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TRIPHENYL PHOSPHATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Triphenyl phosphate is a triaryl phosphate (organophosphate) compound which lacks significant insecticidal activity and is used as a fireproofing agent and plasticizer in lacquers and varnishes. It is also used as an airplane dope, in airplane glues, as a substitute for camphor in celluloid production (acetylcellulose and nitrocellulose), and as an agent for impregnating roofing paper and upholstery. Additional uses are in gasoline additives, surfactants, flotation agents, and stabilizing and antioxidant compounds.

Specific Substances

    1) Triphenyl phosphate
    2) Celluflex TPP
    3) Phenylphosphate
    4) Phenylphosphate (3:1)
    5) Phosphoric acid, triphenyl ester
    6) TPP
    7) Triphenoxyphosphine oxide
    8) CAS 115-86-6
    9) Molecular Formula: C18-H15-O4-P
    10) NIOSH/RTECS TC 8400000
    11) PHENYL PHOSPHATE (3:1)
    12) TRIPHENYLPHOSPHATE
    1.2.1) MOLECULAR FORMULA
    1) C18-H15-O4-P

Available Forms Sources

    A) FORMS
    1) Triphenyl phosphate has been variously described as: nonflammable needles; crystalline solid or powder; crystals from absolute alcohol-petroleum ether; prisms from alcohol; needles from ether-petroleum ether; and, white platelets (ACGIH, 1986; Budavari, 19896 HSDB, 2001; (Sax & Lewis, 1987; Lewis, 1992).
    B) USES
    1) Triphenyl phosphate is a triaryl phosphate (organophosphate) compound which lacks significant insecticidal activity and is used as a fireproofing agent and plasticizer in lacquers and varnishes (ACGIH, 1986; (Clayton & Clayton, 1981; Budavari, 1996; Finkel, 1983).
    2) It is also used as an airplane dope, in airplane glues, as a substitute for camphor in celluloid production (acetylcellulose and nitrocellulose), and as an agent for impregnating roofing paper and upholstery (ACGIH, 1986; (ITI, 1988; Budavari, 1996; Clayton & Clayton, 1981).
    3) Additional uses are in gasoline additives, surfactants, flotation agents, and stabilizing and antioxidant compounds (ACGIH, 1986; (Budavari, 1996; Clayton & Clayton, 1981).
    4) Triphenyl phosphate is prepared from phosphorus pentoxide and phenol or by reaction of triethyl phosphite with chloramine-T (Budavari, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) There are no reported cases of human systemic poisoning from triphenyl phosphate exposure. Skin sensitization has been reported rarely, although triphenyl phosphate is not an irritant and is poorly absorbed through intact skin.
    B) A delayed onset of peripheral neuropathy similar to that produced by tri-orthocresyl phosphate exposure has been seen in experimental animals.
    C) Triphenyl phosphate is thought to be of less toxicity than tri-orthocresyl phosphate in humans. A group of chronically exposed workers had mildly decreased levels of red blood cell cholinesterase, without associated signs or symptoms of cholinergic excess.
    D) Oxides of phosphorus may be released during thermal decomposition and could produce respiratory tract irritation.
    0.2.6) RESPIRATORY
    A) Exposure to oxides of phosphorus evolved during thermal decomposition could produce respiratory tract irritation.
    0.2.7) NEUROLOGIC
    A) No human cases of peripheral neuropathy due to triphenyl phosphate exposure have been reported. In experimental animals, a delayed onset "dying back" or "distal axonopathy" type of peripheral neuropathy is seen.
    0.2.9) HEPATIC
    A) No human cases of increased liver weight have been reported. In experimental animals, increased liver weight was noted following chronic exposure to triphenyl phosphate.
    0.2.14) DERMATOLOGIC
    A) Dermal irritation does not occur. Two cases of skin sensitization have been reported.
    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) A mild decrease in red blood cell cholinesterase may occur and measurements might be useful as an indication of exposure. Monitoring liver function tests is recommended in serious exposures. Monitor arterial blood gases and chest x-ray in patients with respiratory tract irritation.
    B) Electromyograms and nerve conduction studies are useful in assessing and monitoring patients with peripheral neuropathies.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    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) Administer 100% humidified supplemental oxygen with assisted ventilation as required.
    C) Patients exposed to fumes of oxides of phosphorus released during thermal decomposition of triphenyl phosphate should be moved from the contaminated atmosphere and administered 100% humidified supplemental oxygen with assisted ventilation as required.
    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) Hypersensitivity reactions may require systemic antihistamine or corticosteroid treatment.

