Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

TOCP AND RELATED AGENTS

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) TOCP (triorthocresyl phosphate) is the most toxic of the three isomers of tricresyl phosphate (triorthocresyl phosphate, trimetacresyl phosphate (TMCP or tri-m-cresyl phosphate), and triparacresyl phosphate (TPCP or tri-p-cresyl phosphate) in decreasing order of toxicity) (Sittig, 1991; Clayton & Clayton, 1994).
    B) TOCP is used as a polyvinyl chloride, polystyrene, lacquer, varnish, and nitrocellulose plasticizer, as a plastic fire retardant, a water proofing compound, in air filter mediums, in lubricants designed to operate under extremely high pressures, as a hydraulic fluid, in the production of heat-stable lubricating oils, as a gasoline additive, in the manufacture of dopes and certain synthetic fabrics and synthetic lignin resins, and as a heat exchange medium for such uses as cooling fluid in machine guns (ACGIH, 1986) Hathaway, 1996; (Snyder, 1987; Susser & Stein, 1957).
    C) TOCP is devoid of insecticidal activity, and produces a delayed peripheral neurotoxicity but little or no anticholinesterase poisoning in man, although it is an organophosphate compound (Harbison, 1998).
    D) Exposure to a number of other related organophosphate compounds has been shown to produce a similar neurotoxic clinical picture (Hayes & Laws, 1991; Gosselin et al, 1984).

Specific Substances

    1) o-Cresyl phosphate
    2) o-Tolyl phosphate
    3) o-Trikresylphosphate (German)
    4) Phosflex 179-C
    5) Phosphoric acid, tri-o-cresyl ester
    6) Phosphoric acid, tris(2-methylphenyl) ester
    7) TOFK
    8) TOTP
    9) Tri 2-methylphenyl phosphate
    10) Tri-o-cresyl phosphate
    11) Tri-o-tolyl phosphate
    12) Tri-2-tolyl phosphate
    13) Triorthocresyl phosphate
    14) Tris(o-cresyl)-phosphate
    15) Tris(o-methylphenyl) phosphate
    16) Tris(o-tolyl) phosphate
    17) Trojkrezylu fosforan (Polish)
    18) CAS 78-30-8
    1.2.1) MOLECULAR FORMULA
    1) C21-H21-04-P

