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PHOSPHORUS PENTACHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Phosphorus pentachloride is a polychlorinated phosphorus compound used as a catalytic agent in acetylcellulose manufacturing, in producing benzotrichloride from benzal chloride, and for replacing hydroxyl groups with chloride, especially for converting acids to acid chlorides (Windholz, 1983; Sax & Lewis, 1987; Clayton & Clayton, 1982; EPA, 1985; Proctor & Hughes, 1978). It is also used as a dehydrating and chlorinating agent (ACGIH, 1986; ITI, 1985).
    B) Phosphorus pentachloride is used in the manufacture of pharmaceuticals, plasticizers, gasoline additives, chlorinated compounds, and agricultural chemicals (Sittig, 1985).
    C) Phosphorus pentachloride is produced from phosphorus or phosphorus trichloride by the action of chlorine, and is available in technical or reagent grades (Sax & Lewis, 1987).

Specific Substances

    1) Phosphorus pentachloride
    2) Phosphorane, pentachloro-
    3) Fosforo(pentacloruro di) (Italian)
    4) Fosforpentachloride (Dutch)
    5) Pentachlorophosphane
    6) Pentachlorophosphorous
    7) Pieciochlorek fosforu (Polish)
    8) Phosphore(pentachlorure de) (French)
    9) Phosphoric chloride
    10) Phosphorpentachlorid (German)
    11) Phosphorous pentachloride
    12) Phosphorus pentachloride, solid
    13) Phosphorus perchloride
    14) Phosphorus(V) chloride
    15) Molecular Formula: P-Cl5
    16) NIOSH/RTECS TB 6125000
    17) STCC 4932323
    18) CAS 10026-13-8
    19) References: RTECS, 1988; EPA, 1985; Windholz, 1983
    1.2.1) MOLECULAR FORMULA
    1) Cl5-P

Available Forms Sources

    A) SOURCES
    1) Phosphorus pentachloride is produced from phosphorus or phosphorus trichloride by the action of chlorine (Sax & Lewis, 1987).
    B) USES
    1) Phosphorus pentachloride is a polychlorinated phosphorus compound used as a catalytic agent in acetylcellulose manufacturing, in producing benzotrichloride from benzal chloride, and for replacing hydroxyl groups with chloride, especially for converting acids to acid chlorides (Windholz, 1983; Sax & Lewis, 1987; Clayton & Clayton, 1982; EPA, 1985; Proctor & Hughes, 1978). It is also used as a dehydrating and chlorinating agent (ACGIH, 1986; ITI, 1985).
    2) Phosphorus pentachloride is used in the manufacture of pharmaceuticals, plasticizers, gasoline additives, chlorinated compounds, and agricultural chemicals (Sittig, 1985).

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 pentachloride causes irritation of the eyes and respiratory tract. Bronchitis and wheezing or bronchopneumonia may be seen. Pulmonary edema, dyspnea, and chest pain or pleurodynia may be noted, with potentially delayed onset up to 72 hours following exposure. Dermal irritation may occur as phosphorus pentachloride is corrosive.
    B) Headache, dizziness, weakness, hoarseness, nephritis, anorexia, nausea, and vomiting have been reported. Ingestion may produce immediate pain in the mouth and throat, followed by abdominal pain, nausea, vomiting, and hematemesis. Ingestion of large amounts may lead to death in circulatory shock.
    0.2.4) HEENT
    A) Conjunctivitis, nasal irritation, and throat irritation and pain may occur.
    0.2.5) CARDIOVASCULAR
    A) Death may occur in cardiovascular collapse following ingestion.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation, pulmonary edema, and bronchitis may occur.
    0.2.7) NEUROLOGIC
    A) Headache, weakness, and dizziness may occur.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, esophageal or gastrointestinal tract irritation, abdominal pain, or bleeding may occur following ingestion.
    0.2.9) HEPATIC
    A) Elevations of LDH levels may occur.
    0.2.10) GENITOURINARY
    A) Nephritis with oliguria may develop.
    0.2.14) DERMATOLOGIC
    A) Dermal irritation or burns may be seen.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Monitor CBC, urinalysis, and liver and kidney function tests in significant exposures.
    B) Monitor ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) MUCOSAL DECONTAMINATION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
    C) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.
    D) Observe patient for development of GI irritation or burns following an ingestion. Esophagoscopy may be considered to determine the extent of injury in symptomatic patients.
    E) Observe patients for the development of systemic toxicity.
    F) Monitor urine output. Hemodialysis might be required if oliguria develops.
    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) Some authors have recommended flushing exposed skin with a 5 percent copper sulfate solution followed by soap and water washing, but the efficacy and potential complications of this treatment are not well understood.