Range Of Toxicity

    A) The minimum lethal human triphenyl phosphate exposure has not been delineated. A concentration of 1000 mg/m(3) is considered immediately dangerous to life and health.

Clinical Effects

Summary Of Exposure

    A) There are no reported cases of human systemic poisoning from triphenyl phosphate exposure. Skin sensitization has been reported rarely, although triphenyl phosphate is not an irritant and is poorly absorbed through intact skin.
    B) A delayed onset of peripheral neuropathy similar to that produced by tri-orthocresyl phosphate exposure has been seen in experimental animals.
    C) Triphenyl phosphate is thought to be of less toxicity than tri-orthocresyl phosphate in humans. A group of chronically exposed workers had mildly decreased levels of red blood cell cholinesterase, without associated signs or symptoms of cholinergic excess.
    D) Oxides of phosphorus may be released during thermal decomposition and could produce respiratory tract irritation.

Heent

    3.4.3) EYES
    A) Extraocular motor nerve injury has NOT been reported in exposed humans.
    B) Histologic lesions in the motor nerves of the extraocular muscles of experimental animals have been found following triphenyl phosphate poisoning (Grant, 1986).

Respiratory

    3.6.1) SUMMARY
    A) Exposure to oxides of phosphorus evolved during thermal decomposition could produce respiratory tract irritation.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Exposure to oxides of phosphorus evolved during thermal decomposition of triphenyl phosphate (Sax, 1989) could produce respiratory tract irritation.

Neurologic

    3.7.1) SUMMARY
    A) No human cases of peripheral neuropathy due to triphenyl phosphate exposure have been reported. In experimental animals, a delayed onset "dying back" or "distal axonopathy" type of peripheral neuropathy is seen.
    3.7.2) CLINICAL EFFECTS
    A) SECONDARY PERIPHERAL NEUROPATHY
    1) No human cases of peripheral neuropathy due to triphenyl phosphate exposure have been reported, other than one in which there was also exposure to the more potent neurotoxin, tri-orthocresyl phosphate (Clayton & Clayton, 1981). A description of tri-orthocresyl phosphate peripheral neuropathy in humans is given below:
    a) ONSET - Tri-orthocresyl phosphate produces a delayed onset peripheral neuropathy of the "dying back" or "peripheral axonopathy" variety (Gosselin et al, 1984; Hayes, 1982).
    b) EARLY SYMPTOMS - Following an asymptomatic interval lasting from 8 to 35 days (Gosselin et al, 1984), early symptoms are paresthesias and burning pain, especially in the distal areas of the lower extremities.
    c) FLACCID PARALYSIS - Between 10 and 40 days after exposure, the abrupt onset (sometimes over a period of only a few hours) of a flaccid paralysis is noted, which begins in the musculature of the toes and then progresses rapidly over a few days to symmetrically involve the lower and upper extremities, spreading proximally from the periphery with upper extremity involvement lagging 4 to 5 days behind lower extremity involvement. This flaccid paralysis has signs of a lower motor neuron lesion and involves muscle wasting (Namba et al, 1971).
    d) SPASTICITY - Some patients may have sphincteric incompetence during this phase (Aring, 1942). This flaccid paralysis may be followed by pyramidal signs and spasticity of the lower extremities with clonus, hyperreflexia, hypertonus, and a peculiar spastic gait with foot drop and high steps (Gosselin et al, 1984; Aring, 1942).
    e) REFLEXES - In some patients, diminished or abolished ankle jerks and abdominal reflexes with positive Babinski signs may be noted (Vasilescu & Florescu, 1980).
    f) HYPOESTHESIA - Thermal, tactile, and painful hypoesthesia occurs in some patients (Vasilescu & Florescu, 1980).
    g) PEAK EFFECT - The complete clinical picture may become apparent after 8 to 10 days of progression, although in severe cases the full extent of paralysis may not be reached until after two to three months (Gosselin et al, 1984).
    h) PROGNOSIS - The prognosis is often favorable with a low mortality. Many patients do not require further treatment after one or two years, although 5% of victims may remain incapacitated (Gosselin et al, 1984).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEUROPATHY PERIPHERAL
    a) In experimental animals, triphenyl phosphate exposure produces a delayed "dying back" or "distal axonopathy" type of peripheral neuropathy similar to that produced by tri-orthocresyl phosphate (Hayes, 1982; Clayton & Clayton, 1981; Anger & Johnson, 1985).
    1) This neuropathy is primarily motor, with little or no sensory component (Gosselin et al, 1984).