Available Forms Sources

    A) FORMS
    1) TOCP is an almost colorless, odorless, oily liquid (Lewis, 1997).
    B) SOURCES
    1) It is derived from cresol and phosphorous oxychloride (Lewis, 1997).
    C) USES
    1) TOCP is used as a polyvinyl chloride, polystyrene, lacquer, varnish, and nitrocellulose plasticizer, as a plastic fire retardant, a water proofing compound, in air filter mediums, in lubricants designed to operate under extremely high pressures, as a hydraulic fluid, in the production of heat-stable lubricating oils, as a gasoline additive, in the manufacture of dopes and certain synthetic fabrics and synthetic lignin resins, and as a heat exchange medium for such uses as cooling fluid in machine guns (ITI, 1995; ACGIH, 1986) Hathaway, 1988; (Susser & Stein, 1957).
    2) A rapid onset of peripheral neuropathy has been reported in experimental animals administered Abate (bithion), azinphos-methyl, carbophenothion (Trithion; S-(p-chlorophenylthio)methyl O,O- diethylphosphorodithioate), Ciodrin, coumaphos, dicapthon, dioxathion, EPN (O-ethyl O-p-nitrophenyl phenylphosphonothioate), Ethion (Embathion, Nialate; O,O,O',O',-tetraethyl S,S'- methylenebisphosphorodithioate), fenthion, malathion, menazon, methyl parathion, Methyl Trithion, phorate, ronnel, and Ruelene (Dowco 132; 4-tert-butyl-2-chlorophenyl methyl methylphosphoramidate) (Gosselin et al, 1984; Namba et al, 1971). Peripheral neuropathy has not been reported in humans exposed to these agents.
    3) Delayed onset of peripheral neuropathy has been found in poisoning with triphenyl phosphate, DFP (diisopropylphosphorotrithioate), Mipafox (Isopestox; bis-(monoisopropylamino)-fluorophosphate), DEF (S,S,S,-tributyl phosphorotrithioate), Dursban (Dowco 179; O,O-diethyl O-(3,5,6-trichloro-2-pyridyl)-phosphorothioate), and Merphos (tributyl phosphorotrithioate) (Gosselin et al, 1984; Clayton & Clayton, 1994; Hayes & Laws, 1991; Namba et al, 1971).
    4) A pure motor neuropathy has been described in two patients, one exposed to Dipterex and one exposed to Divipan (Vasilescu & Florescu, 1980).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) EARLY EFFECTS - TOCP poisoning is characterized by early nausea, vomiting, diarrhea, and abdominal pain, with no signs and symptoms of anticholinesterase (cholinergic) poisoning. Early GI effects then clear, followed by an 8 to 35- day asymptomatic latent period.
    B) LATE EFFECTS -
    1) A pre-paralytic phase occurs in some patients, manifesting with diarrhea, conjunctivitis, laryngitis, rhinitis, pharyngitis, distal extremity paresthesias, and cramping calf pain.
    2) Flaccid paralysis usually begins in the toes and extends proximally and symmetrically in both upper and lower extremities. Paralysis peaks in intensity over a period of 2 to 3 months and its resolution is variable.
    C) PERMANENT SEQUELAE - Some patients make an apparent full recovery while others remain with more or less severe disability.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) A feverish feeling has been described following exposure.
    0.2.7) NEUROLOGIC
    A) A delayed peripheral neuropathy of the "dying back" or "peripheral axonopathy" variety predominates.
    B) Between 10 and 40 days after exposure, abrupt onset of flaccid paralysis is noted. This may be followed by lower extremity spasticity with clonus, hyperreflexia, hypertonus, and a peculiar spastic gait. In severe cases the full extent of paralysis may not be reached until after 2 to 3 months. Recovery is variable. Mortality is usually low and approximately 5% of victims may remain paralyzed.
    0.2.8) GASTROINTESTINAL
    A) Abdominal pain, nausea, and vomiting often occur. Diarrhea may last several weeks.
    0.2.14) DERMATOLOGIC
    A) The soles of the feet and palms may be cold, cyanotic, and profusely diaphoretic.
    0.2.20) REPRODUCTIVE
    A) TOCP produced toxic effects on both male and female REPRODUCTIVE SYSTEMS when Long-Evans rats were given doses of 0 to 400 mg/kg by gavage prior to, and during breeding. Spermatotoxic effects, includes reduced motility, concentration, velocity, and abnormal morphology. Damage to ovarian and uterine tissue also contributed to severely lowered fertility rates (HSDB , 1999).

Laboratory Monitoring

    A) Plasma pseudocholinesterase levels may be decreased but do not correlate with either the severity of symptoms or the degree of exposure.
    B) Electromyograms and nerve conduction velocity studies may be useful in evaluating a patient with neuropathy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    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.
    C) 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.
    D) Avoid cathartic administration.
    E) Treatment is symptomatic and supportive.
    F) Atropine and 2-PAM chloride do not prevent delayed peripheral neuropathy, and as there is no cholinergic component to the poisoning, these agents should not be given.
    G) Many nonspecific treatments including administration of vitamins B1 and B12, corticosteroids, and pilocarpine have been described by various authors, but only physical and occupational therapy and related orthopedic interventions have shown actual benefit.
    H) If profuse diarrhea occurs, monitor fluid and electrolyte status and replace as needed.
    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.
    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).

Range Of Toxicity

    A) The human lethal oral dose of TOCP is about 1 g/kg; doses of 6 to 7 mg/kg have produced serious paralysis.

Clinical Effects

Summary Of Exposure

    A) EARLY EFFECTS - TOCP poisoning is characterized by early nausea, vomiting, diarrhea, and abdominal pain, with no signs and symptoms of anticholinesterase (cholinergic) poisoning. Early GI effects then clear, followed by an 8 to 35- day asymptomatic latent period.
    B) LATE EFFECTS -
    1) A pre-paralytic phase occurs in some patients, manifesting with diarrhea, conjunctivitis, laryngitis, rhinitis, pharyngitis, distal extremity paresthesias, and cramping calf pain.
    2) Flaccid paralysis usually begins in the toes and extends proximally and symmetrically in both upper and lower extremities. Paralysis peaks in intensity over a period of 2 to 3 months and its resolution is variable.
    C) PERMANENT SEQUELAE - Some patients make an apparent full recovery while others remain with more or less severe disability.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) A feverish feeling has been described following exposure.
    3.3.3) TEMPERATURE
    A) Part of the pre-paralytic phase may include a feverish feeling despite normal body temperature (Gosselin et al, 1984).

