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PHOSPHORUS TRICHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Phosphorus trichloride is produced by the reaction of yellow phosphorus with chlorine or red phosphorus and dry chlorine. It is used as an intermediate in chemical manufacturing.

Specific Substances

    1) Phosphorus trichloride
    2) Phosphorus chloride
    3) Chloride of phosphorus
    4) Fosforo (tricloruro di)
    5) Fosfortrichloride
    6) Phosphine, trichloro-
    7) Phosphore (trichlorure de)
    8) Phosphorous chloride
    9) Phosphortrichlorid
    10) Trichlorophosphine
    11) Trojchlorek fosforu
    12) STCC 4932359
    13) NIOSH/RTECS TH 3675000
    14) Molecular Formula: Cl3-P
    15) CAS 7719-12-2
    16) PHOSPHOROUS TRICHLORIDE
    17) TROJCHLOREK FORFORU
    1.2.1) MOLECULAR FORMULA
    1) Cl3-P

Available Forms Sources

    A) SOURCES
    1) Phosphorus trichloride is produced by the reaction of yellow phosphorus with chlorine (Clayton & Clayton, 1994). It may also be prepared from red phosphorus and dry chlorine in the presence of refluxing phosphorus trichloride (Budavari, 1996).
    2) Phosphorus trichloride is produced by passing a current of dry chlorine over phosphorus which is gently heated. A mixture of mostly phosphorus trichloride with some phosphorus pentachloride distills over. Phosphorus is then added to the process, and the whole mixture is distilled (Sax & Lewis, 1987).
    B) USES
    1) It is used as an intermediate in chemical manufacturing of many industrial chemicals, which have included insecticides to synthetic surfactants to ingredients found in household products (i.e. silver polish)(HSDB , 2000).
    2) Phosphorus trichloride is used in the process of depositing metal on rubber, and as a chemical intermediate in the production of organophosphate pesticides, agricultural chemicals, surfactants, phosphites (by reaction with alcohols and phenol), laboratory reagents, gasoline additives, plasticizers, dyestuffs, germicidal preparations, medications, and other products, and as a finishing agent for textiles (AAR, 1987; ACGIH, 1986; Sax & Lewis, 1987; EPA, 1985; ITI, 1985; Sittig, 1985; HSDB , 2000).
    3) Phosphorus trichloride is used as a chlorinating agent and catalyst (ACGIH, 1986; HSDB , 2000).
    4) Phosphorus trichloride is used in the process of producing iridescent metal deposits and in the production of phosphorus oxychloride and phosphorus pentachloride (Budavari, 1996).
    5) AVAILABILITY - Phosphorus trichloride is available and is shipped in pure (99.5% plus) and technical (98.5% plus) grades (CHRIS , 2000).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Phosphorus trichloride vapors are irritating to the eyes, skin, and respiratory tract.
    B) ONSET - Pulmonary edema may occur with onset delayed from 12 to 24 hours. This delay is similar to what may occur following chlrine gas exposures.
    C) SYMPTOMS - Direct contact may cause severe acid burns of any moist tissues including the eyes and mucosa of the respiratory and gastrointestinal tracts. Severe irritation or burns of the mouth, throat, esophagus, or gastrointestinal tract may follow ingestion. Subclinical elevations of liver enzymes or mild renal injury could occur.
    1) Dermatitis, dermal burns, vertigo, headache, dizziness, anorexia, nausea, vomiting, pleuritic chest discomfort, coughing, bronchitis, pneumonitis, and renal injuries (in experimental animals) have all been caused by phosphorus trichloride exposure.
    D) CHRONIC TOXICITY - At lower chronic exposure levels, asthma-like syndromes may develop followed by a chronic chemical pneumonitis or emphysema.
    E) When heated to decomposition phosphorus chloride emits highly toxic fumes of chloride and oxides of phosphorus.
    0.2.3) VITAL SIGNS
    A) Fever may develop.
    0.2.4) HEENT
    A) Lacrimation, conjunctivitis, corneal clouding, photophobia, and loss of vision may occur. Vapor exposure can cause irritation of the nose and throat, necrosis of the nostrils, and mouth ulcers.
    0.2.6) RESPIRATORY
    A) Irritation, dyspnea, decreases in pulmonary function tests, hypoxemia, and pulmonary edema may be seen.
    0.2.7) NEUROLOGIC
    A) Headache and vertigo may occur.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur. Severe burns of the gastrointestinal tract may occur after ingestion.
    0.2.9) HEPATIC
    A) Asymptomatic transient elevations of LDH have been observed.
    0.2.10) GENITOURINARY
    A) Nephritis has been seen in exposed experimental animals.
    0.2.14) DERMATOLOGIC
    A) Dermal irritation or severe acid burns, skin ulcers, and skin thickening may occur.
    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) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    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) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    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.
    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) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Workers exposed to vapor concentrations ranging from 10 to 150 mg/m(3) complained of burning in the eyes and throat, photophobia, an oppressive feeling in the chest, and bronchitis.