Hepatic

    3.9.1) SUMMARY
    A) No human cases of increased liver weight have been reported. In experimental animals, increased liver weight was noted following chronic exposure to triphenyl phosphate.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) RATS chronically fed diets containing triphenyl phosphate were found to have increased liver weights at necropsy (ACGIH, 1986).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal irritation does not occur. Two cases of skin sensitization have been reported.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) While dermal irritation does not occur with triphenyl phosphate exposure, two cases of skin sensitization to the material have been reported (Carlsen et al, 1986).

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.
    3.20.3) 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 CAS115-86-6 (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 potential carcinogenicity of triphenyl phosphate, other than one negative study in mice (Sax, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A mild decrease in red blood cell cholinesterase may occur and measurements might be useful as an indication of exposure. Monitoring liver function tests is recommended in serious exposures. Monitor arterial blood gases and chest x-ray in patients with respiratory tract irritation.
    B) Electromyograms and nerve conduction studies are useful in assessing and monitoring patients with peripheral neuropathies.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A mild decrease in RED BLOOD CELL CHOLINESTERASE was noted in one group of workers, but was not well correlated with exposure (ACGIH, 1986; (Clayton & Clayton, 1981).
    a) Measurement of RED BLOOD CELL CHOLINESTERASE might be useful as an indication of exposure in acute poisoning.
    2) In humans, PLASMA PSEUDOCHOLINESTERASE does not seem to be affected (Clayton & Clayton, 1981).
    3) LIVER FUNCTION TESTS - As some hepatic effects have been demonstrated in exposed experimental animals (ACGIH, 1986), monitoring liver function tests is recommended in serious exposures.
    4) NEUROTOXIC ESTERASE - Like tri-orthocresyl phosphate, triphenyl phosphate inhibits neurotoxic esterase (NTE) which is found in circulating lymphocytes as well as nervous tissue (Hayes, 1982).
    a) Assays of NTE in circulating lymphocytes have correlated well with exposure to the neurotoxic agents DEF and merphos (Lotti et al, 1983).
    b) NTE assays are, however, not currently readily available for monitoring of either exposed workers or patients with acute poisoning.
    B) ACID/BASE
    1) Pulse oximetry and/or arterial blood gases should be monitored in patients with respiratory tract irritation following exposure to oxides of phosphorus evolved from thermal decomposition of triphenyl phosphate.
    4.1.4) OTHER
    A) OTHER
    1) ELECTROPHYSIOLOGICAL TESTING
    a) NERVE CONDUCTION - Electromyograms and nerve conduction studies are useful in assessing and monitoring patients with peripheral neuropathies (Vasilescu & Florescu, 1980).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Chest x-ray should be monitored in patients with respiratory tract irritation following exposure to oxides of phosphorus evolved from thermal decomposition of triphenyl phosphate.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) A photometric method has been recommended by NIOSH for triphenyl phosphate measurement (Clayton & Clayton, 1981).
    2) WATER - Triphenyl phosphate has been isolated from water with XAD-2 resin, followed by gas chromatographic determination (LeBel et al, 1981).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) A mild decrease in red blood cell cholinesterase may occur and measurements might be useful as an indication of exposure. Monitoring liver function tests is recommended in serious exposures. Monitor arterial blood gases and chest x-ray in patients with respiratory tract irritation.
    B) Electromyograms and nerve conduction studies are useful in assessing and monitoring patients with peripheral neuropathies.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) ATROPINE
    1) Atropine and oximes should only be administered if there is a clear anticholinesterase component to the poisoning. In all other cases, they should be withheld.
    B) CONTRAINDICATED TREATMENT
    1) A variety of treatments including administration of corticosteroids, vitamins B1 and B12, and pilocarpine have sometimes been recommended in poisoning with the similar agent, tri-orthocresyl phosphate.
    2) There is, however, no evidence that administration of these agents has any beneficial effect in this poisoning and they should most likely be withheld.
    C) MONITORING OF PATIENT
    1) Monitor red blood cell cholinesterase levels and liver function tests in serious poisoning cases.
    D) REHABILITATION THERAPY
    1) Physical and occupational therapy with various orthopedic procedures when indicated aimed at maintaining neuromuscular function should be provided.