Heent

    3.4.2) HEAD
    A) Non-tender, symmetrical swelling of the parotid glands has been described in some cases of TOCP poisoning (Plunkett, 1976; Susser & Stein, 1957).
    3.4.3) EYES
    A) Accommodation disturbances and nystagmus may occur (Plunkett, 1976; Grant, 1993).
    B) Inflammation of the conjunctiva lasting about 24 to 36 hours may occur during the pre-paralytic phase in about a third of cases (Namba et al, 1971).
    C) A single accidental splash contact with TOCP does not produce corneal burns (Grant, 1993).
    3.4.5) NOSE
    A) During the pre-paralytic phase, inflammation of mucous membranes with rhinitis, pharyngitis, laryngitis, and dysphagia may occur in about a third of cases, lasting for 24 to 36 hours (Namba et al, 1971).
    3.4.6) THROAT
    A) During the pre-paralytic phase, inflammation of mucous membranes with rhinitis, pharyngitis, laryngitis, and dysphagia may occur in about a third of cases, lasting for 24 to 36 hours (Namba et al, 1971).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) CASE SERIES - Three of 10 patients involved in one outbreak of TOCP poisoning had inverted T waves or elevated ST segments in the precordial ECG leads, but these findings were not definitely connected with the TOCP poisoning (Susser & Stein, 1957).
    2) No other authors have noted EKG effects associated with TOCP exposure.

Neurologic

    3.7.1) SUMMARY
    A) A delayed peripheral neuropathy of the "dying back" or "peripheral axonopathy" variety predominates.
    B) Between 10 and 40 days after exposure, abrupt onset of flaccid paralysis is noted. This may be followed by lower extremity spasticity with clonus, hyperreflexia, hypertonus, and a peculiar spastic gait. In severe cases the full extent of paralysis may not be reached until after 2 to 3 months. Recovery is variable. Mortality is usually low and approximately 5% of victims may remain paralyzed.
    3.7.2) CLINICAL EFFECTS
    A) SECONDARY PERIPHERAL NEUROPATHY
    1) The major toxicity of TOCP is a delayed peripheral neuropathy of the "dying back" or "peripheral axonopathy" variety (Gosselin et al, 1984; Hayes & Laws, 1991; Woolf, 1995).
    a) Following an asymptomatic interval lasting from 8 to 35 days (Gosselin et al, 1984; CHRIS , 1999), early symptoms are paresthesias and causalgias, especially in the distal portions of the lower extremities (Srivastava et al, 1990; Wang et al, 1995; Tosi et al, 1994).
    b) Between 10 and 40 days after exposure, there is abrupt onset (sometimes over a period of only a few hours) of flaccid paralysis, 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. Some patients may have sphincteric incompetence during this phase (Aring, 1942).
    2) 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 (the "Jake Walk" named for victims of a poisoning epidemic who consumed a Jamaican ginger extract contaminated with TOCP) (Gosselin et al, 1984; Morgan & Tulloss, 1976; Vasilescu & Florescu, 1980; Aring, 1942; Woolf, 1995).
    a) In some patients, diminished or abolished ankle jerks and abdominal reflexes with positive Babinski signs may be noted (Vasilescu & Florescu, 1980).
    b) Thermal, tactile, and painful hypoesthesia occurs in some patients (Vasilescu & Florescu, 1980; Wang et al, 1995).
    c) 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; Wang et al, 1995).
    d) This flaccid paralysis has signs of a lower motor neuron lesion and involves muscle wasting (Namba et al, 1971; Tosi et al, 1994; Wang et al, 1995).
    3) There is usually a low mortality.
    4) Autopsy of 6 human cases revealed demyelination of nerve cells and involvement of the anterior horn cells (Hathaway, 1996).
    5) Muscular weakness among survivors may increase over a period of several weeks or months; recovery may take months or years, and, in 5% to 30% of cases, permanent incapacitating residual effects remain, usually confined to the lower limbs (Gosselin et al, 1984; Hunter et al, 1944; Susser & Stein, 1957; Srivastava et al, 1990; Tosi et al, 1994; Wang et al, 1995).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEUROPATHY
    a) SWINE treated with TOCP at oral doses of 800 milligrams/kilogram developed depression in cholinesterase and neurotoxic esterase activity in the brain and spinal cord (Barrett & Oehme, 1994).
    b) SWINE treated with TOCP at oral doses of 400, 800 or 1,000 milligrams/kilogram developed delayed neurotoxicity 10 to 12 days post exposure (Barrett & Oehme, 1994). The severity of the neurotoxicity was dose related.
    c) In Japanese QUAIL, oral administration of tri-ortho-tolyl-phosphate (500 milligrams/kilogram) did not cause delayed neurotoxicity while subcutaneous administration of triphenyl phosphite (6.25 to 500 milligrams/kilogram) caused delayed neurotoxicity with dose related severity (Varghese et al, 1995).