Clinical Effects

Summary Of Exposure

    A) Phosphorus trichloride vapors are irritating to the eyes, skin, and respiratory tract.
    B) ONSET - Pulmonary edema may occur with onset delayed from 12 to 24 hours. This delay is similar to what may occur following chlrine gas exposures.
    C) SYMPTOMS - Direct contact may cause severe acid burns of any moist tissues including the eyes and mucosa of the respiratory and gastrointestinal tracts. Severe irritation or burns of the mouth, throat, esophagus, or gastrointestinal tract may follow ingestion. Subclinical elevations of liver enzymes or mild renal injury could occur.
    1) Dermatitis, dermal burns, vertigo, headache, dizziness, anorexia, nausea, vomiting, pleuritic chest discomfort, coughing, bronchitis, pneumonitis, and renal injuries (in experimental animals) have all been caused by phosphorus trichloride exposure.
    D) CHRONIC TOXICITY - At lower chronic exposure levels, asthma-like syndromes may develop followed by a chronic chemical pneumonitis or emphysema.
    E) When heated to decomposition phosphorus chloride emits highly toxic fumes of chloride and oxides of phosphorus.

Vital Signs

    3.3.1) SUMMARY
    A) Fever may develop.
    3.3.3) TEMPERATURE
    A) FEVER may be present in either acute or subacute poisoning (Sassi, 1952).

Heent

    3.4.1) SUMMARY
    A) Lacrimation, conjunctivitis, corneal clouding, photophobia, and loss of vision may occur. Vapor exposure can cause irritation of the nose and throat, necrosis of the nostrils, and mouth ulcers.
    3.4.3) EYES
    A) LACRIMATION - Burning of the eyes and lacrimation have been reported in patients exposed to phosphorus trichloride (includes vapor exposure) and its hydration products (Watson et al, 1984; (Proctor et al, 1988; Clayton & Clayton, 1994).
    B) CONJUNCTIVITIS has been seen in some experimental animals exposed to 2 to 4 ppm in air. Corneal clouding occurred with exposure to 23 to 90 ppm over 6 hours and included severe systemic effects (Grant & Schuman, 1993).
    C) PHOTOPHOBIA - Exposed workers have complained of photophobia (Sassi, 1952).
    D) ANIMAL STUDIES -
    1) Eye irritation has been seen in experimental animals exposed to the vapor. Corneal clouding occurred with exposure to higher vapor concentrations (23 to 90 ppm) and included severe systemic effects (Grant & Schuman, 1993).
    2) Molodkina (1974) reported necrosis in the eye causing irreversible loss of vision in experimental animals following acute exposure.
    3.4.5) NOSE
    A) IRRITATION - Vapor exposure can cause irritation of the nose and throat (Sittig, 1985; HSDB , 2000).
    B) NECROSIS of the nostrils occurred in experimental animals after acute inhalation exposure to phosphorus trichloride (Weeks et al, 1964).
    3.4.6) THROAT
    A) IRRITATION - Vapor exposure can cause irritation of the nose and throat (Sittig, 1985; HSDB , 2000).
    B) ANIMAL STUDIES - Acute exposure caused skin and mouth ulcers in experimental animals (Molodkina, 1974).

