation should be acquired.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) For burns, clean with a mild disinfectant and water, debride devitalized skin, apply topical antibiotic. Optimal dressing may vary with type and location of burn. Determine tetanus immunization status and administer tetanus toxoid 0.5 mL IM if required.
    3) Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.
    B) TOXICITY: Serious burns are less likely if the pH >3. Injury is usually greater with either a large ingestion (usually deliberate), or a high concentration acid (usually not a household product). With highly concentrated liquids, severe burns may occur in up to 100% of all patients.
    C) In a case series of unintentional caustic ingestions (mixed liquid and solid, acids and bases) among children, the incidence of significant esophageal or gastric burns was 5% to 35%. However, adults with deliberate acid ingestions are more likely to develop significant esophageal and/or gastric burns (40% to 95%).

Clinical Effects

Summary Of Exposure

    A) USES: Benzotrichloride is used as a raw material in synthetic dyes, as an intermediate in the synthesis of ethyl benzoate and benzenyl groups, and in the production of benzotrifluoride, which is an important additive in herbicide, pharmaceutical, and antimicrobial agents. This compound is also used in the production of hydroxybenzophenone ultra-violet stabilizers which are used to prevent discoloration of plastics.
    B) TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars. Benzotrichloride is a possible human carcinogen and may be associated with lung tumors from occupational exposure.
    C) EPIDEMIOLOGY: Exposure is rare. Benzotrichloride is typically available for industrial purposes.
    D) In experimental animals, signs and symptoms of exposure have included slowed respiration; hyperemia of extremities; motor automatism; twitching of peripheral muscles; leukopenia; mild anemia; decreased renal function; and mild histological changes in the liver, kidney, and thyroid.
    E) WITH POISONING/EXPOSURE
    1) Benzotrichloride exposure is unusual; limited data regarding specific toxicity following exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    2) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or Grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop Grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation, particularly gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema. Exposure to large doses may cause CNS depression.
    3) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Other rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because acidic products available in the home are generally of low concentration.
    a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.
    4) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported. Exposure to large doses may cause CNS depression.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    6) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis, and systemic toxicity.

Heent

    3.4.1) SUMMARY
    A) Irritation of the eyes, nose, throat, and mucous membranes may occur from contact with the fumes. Direct contact with the liquid may cause serious burns.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CONJUNCTIVITIS - Exposure to the fumes of benzotrichloride would be expected to irritate the eyes, and direct contact may cause severe burns and injury. Benzotrichloride induced severe eye irritation in the rabbit in the Standard Draize Test (RTECS, 1996; Lewis, 1996).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) MUCOSAL IRRITATION - Irritation of the mucosa of the nose and throat occurs with exposure to low concentrations of benzyl chloride vapor (Proctor et al, 1988), and would also be expected with benzotrichloride.
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) MUCOSAL IRRITATION - Irritation of the mucosa of the nose and throat occurs with exposure to low concentrations of benzyl chloride vapor (Proctor et al, 1988), and would also be expected with benzotrichloride.

Cardiovascular

    3.5.1) SUMMARY
    A) Degenerative changes were seen in the myocardium of animals exposed to lethal doses of benzyl chloride, a closely related compound.
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MYOCARDIUM CHANGES
    a) Degenerative changes were seen in the myocardium in experimental animals exposed to lethal doses of benzyl chloride, a closely related compound (Mikhailova, 1965). This effect has not been reported in exposed humans.

Respiratory

    3.6.1) SUMMARY
    A) The fumes of benzotrichloride are highly irritating. Severe respiratory tract irritation with possible pulmonary edema or lung injury may develop.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) The fumes of benzotrichloride are highly irritating (Lewis, 1996). Lung damage may occur with heavy exposure to benzyl chloride, a closely related compound (CHRIS , 1996), and would be expected to occur with benzotrichloride.
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Pulmonary edema may be seen after significant inhalation exposure to benzyl chloride (CHRIS , 1996). Similar effects would be expected with benzotrichloride, due to the liberation of hydrochloric acid in the body.

Neurologic

    3.7.1) SUMMARY
    A) CNS depression and excitation has occurred in experimental animals exposed to large doses of benzotrichloride.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEFICIT
    a) Central nervous depression was seen in experimental animals exposed to large doses of benzotrichloride (Lewis, 1996).
    2) CNS STIMULANT
    a) CNS excitation was noted in rats (Hathaway et al, 1996).