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) Administer 100% humidified supplemental oxygen with assisted ventilation as required.
    B) MONITORING OF PATIENT
    1) Monitor pulse oximetry and/or arterial blood gases and chest x-ray in patients with respiratory tract irritation from exposure to oxides of phosphorus released from thermal decomposition of triphenyl phosphate.
    C) 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) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) ACUTE ALLERGIC REACTION
    1) Hypersensitivity reactions may require systemic antihistamine or corticosteroid treatment.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) No studies have addressed the use of extracorporeal elimination techniques in triphenyl phosphate poisoning.

Range Of Toxicity

Summary

    A) The minimum lethal human triphenyl phosphate exposure has not been delineated. A concentration of 1000 mg/m(3) is considered immediately dangerous to life and health.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human triphenyl phosphate exposure has not been delineated.
    B) ANIMAL DATA
    1) In experimental animals, subcutaneous administration of 1,000 milligrams per kilogram is fatal to rabbits, 300 to 1,000 milligrams per kilogram is fatal to cats, and 500 milligrams per kilogram is fatal to monkeys (ACGIH, 1986).
    2) One part per million of triphenyl phosphate in water kills goldfish in 8 hours, while 3 to 5 parts per million kills goldfish in 5 hours (ACGIH, 1986).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) A group of 32 workers engaged in manufacturing triphenyl phosphate showed no adverse health effects following exposure for as long as 10 years to dust, vapor, and mist at concentrations as high as 3.5 milligrams per cubic meter (ACGIH, 1986). A slight and subclinical decrease in red blood cell cholinesterase levels was noted in these workers (ACGIH, 1986).
    2) In vitro studies have indicated a 50 milligrams per kilogram no effect level on cholinesterase inhibition, while 100 milligrams per kilogram produced a 20 percent inhibition of red blood cell cholinesterase (Clayton & Clayton, 1981).
    3) A concentration of 1000 mg/m(3) is considered immediately dangerous to life and health (NIOSH , 1996).
    B) ANIMAL DATA
    1) Subcutaneous administration of 200 milligrams per kilogram causes paralysis in cats, but humans are thought to be less susceptible (ACGIH, 1986; (Gosselin et al, 1984).
    2) Between 0.38 and 1.8 grams of triphenyl phosphate per kilogram administered orally to rats for 3 months caused no deaths. With diets containing 0.1 percent to 0.5 percent triphenyl phosphate fed for 35 days, rats had slight decreases in growth weights and increased liver weights at necropsy (ACGIH, 1986).
    3) Plasma cholinesterase has been found to be inhibited by up to 50 percent of activity following oral triphenyl phosphate administration at 200 milligrams per kilogram to mice and 1,000 milligrams per kilogram to chickens (ACGIH, 1986).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) Triphenyl phosphate blood levels are not readily available and have not been correlated with either exposure or toxicity.
    b) One group of exposed workers had subclinical decreases in red blood cell cholinesterase levels (ACGIH, 1986).
    c) Human blood tested in vitro showed a greater sensitivity to cholinesterase inhibition by triphenyl phosphate than did rodent blood (ACGIH, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS115-86-6 (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) Triphenyl phosphate