Respiratory

    3.6.1) SUMMARY
    A) Irritation, dyspnea, decreases in pulmonary function tests, hypoxemia, and pulmonary edema may be seen.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Patients exposed to vapors from spilled material complained of dyspnea (Wason et al, 1984; Finnegan & Hodson, 1989).
    B) RESPIRATORY FAILURE
    1) PULMONARY FUNCTION - Patients exposed to vapors from spilled material had decreases in a variety of pulmonary function tests which improved over the following month (Wason et al, 1984; Finnegan & Hodson, 1989).
    C) BRONCHOSPASM
    1) IRRITATION - Vapor exposure causes irritation of the respiratory tract (Proctor & Hughes, 1978; Finnegan & Hodson, 1989; HSDB , 2000). Bronchospasm, cough, and wheezing may be seen.
    D) ACUTE LUNG INJURY
    1) More serious inhalation exposures can produce pulmonary edema, which may delayed in onset as long as 12 to 24 hours after exposure (generally symptoms are delayed in minor to moderate exposures) (Proctor & Hughes, 1978; Clayton & Clayton, 1994).
    E) HYPOXEMIA
    1) HYPOXEMIA and asthma developed in a 34-year-old woman for a protracted period of time following a single 15 minute exposure to a high concentration of hydrogen chloride and phosphorus trichloride vapor (Finnegan & Hodson, 1989).
    F) RESPIRATORY FINDING
    1) CHRONIC TOXICITY
    a) Repeated or prolonged low-level exposure, even to low concentrations, can result in an asthma-like syndrome with wheezing and a chronic cough (Sassi, 1952; Hathaway et al, 1996). This reaction may be characterized today as RAD (reactive airway disease) in which prolonged or repeated exposure to low concentrations may result in chronic cough and wheezing; pulmonary changes are nonfibrotic and nonprogressive (Hathaway et al, 1996).
    b) Some patients with occupational exposure have developed emphysema with increased pulmonary markings on chest x-ray (Sassi, 1952).
    c) One to 8 weeks after exposure, patients experienced irritation of the pharynx, coughing, dyspnea, and severe asthmatic bronchitis. Emphysema was noted in some patients at least 1 year following exposure (Sassi, 1952).

Neurologic

    3.7.1) SUMMARY
    A) Headache and vertigo may occur.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Headache and vertigo may occur with phosphorus trichloride exposure (ITI, 1985).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur. Severe burns of the gastrointestinal tract may occur after ingestion.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Patients exposed to phosphorus trichloride vapors developed nausea and vomiting (Wason et al, 1984).
    B) CHEMICAL BURN
    1) Severe burns of the mouth, throat, esophagus, or gastrointestinal tract may occur if phosphorus trichloride is ingested (Proctor & Hughes, 1978; HSDB , 2000).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) STOMATITIS ULCERATIVE
    a) Mouth ulcers developed in experimental animals following acute exposure (Molodkina, 1974).
    2) SKIN ULCERATION
    a) Skin ulcers developed in experimental animals following acute exposure (Molodkina, 1974).

Hepatic

    3.9.1) SUMMARY
    A) Asymptomatic transient elevations of LDH have been observed.
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) HEPATOTOXICITY - Some patients exposed to vapors from spilled material developed asymptomatic transient elevations of LDH (Wason et al, 1984).

Genitourinary

    3.10.1) SUMMARY
    A) Nephritis has been seen in exposed experimental animals.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHRITIS
    a) Nephritis has been seen in exposed experimental animals (ITI, 1985; Proctor & Hughes, 1978). This effect has not been reported in exposed humans.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) Elevated leukocyte counts with neutrophilia have been described in chronically exposed workers (Sassi, 1952).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal irritation or severe acid burns, skin ulcers, and skin thickening may occur.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Dermal irritation may occur from direct exposure (Proctor & Hughes, 1978; Clayton & Clayton, 1994).
    B) CHEMICAL BURN
    1) Ulceration or severe acid burns may occur from direct exposure (Proctor & Hughes, 1978; Clayton & Clayton, 1994).
    2) Release of hydrochloric and phosphoric acid occurs and can cause burns when phosphorus trichloride is wet or in contact with moist tissues (Proctor & Hughes, 1978).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SKIN DISORDER
    a) Acute exposure caused thickening of skin fold and bleeding in experimental animals (Molodkina, 1974).
    2) NECROSIS ISCHEMIC
    a) NECROSIS of the paws occurred after acute inhalation exposure in experimental animals (Weeks et al, 1964).

Musculoskeletal

    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) NECROSIS of the paws occurred after acute inhalation exposure in experimental animals (Weeks et al, 1964).

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.
    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.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7719-12-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Genotoxicity

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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

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

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Air concentrations can be collected by impinger or a fritted bubbler and measured by a colorimetric method or an ion specific electrode (Sittig, 1985).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) The onset of pulmonary edema may be delayed for up to 12 to 24 hours after cessation of inhalation exposure. Patients should be observed in a controlled setting for at least 24 hours.
    B) Patients with significant or chronic exposure should have periodic monitoring for the development of an asthma-like syndrome or emphysema.