Gastrointestinal

    3.8.1) SUMMARY
    A) Irritation or burns of the esophagus or gastrointestinal tract may occur. Anorexia, nausea, vomiting, diarrhea, and abdominal cramping or pain may be noted.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Anorexia, nausea, vomiting, diarrhea, and abdominal cramping may occur following ingestion of benzyl chloride (CHRIS , 1996; Plunkett, 1976), and would be expected to occur with benzotrichloride.
    B) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Severe irritation or burns of the mouth, throat, esophagus, or gastrointestinal tract could occur following ingestion of benzyl chloride (CHRIS , 1996). Similar effects would be expected with benzotrichloride because of the generation of hydrochloric acid.

Hepatic

    3.9.1) SUMMARY
    A) Degenerative changes were seen in animals fatally poisoned with benzyl chloride.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LIVER DAMAGE
    a) Degenerative changes were seen in the liver in poisoned experimental animals exposed to fatal doses of benzyl chloride, a closely related compound (Mikhailova, 1965). This effect has not been reported in exposed humans.

Genitourinary

    3.10.1) SUMMARY
    A) Degenerative changes were found in animals lethally poisoned with benzyl chloride.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TOXIC NEPHROPATHY
    a) Degenerative changes were seen in the kidneys in experimental animals fatally poisoned with benzyl chloride (Mikhailova, 1965). This effect has not been reported in exposed humans.

Acid-Base

    3.11.1) SUMMARY
    A) Because benzotrichloride liberates hydrochloric acid upon contact with moisture, significant exposures would be expected to result in acidosis.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Significant exposures would be expected to cause some degree of acidosis because benzotrichloride liberates hydrochloric acid upon contact with moisture.

Dermatologic

    3.14.1) SUMMARY
    A) Benzotrichloride is corrosive to skin. It produced depigmentation of the hair in mice. Skin irritation or burns may be seen.
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SKIN NECROSIS
    a) Benzotrichloride is corrosive to skin (Lewis, 1996). Benzotrichloride induced moderate skin irritation in the rabbit in the Standard Draize Test and severe skin irritation in the rabbit in the Open Draize Test (RTECS, 1996). In the course of a mouse skin painting assay, benzotrichloride induced erythema and swelling (Fukuda et al, 1981).
    2) VITILIGO
    a) Benzotrichloride produced depigmentation of the hair in C57 black mice which had been injected intradermally with a dose of 5 mg (HSDB, 1996).