    a) TLV:
    1) TLV-TWA: 3 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Cholinesterase inhib
    d) Molecular Weight: 326.28
    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 CAS115-86-6 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Triphenyl phosphate
    2) REL:
    a) TWA: 3 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: 1000 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS115-86-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Triphenyl phosphate
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    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: Triphenyl phosphate
    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 CAS115-86-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Triphenyl phosphate
    2) Table Z-1 for Triphenyl phosphate:
    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: 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) References: RTECS, 1992 Lewis, 1992
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 1273 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 1320 mg/kg
    3) LD50- (ORAL)RAT:
    a) 3500 mg/kg
    b) 3800 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) CHOLINESTERASE - Although triphenyl phosphate inhibits red blood cell cholinesterase, this is thought to be only an incidental finding and not the neurotoxic mechanism (Hayes, 1982).
    B) NEUROTOXIC ESTERASE - Inhibition of a neurotoxic esterase (NTE) may be responsible for the peripheral neuropathy seen in triphenyl phosphate poisoning (Hayes, 1982). Neither carbamylation nor sulfation of neurotoxic esterase cause axonal damage, while phosphorylation does produce axonopathy (Gosselin et al, 1984).
    C) PERIPHERAL NEUROPATHY -
    1) Triphenyl phosphate produces a delayed onset peripheral neuropathy of the "dying back" or "distal axonopathy" type (Hayes, 1982).
    2) This involves Wallerian degeneration beginning at the portion of the nerve most distal from the cell body and extending a varying distance proximally (Hayes, 1982).
    3) Myelin degeneration may be seen as a secondary effect (Hayes, 1982).
    4) It is not presently clear whether the nerve lesion involves a direct attack on the axon or some metabolic disturbance in the cell body (Hayes, 1982). Although there appears to be no disturbance of protein transport by the axon, disordered axonal transport of other essential substances has not been investigated (Hayes, 1982).
    D) DEMYELINATION in the peripheral nerves and spinal cord was noted in animals studies, which may have been due to contaminations with other phosphate esters (Menzer, 1987).

Physicochemical

Physical Characteristics

    A) Triphenyl phosphate is a colorless, crystalline needle-shaped solid (at room temperature) with a characteristic phenol-like odor (ACGIH, 1986; (Sax, 1989).
    B) Triphenyl phosphate has been variously described as: nonflammable needles; crystalline solid or powder; crystals from absolute alcohol-petroleum ether; prisms from alcohol; needles from ether-petroleum ether; and white platelets (HSDB, 2005; Budavari, 1996; Sax & Lewis, 1987; Lewis, 1992).
    C) Several sources indicate it may be odorless (HSDB, 2005; Budavari, 1996) .

Ph

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

Molecular Weight

    A) 326.28

Animal Toxicology

Clinical Effects

    11.1.6) FELINE/CAT
    A) PARALYSIS - A single intraperitoneal injection of 0.1 to 0.5 g/kg of triphenyl phosphate given to 6 cats produced paralysis after 16 to 18 days (Sutton, 1960).

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