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.
    B) 120 to 130 ppm was fatal to mice with a 10 minute inhalation exposure.

Clinical Effects

Hepatic

    3.9.1) SUMMARY
    A) Elevations of LDH levels may occur.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) Transient, asymptomatic elevations of LDH levels were noted in some workers exposed to a mixture of irritant fumes and vapors, including phosphorus pentachloride (Rosenthal et al, 1978).

Genitourinary

    3.10.1) SUMMARY
    A) Nephritis with oliguria may develop.
    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) Nephritis with oliguria has been reported (ITI, 1985; Plunkett, 1976; Rosenthal et al, 1978).
    B) BLOOD IN URINE
    1) A trace of albumin and a few red blood cells were noted in the urine of some workers exposed to a mixture of irritant fumes and vapors, including phosphorus pentachloride (Rosenthal et al, 1978).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal irritation or burns may be seen.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Dermal irritation or burns may occur as phosphorus pentachloride is corrosive (ITI, 1985; Sax, 1984; Proctor & Hughes, 1978).

Reproductive

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

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS10026-13-8 (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
    3.21.3) 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.

Summary Of Exposure

    A) Phosphorus pentachloride causes irritation of the eyes and respiratory tract. Bronchitis and wheezing or bronchopneumonia may be seen. Pulmonary edema, dyspnea, and chest pain or pleurodynia may be noted, with potentially delayed onset up to 72 hours following exposure. Dermal irritation may occur as phosphorus pentachloride is corrosive.
    B) Headache, dizziness, weakness, hoarseness, nephritis, anorexia, nausea, and vomiting have been reported. Ingestion may produce immediate pain in the mouth and throat, followed by abdominal pain, nausea, vomiting, and hematemesis. Ingestion of large amounts may lead to death in circulatory shock.

Heent

    3.4.1) SUMMARY
    A) Conjunctivitis, nasal irritation, and throat irritation and pain may occur.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Eye irritation may be noted (Grant, 1986).
    3.4.5) NOSE
    A) Irritation of the mucosa of the nose and throat may be noted following inhalation exposure (EPA, 1985; Plunkett, 1976; Proctor & Hughes, 1978).
    3.4.6) THROAT
    A) Irritation of the mucosa of the nose and throat may be noted following inhalation exposure (EPA, 1985; Plunkett, 1976; Proctor & Hughes, 1978).
    B) Immediate pain in the mouth and throat may occur if this agent is ingested (EPA, 1985).

Cardiovascular

    3.5.1) SUMMARY
    A) Death may occur in cardiovascular collapse following ingestion.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) With severe gastrointestinal tract irritation and bleeding following ingestion, death may occur in cardiovascular collapse (EPA, 1985).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation, pulmonary edema, and bronchitis may occur.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Respiratory tract irritation may be seen following inhalation exposure (ACGIH, 1986; Clayton & Clayton, 1982).
    B) ACUTE LUNG INJURY
    1) Pulmonary edema, dyspnea, and chest pain or pleurodynia may be seen, with potentially delayed onset up to 72 hours following exposure (ITI, 1985; Plunkett, 1976; Proctor & Hughes, 1978).
    C) BRONCHITIS
    1) Bronchitis and wheezing or bronchopneumonia may develop following exposure (ACGIH, 1986; ITI, 1985; Plunkett, 1976; Rosenthal et al, 1978).
    2) CHRONIC BRONCHITIS - Chronic bronchitis may develop following a severe, acute exposure (Plunkett, 1976; Rosenthal et al, 1978).
    a) Abnormalities on pulmonary function testing and hypoxemia may be seen following inhalation exposure, and may not completely resolve in all cases (Rosenthal et al, 1978).