Gastrointestinal

    3.8.1) SUMMARY
    A) Abdominal pain, nausea, and vomiting often occur. Diarrhea may last several weeks.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Abdominal pain, nausea, and vomiting occur in most patients immediately after ingestion of TOCP (Aring, 1942; Gosselin et al, 1984; Namba et al, 1971; HSDB , 1999; Srivastava et al, 1990; Wang et al, 1995).
    B) DIARRHEA
    1) Diarrhea occurs in most patients almost immediately after TOCP ingestion and may last for several weeks (Aring, 1942).

Dermatologic

    3.14.1) SUMMARY
    A) The soles of the feet and palms may be cold, cyanotic, and profusely diaphoretic.
    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) The soles of the feet and palms have been noted to be cold, sometimes cyanotic, and to sweat profusely in victims of TOCP poisoning, an effect which may last for months (Aring, 1942; Susser & Stein, 1957).
    B) SKIN ABSORPTION
    1) TOCP is absorbed easily through the skin (ACGIH, 1986; CHRIS , 1999).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Cramping pain in the calf muscles is a common early finding which precedes the development of neuropathy (Gosselin et al, 1984; Tosi et al, 1994; Wang et al, 1995).

Reproductive

    3.20.1) SUMMARY
    A) TOCP produced toxic effects on both male and female REPRODUCTIVE SYSTEMS when Long-Evans rats were given doses of 0 to 400 mg/kg by gavage prior to, and during breeding. Spermatotoxic effects, includes reduced motility, concentration, velocity, and abnormal morphology. Damage to ovarian and uterine tissue also contributed to severely lowered fertility rates (HSDB , 1999).
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) TOCP was negative in one rat teratogenicity study (Schardein, 1993).
    b) TOCP is transferred to the fetus in rats (Ahmed et al, 1993). TOCP was not teratogenic or fetotoxic in rats given up to 350 mg/kg/day on days 6 through 18 of gestation (Tocco et al, 1987). A similar lack of effect was seen in rats given up to 750 mg/kg on days 18 and 19 (Mele & Jensh, 1977). Tricresyl phosphate containing less than 9.0% TOCP produced fewer litters with live young, smaller litter size, and decreased pup viability in rats when both males and females received 400 mg/kg (Carlton et al, 1987). The rat is relatively resistant to the neurotoxic effects of TOCP; it may not be a good model for reproductive studies.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the possible effects of TOCP exposure during pregnancy.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) HUMANS
    1) LACK OF INFORMATION
    a) At the time of this review, no data were available to assess the potential effects of breast feeding during TOCP exposure. One patient exposed to TOCP who subsequently developed peripheral neuropathy had breast fed an infant for one month during the early phases of the illness, but no details of the infant's examination or clinical course were reported (Susser & Stein, 1957).
    b) One patient exposed to TOCP who subsequently developed peripheral neuropathy had breast fed an infant for one month during the early phases of the illness, but no details of the infant's examination or clinical course were reported (Susser & Stein, 1957).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS78-30-8 (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 potential of TOCP in humans or experimental animals.

Genotoxicity

    A) At the time of this review, no genetic studies were found for TOCP. There is some evidence that the reactive metabolite is an alkylating agent (Burka & Chapin, 1993).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma pseudocholinesterase levels may be decreased but do not correlate with either the severity of symptoms or the degree of exposure.
    B) Electromyograms and nerve conduction velocity studies may be useful in evaluating a patient with neuropathy.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Plasma pseudocholinesterase levels have been noted to be decreased to as low as 70% of normal in exposed individuals, but these levels do not correlate with either the severity of symptoms or the degree of exposure (Hathaway, 1996; (Snyder, 1987).
    a) Obtaining plasma pseudocholinesterase levels could conceivably be useful as confirmation of exposure when inhibition of pseudocholinesterase activity is present, but cannot be used to guide therapy.
    2) TOCP inhibits neurotoxic esterase (NTE) which is found in circulating lymphocytes as well as nervous tissue (Hayes & Laws, 1991; Lotti et al, 1983).
    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, and the relationship between NTE levels and degree of symptomatology has not yet been demonstrated.
    4.1.4) OTHER
    A) OTHER
    1) ELECTROPHYSIOLOGICAL TESTING
    a) Electromyograms and nerve conduction velocity studies may be useful in evaluating a patient's neuropathy (Abou-Donia et al, 1986; Snyder, 1987; Vasilescu & Florescu, 1980).
    2) CEREBROSPINAL FLUID
    a) Although cerebrospinal fluid (CSF) analysis is often normal in patients with TOCP-induced peripheral neuropathy, elevated CSF protein levels with elevated CSF lymphocyte counts may occasionally be found (Hathaway, 1996; (Plunkett, 1976).
    3) POSTMORTEM
    a) TOCP-induced neuropathy identified in fatalities showed anterior horn cell involvement and nerve cell demyelination (Hathaway, 1996).