Reproductive

    3.20.1) SUMMARY
    A) Teratogenic effects have been reported in rats.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) Teratogenic effects have been reported in rats (Schardein, 1993).
    B) FETOTOXICITY
    1) Benzyl chloride, a closely related compound, was fetotoxic but not teratogenic in rats (Skowronski & Abdel-Rahman, 1986).
    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.
    B) ANIMAL STUDIES
    1) RETARDED OFFSPRING DEVELOPMENT - In rats administered 208 milligrams per kilogram benzyl chloride orally from days 1 through 19 of gestation, fertility, postnatal development, and decreased resistance to anoxia were noted in the offspring (IARC, 1982b).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS98-07-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: benzotrichloride
    b) Carcinogen Rating: 2A
    1) The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
    3.21.2) SUMMARY/HUMAN
    A) Lung cancer deaths were elevated in workers exposed to benzotrichloride and other substances. Benzotrichloride has induced lung tumors in animals by various routes of exposure. Skin tumors, leukemias, and lymphomas have also occurred in animal studies.
    3.21.3) HUMAN STUDIES
    A) NEOPLASM
    1) IARC Classifications (IARC, 1982)
    a) Animals - Sufficient evidence
    b) Human - Limited evidence
    2) In the NTP Seventh Annual Report on Carcinogens, 1992, benzotrichloride was anticipated to be a carcinogen (RTECS, 1996).
    3) Deaths from lung cancer were elevated in a Japanese occupational group exposed to benzotrichloride and other substances in the production of benzoyl chloride. Two deaths were observed versus 0.06 expected. Benzotrichloride was thought to be the causative agent (Sakabe et al, 1976; Sakabe & Fukuda, 1977).
    4) Two deaths occurred in benzotrichloride-exposed American male employees with more than 15 years of exposure. Deaths from respiratory cancers as a whole were also elevated (7 observed versus 2.8 expected), but this difference was not statistically significant (Wong, 1988).
    5) Benzotrichloride was possibly the cause of cancers of the mouth and throat, digestive system, respiratory system, genitourinary system, and lymphatic hematopoietic system in a group of 953 British workers exposed to chlorinated toluenes (Sorahan & Waterhouse, 1983; (Sorahan et al, 1983). A follow-up study concluded that deaths from lung cancer and Hodgkin's disease were significantly elevated in workers exposed through 1984 (Sorahan & Cathcart, 1989).
    3.21.4) ANIMAL STUDIES
    A) ANIMAL STUDIES
    1) Lung adenomas were induced in A/J mice by benzotrichloride at a total dose of 1,440 mg/kg by IP injection given three times weekly for eight weeks (Stoner et al, 1986). Activation of the K-ras oncogene occurs consistently in these tumors (You et al, 1993).
    2) Tumors of the lung, skin, and lymphatic tissues developed in mice inhaling benzotrichloride vapor 30 minutes per day, two days per week, for 5 months (Yoshimura et al, 1986). In an earlier study, 1.6 ppm benzotrichloride inhaled for 30 minutes, twice per week, for 12 months, induced lung tumors, skin lesions, and inflammatory lesions of the lymph nodes, liver, spleen, and kidney in mice (Yoshimura et al, 1979).
    3) Benzotrichloride induced leukemia and tumors of the skin and lung in a mouse skin painting study (Fukuda et al, 1981).
    4) In mouse studies, benzotrichloride was found to be an equivocal tumorigenic, neoplastic and carcinogenic agent by RTECS criteria with skin and appendages tumors; lungs and thorax tumors; kidney, ureter, and bladder tumors; and the presence of lymphomas including Hodgkin's disease (RTECS , 1991).
    5) Benzotrichloride induced papillomas, carcinomas, and leukemia in mice (Sittig, 1985).

Genotoxicity

    A) Benzotrichloride has induced DNA damage, repair and mutations in bacteria.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. Serum lactate and base deficit may also be useful in these patients.
    C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings does NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade 2 or 3 burns, to evaluate for strictures.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion. In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests and liver enzymes.
    B) COAGULATION STUDIES
    1) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain INR, PT, PTT, fibrinogen, fibrin degradation products, and type and crossmatch for blood.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Elevated levels of hippuric acid in the urine confirmed exposure to benzotrichloride in rats (HSDB, 1996).
    B) OTHER
    1) Monitor urine output and urinalysis in patients with significant gastrointestinal burns, perforation, or bleeding.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway burns.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm.
    2) The absence of these findings does NOT rule out the possibility of necrosis or perforation of the esophagus or stomach.
    3) Obtain a chest radiograph in patients with pulmonary signs or symptoms.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, or extensive grade II burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor Grade I burns and who can tolerate oral intake can be discharged to home.