Monitoring

    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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.
    B) EMESIS/NOT RECOMMENDED -
    1) DO NOT induce emesis as it may worsen caustic injury.
    C) ACTIVATED CHARCOAL/NOT RECOMMENDED
    1) Activated charcoal is of no value and may obscure endoscopy findings; it should be avoided.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS
    1) Do NOT induce emesis.
    B) NASOGASTRIC TUBE
    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.
    6.5.3) TREATMENT
    A) 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).
    B) IRRITATION SYMPTOM
    1) There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of phosphorus trichloride ingestion. The following information is derived from experience with other corrosives.
    C) 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.
    D) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    E) 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, 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.
    F) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    G) AIRWAY MANAGEMENT
    1) If severe upper airway irritation with swelling or burns occurs, ensure airway patency and adequacy of oxygenation and ventilation. Endotracheal intubation or creation of a surgical airway might be necessary in severe cases with airway compromise.
    H) FLUID/ELECTROLYTE BALANCE REGULATION
    1) If significant vomiting occurs, monitor fluid and electrolyte status and replace losses as necessary.

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) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    B) IRRITATION SYMPTOM
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) Onset of pulmonary edema may be delayed for up to 12 to 24 hours after exposure.
    C) PULMONARY EDEMA
    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) LABORATORY TEST
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    2) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    E) MEASUREMENT OF RESPIRATORY FUNCTION
    1) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) CONSULTATION
    1) Because severe irritation may occur with direct liquid splashes in the eye, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) 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) 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) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) LACK OF INFORMATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) Workers exposed to vapor concentrations ranging from 10 to 150 mg/m(3) complained of burning in the eyes and throat, photophobia, an oppressive feeling in the chest, and bronchitis.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) OCCUPATIONAL
    1) Workers exposed to phosphorus trichloride vapor concentrations ranging from 10 to 150 milligrams/cubic meter during production of the chemical complained of burning in the eyes and throat, photophobia, an oppressive feeling in the chest, and bronchitis (Sassi, 1952).
    a) Subacute exposure resulted in throat irritation, catarrh, coughing, nocturnal dyspnea, dyspnea on exertion, and emphysema after 1 to 2 years of employment (Sassi, 1952).
    B) ANIMAL DATA
    1) Eye and respiratory tract irritation was noted in cats exposed to vapor concentrations of 2 to 4 parts per million for 6 hours (Grant, 1986).
    a) Severe systemic effects and corneal clouding were seen in cats exposed to vapor concentrations of 23 to 90 parts per million for 6 hours (Grant, 1986).
    2) Only slight systemic illness was produced in cats exposed to 0.7 part per million for 6 hours (ACGIH, 1986).
    a) A one hour exposure to between 50 and 90 parts per million caused serious systemic injury in cats (ACGIH, 1986).
    C) CASE REPORTS
    1) Severe hypoxemia and asthma developed in a 34-year-old woman for a protracted period of time following a single 15 minute exposure to a high concentration of hydrogen chloride and phosphorus trichloride vapor (Finnegan & Hudson, 1989).

Workplace Standards

    A) ACGIH TLV Values for CAS7719-12-2 (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) Phosphorus trichloride
    a) TLV:
    1) TLV-TWA: 0.2 ppm
    2) TLV-STEL: 0.5 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): URT, eye, and skin irr
    d) Molecular Weight: 137.35
    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 CAS7719-12-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Phosphorus trichloride
    2) REL:
    a) TWA: 0.2 ppm (1.5 mg/m(3))
    b) STEL: 0.5 ppm (3 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 25 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7719-12-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Phosphorus trichloride
    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 ; Listed as: Phosphorus trichloride
    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 CAS7719-12-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Phosphorus trichloride
    2) Table Z-1 for Phosphorus trichloride:
    a) 8-hour TWA:
    1) ppm: 0.5
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 3
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) Reference: RTECS, 1991
    1) LD50- (ORAL)RAT:
    a) 550 mg/kg
    b) 18 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Phosphorus trichloride is a direct irritant of skin, eyes, and mucous membranes (Sittig, 1985; Clayton & Clayton, 1982). This material decomposes to hydrochloric and phosphoric acids on contact with moisture, and can produce severe corrosive effects on tissues (Proctor & Hughes, 1978).

Physicochemical

Physical Characteristics

    A) Phosphorus trichloride is a clear, colorless to yellow colored fuming nonflammable liquid with an irritating, pungent acid-like odor (AAR, 1987; ACGIH, 1986; Budavari, 1996).
    1) Phosphorus trichloride fumes in air. It sinks in water and reacts with water, producing a harmful vapor (CHRIS , 2000).
    2) Phosphorus trichloride rapidly decomposes in moist air (ITI, 1985).

Molecular Weight

    A) 137.35 (RTECS , 2000)

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