Methods

    A) CHROMATOGRAPHY
    1) Tricresyl phosphate levels can be determined by thin-layer and gas-liquid chromatography (HSDB , 1999).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Plasma pseudocholinesterase levels may be decreased but do not correlate with either the severity of symptoms or the degree of exposure.
    B) Electromyograms and nerve conduction velocity studies may be useful in evaluating a patient with neuropathy.

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) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    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.
    C) ACTIVATED CHARCOAL
    1) Avoid cathartic administration, as prolonged diarrhea may occur.
    2) 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.
    3) 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).
    6.5.3) TREATMENT
    A) CONTRAINDICATED TREATMENT
    1) Avoid administration of atropine and 2-PAM chloride (protopam) as these agents are ineffective (Gosselin et al, 1984).
    B) NEUROPATHY
    1) A variety of nonspecific treatments including administration of daily doses of 300 milligrams of vitamin B1 orally with 1 milligram of vitamin B12 intramuscularly, a 30 day course of corticosteroids, and pilocarpine 10 to 20 milligrams daily subcutaneously in divided doses have been proposed (Gosselin et al, 1984).
    2) There is no evidence that these treatments change the course of the peripheral neuropathy.
    C) FLUID/ELECTROLYTE BALANCE REGULATION
    1) If profuse diarrhea occurs in the initial stages of the poisoning, monitoring of fluid and electrolyte status with replacement therapy as required may be necessary.
    D) REHABILITATION THERAPY
    1) Physical and occupational therapy with orthopedic intervention when necessary may be important in preserving motor functioning.
    2) Prolonged followup and rehabilitation measures are indicated in patients whose peripheral neuropathies do not completely resolve.

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) PULMONARY ABSORPTION
    1) As serious poisoning may occur by the inhalation route, patients exposed to vapors should be carefully evaluated and followed for potential delayed peripheral neuropathy.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) SKIN ABSORPTION
    1) As serious poisoning may occur by the dermal route, exposed patients should be carefully evaluated and followed for potential delayed peripheral neuropathy.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) LACK OF INFORMATION
    1) No studies have assessed extracorporeal removal techniques in the treatment of TOCP poisoning.

Abstracts

Case Reports

    A) ADVERSE EFFECTS
    1) Several outbreaks involving up to thousands of victims each have occurred in the past from consumption of contaminated Jamaican ginger extract, TOCP-contaminated foodstuffs or alcohol, and TOCP mixed with or used instead of cooking oil (Gosselin et al, 1984; Morgan, 1982; Senanayake & Jeyaratnam, 1981; Smith & Spalding, 1959; Susser & Stein, 1957; Vora et al, 1962; Sarkar, 1974; Vasilescu & Florescu, 1980; Yuasa et al, 1970).
    2) Vasilescu & Florescu (1980) reported on 12 patients who consumed TOCP-contaminated industrial alcohol with 13 years of followup in two of the victims.
    a) All developed both peripheral nerve lesions and central pyramidal lesions such as hyperreflexia and spasticity.
    b) Those with predominantly peripheral involvement showed the best improvement, while there was little improvement in the pyramidal lesions during the period of followup.
    c) Electrophysiologic studies showed that the lesions resembled the picture of amyotrophic lateral sclerosis and suggested neuronal and axonal degeneration.
    3) Sarkar (1974) described three separate outbreaks of TOCP poisoning in West Bengal.
    a) The first involved over 400 people and was the result of eating foods made from flour which had been contaminated with TOCP during transport.
    b) The other two outbreaks involved more than 55 people, and resulted from the use of cooking or mustard oil stored in drums which had previously held TOCP.
    c) A similar incident in Bombay involved 58 patients and also resulted from preparing food in contaminated mustard oil (Vora et al, 1962). One of the victims of this last incident claimed not to have consumed any of the contaminated oil, but had used it for massaging the body (Vora et al, 1962).
    4) An outbreak involving 11 people in Durban, South Africa from the brewing of illicit liquor in drums which had previously contained TOCP was reported by Susser & Stein (1957).
    5) Three cases of what appeared to be permanent lower extremity paralysis were reported in TOCP manufacturing workers during World War II blackout conditions (ACGIH, 1986). Dermal contact as well as inhalation of vapors may have been responsible for these cases (ACGIH, 1986).
    B) PEDIATRIC
    1) Acute ingestion of a mouthful of lubricating oil containing non-ortho isomers of tricresyl phosphate and triphenyl phosphate by a 4.5 year old boy resulted in neuropathy and gastrointestinal symptoms (Goldstein et al, 1988).
    a) Vomiting occurred 4 hours postingestion and resolved over 2 days. Five days postingestion, vomiting resumed, with diarrhea, abdominal pain, and weakness, followed by drowsiness, slurred speech, and inability to walk. Drooling, increased respiratory secretions, facial weakness, myoclonic jerking, and cyanosis developed over several hours. Red cell and plasma cholinesterase was 4.5% and 2.9% of normal, respectively.
    b) He improved and was discharged with residual axonal neuropathy. Five weeks postingestion full function had returned.