Monitoring

    A) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. Serum lactate and base deficit may also be useful in these patients.
    C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings does NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade 2 or 3 burns, to evaluate for strictures.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Activated charcoal should NOT be used. It may cause vomiting which can worsen caustic gastrointestinal injury, and may obscure endoscopy findings.
    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; Penner, 1980).
    2) A report concerning emergency surgical resection of the alimentary tract following caustic ingestions has indicated that 5 out of 6 patients sustained injuries beyond the pylorus as a result of gastric lavage (Wu & Lai, 1993).
    B) 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).
    C) INSERTION OF NASOGASTRIC TUBE
    1) It has been suggested 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 and worsen the burn (Penner, 1980).
    2) Many authorities oppose this procedure fearing esophageal or gastric perforation. A soft nasogastric or orogastric tube should only be passed within 90 minutes following the large ingestion of a strong acid.
    D) BURN
    1) Burns of the oropharynx, esophagus, stomach, and duodenum may occur. Complications such as stricture, perforation, gastrointestinal bleeding and gastric outlet obstruction are related to the depth of burn. Early (within 24 hours) endoscopy should be performed to assess the severity of injury and guide future management.
    E) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    F) ULTRASONOGRAPHY
    1) A small study suggests that esophageal ultrasonography may be useful in predicting the likelihood of strictures after corrosive ingestion (Kamijo et al, 2004).
    a) Miniprobe ultrasonography was performed endosopically at the site of the most severe lesion in 11 patients with corrosive esophageal injury. Grading was as follows: grade 0 distinct muscular layers without thickening (5 patients); grade I distinct muscular layers with thickening (4 patients): grade II obscured muscular layers with indistinct margins (1 patient); and grade III muscular layers that could not be differentiated (1 patient). Lesions were also classified as to whether the area of worst damage involved part of the circumference (type a) or the entire circumference (type b).
    b) Strictures did not develop in patients with grade 0 or 1 lesions. A transient stricture developed in the patient with a grade IIa lesion. A stricture that required repeated dilatation developed in the patient with a grade IIIb lesion.
    G) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989a; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    H) 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, 1984).
    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, 1993a). 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.
    I) 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.
    2) A 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).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) OXYGEN
    1) Move patients with inhalation exposure from the toxic environment and administer 100% humidified supplemental oxygen with assisted ventilation as required.
    B) AIRWAY MANAGEMENT
    1) Assure airway patency and oxygenation. Endotracheal intubation could be necessary if severe irritation of the upper airway occurs.
    C) 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.
    D) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) 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.
    2) 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).
    3) 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.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) Minimum lethal human exposure is unknown.
    B) TOXICITY: Serious burns are less likely if the pH >3. Injury is usually greater with either a large ingestion (usually deliberate), or a high concentration acid (usually not a household product). With highly concentrated liquids, severe burns may occur in up to 100% of all patients.
    C) In a case series of unintentional caustic ingestions (mixed liquid and solid, acids and bases) among children, the incidence of significant esophageal or gastric burns was 5% to 35%. However, adults with deliberate acid ingestions are more likely to develop significant esophageal and/or gastric burns (40% to 95%).

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    2) CARCINOGENICITY: IARC (2000) classifies alpha-chlorinated toluenes and benzoyl chloride as Group 2A, probably carcinogenic to humans.

Maximum Tolerated Exposure

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

Workplace Standards

    A) ACGIH TLV Values for CAS98-07-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Benzotrichloride
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.1 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A2
    2) Codes: Skin
    3) Definitions:
    a) A2: Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Eye, skin, and URT irr
    d) Molecular Weight: 195.5
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS98-07-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS98-07-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: Benzotrichloride
    a) A2 :Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Benzotrichloride
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    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): 2A ; Listed as: benzotrichloride
    a) 2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Category 1 ; Listed as: alpha-Chlorinated toluenes: benzyl trichloride
    a) Category 1 : Substances that cause cancer in man and can be assumed to make a significant contribution to cancer risk. Epidemiological studies provide adequate evidence of a positive correlation between the exposure of humans and the occurence of cancer. Limited epidemiological data can be substantiated by evidence that the substance causes cancer by a mode of action that is relevant to man.
    6) MAK (DFG, 2002): Category 2 ; Listed as: Benzyl trichloride
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS98-07-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: IARC, 1982 HSDB, 2000 ITI, 1995 ) Lewis, 1996 RTECS, 2000
    1) LD50- (ORAL)MOUSE:
    a) 702 mg/kg
    2) LD50- (ORAL)RAT:
    a) 6 g/kg
    b) 6 g/kg for 14D
    3) TCLo- (INHALATION)MOUSE:
    a) 1620 ppb for 30M for 22W-I -- NEO
    4) TCLo- (INHALATION)RAT:
    a) 100 mg/m(3) for 2H for 9W-I
    b) 49 mg/m(3) for 4W-I

Physicochemical

Physical Characteristics

    A) Benzotrichloride exists as a clear, colorless to yellow, oily, unstable, fuming liquid with a penetrating odor (Lewis, 1997; Lewis, 1996; Lewis, 1998). It will fume in air (Budavari, 1996; Lewis, 1997). In water and moist air, it will hydrolyze to benzoic and hydrochloric acids (Budavari, 1996; Lewis, 1998; Lewis, 1997).

Molecular Weight

    A) 195.48

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