Neurologic

    3.7.1) SUMMARY
    A) Headache, weakness, and dizziness may occur.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Headache, weakness, and dizziness have been reported (ITI, 1985; Plunkett, 1976; Rosenthal et al, 1978).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, esophageal or gastrointestinal tract irritation, abdominal pain, or bleeding may occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting have been reported (ITI, 1985; Plunkett, 1976; Rosenthal et al, 1978).
    B) GASTROINTESTINAL IRRITATION
    1) Ingestion may produce immediate pain in the mouth and throat, followed by abdominal pain, nausea, vomiting, and hematemesis (EPA, 1985). Ingestion of large amounts with severe gastrointestinal tract irritation may lead to death in circulatory shock (EPA, 1985).
    2) Esophageal irritation or burns may be predicted to occur in some cases of ingestion.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor CBC, urinalysis, and liver and kidney function tests in significant exposures.
    B) Monitor ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.
    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: Phosphorus pentachloride measurements in air can be done by collecting samples with an impinger or fritted bubbler which are then analyzed by either a colorimetric or ion specific electrode technique (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.

Monitoring

    A) Monitor CBC, urinalysis, and liver and kidney function tests in significant exposures.
    B) Monitor ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    B) NASOGASTRIC SUCTION
    1) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    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) Patients should initially be kept NPO following ingestion until the degree and site of injury is determined.
    2) 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.
    3) Surgical consultation and intervention could be required if bleeding or perforation develop.
    4) The role of steroids and H2-blocking agents (cimetidine, ranitidine) in ingestions of phosphorus pentachloride is controversial.
    C) MONITORING OF PATIENT
    1) Monitor vital signs, fluid and electrolyte status, urinalysis, urine output, and renal and liver function tests in significant exposures.
    2) Monitor nasogastric aspirate and stools for frank or occult bleeding.
    D) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment 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) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    B) 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).
    C) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) OBSERVATION REGIMES
    1) CHRONIC BRONCHITIS - Following severe acute exposure, chronic bronchitis may develop in some cases (Rosenthal et al, 1978; Plunkett, 1976). Prolonged followup and monitoring of pulmonary function tests may be required.
    2) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    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).
    6.8.2) TREATMENT
    A) OPHTHALMIC EXAMINATION AND EVALUATION
    1) CONSULTATION - If severe eye irritation is present, prolonged initial flushing with tap water or normal saline and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Some references have recommended washing contaminated skin with a 5 percent solution of copper sulfate followed by a soap and water wash (ITI, 1985; Plunkett, 1976). The efficacy and potential complications of this treatment modality are not well studied.
    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) SKIN ABSORPTION
    1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.
    2) If severe nephritis with oliguria should develop, hemodialysis may be useful as supportive therapy.

Range Of Toxicity

Summary

    A) Minimum lethal human exposure is unknown.
    B) 120 to 130 ppm was fatal to mice with a 10 minute inhalation exposure.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) A concentration of 120 to 130 parts per million has been reported to be fatal to mice with a 10 minute inhalation exposure (ACGIH, 1986; Proctor et al, 1988).

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 CAS10026-13-8 (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 pentachloride
    a) TLV:
    1) TLV-TWA: 0.1 ppm
    2) TLV-STEL:
    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 and eye irr
    d) Molecular Weight: 208.24
    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 CAS10026-13-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Phosphorus pentachloride
    2) REL:
    a) TWA: 1 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 70 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS10026-13-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Phosphorus pentachloride
    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 pentachloride
    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 CAS10026-13-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Phosphorus pentachloride
    2) Table Z-1 for Phosphorus pentachloride:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1
    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, 1992
    1) LD50- (ORAL)RAT:
    a) 660 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Phosphorus pentachloride is a direct irritant of eyes, skin, and mucous membranes (EPA, 1985).
    1) When phosphorus pentachloride contacts water, it releases hydrochloric acid which may be responsible for its irritant effects (Rosenthal et al, 1978).
    2) Under conditions of high pressure or temperature, phosphorus pentachloride can release chloride fumes (Sax, 1984; Rosenthal et al, 1978) which might also be responsible for some of the irritant effects noted from exposure in fires or explosions (Rosenthal et al, 1978).

Physicochemical

Physical Characteristics

    A) Phosphorus pentachloride is a white to pale yellow deliquescent crystalline solid with an irritating, pungent, unpleasant, hydrochloric acid-like odor. It fumes in moist air (ACGIH, 1986; EPA, 1985; Windholz, 1983; Clayton & Clayton, 1982).
    1) It has also been described as greenish-yellow in color (AAR, 1987).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 208.27 (Budavari, 1989)

References

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