Range Of Toxicity

Summary

    A) The human lethal oral dose of TOCP is about 1 g/kg; doses of 6 to 7 mg/kg have produced serious paralysis.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The human lethal dose of TOCP by ingestion is estimated to be about 1 gram per kilogram (ACGIH, 1986) Hathaway, 1996).
    1) LDLo (ORAL) HUMAN - 1,000 mg/kg (Hathaway, 1996)
    2) LDLo (ORAL) DOG - 500 mg/kg (ITI, 1995)
    3) LDLo (Subcutaneous) DOG - 100 mg/kg (Lewis, 1996)
    4) LDLo (Subcutaneous) DOG - 300 mg/kg (RTECS, 1999)
    5) LDLo (Subcutaneous) CAT - 185 mg/kg (Lewis, 1996)
    6) LDLo (ORAL) RABBIT - 100 mg/kg (RTECS, 1999)
    7) LDLo (Subcutaneous) RABBIT - 100 mg/kg (RTECS, 1999)
    8) LDLo (IV) RABBIT - 100 mg/kg (RTECS, 1999)
    9) LDLo (IM) RABBIT - 135 mg/kg (RTECS, 1999)
    10) LDLo (IP) RABBIT - 100 mg/kg (RTECS, 1999)
    11) LDLo (Subcutaneous) GUINEA PIG - 300 mg/kg (RTECS, 1999)
    12) LDLo (IP) MOUSE - 50 mg/kg (Lewis, 1996)
    13) LDLo (Subcutaneous) RAT - 10 mg/kg (Clayton & Clayton, 1994)
    14) LDLo (ORAL) CHICKEN - 1,000 mg/kg (Clayton & Clayton, 1994)

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Oral doses of 6 to 7 milligrams/kilogram have produced serious human paralysis (ACGIH, 1986) Hathaway, 1996).
    B) CASE REPORTS
    1) PEDIATRIC
    a) Ingestion of a mouthful (5 to 10 mL or up to 0.5 mL/kg) produced severe toxicity in a 4.5 year old child (Goldstein et al, 1988).
    2) OCCUPATIONAL
    a) Air concentrations of TOCP in different areas of an industrial facility where three workers developed polyneuritis were lower than 2.5 milligrams per cubic meter, lower than 1 milligram per cubic meter, and between 0.55 and 1.7 milligrams per cubic meter, although dermal absorption was not excluded in these cases (ACGIH, 1986).
    b) A worker exposed to tricresyl phosphate containing 6% to 10% TOCP developed an apparently permanent lower extremity paralysis, but further exposure details were not available (ACGIH, 1986).
    c) With occupational exposure to various triaryl phosphates containing up to 20% TOCP, no adverse health effects were noted when air concentrations ranged from 0.27 milligram per cubic meter to greater than 3 milligrams per cubic meter, although decreased plasma pseudocholinesterase values were found in some workers (ACGIH, 1986; Clayton & Clayton, 1994).
    d) In an outbreak associated with the consumption of TOCP contaminated industrial alcohol, ingestion of as little as 100 milliliters resulted in peripheral neuropathy (Vasilescu & Florescu, 1980).
    e) In one industrial hygiene study of workers with an average 8.9 year exposure to tricresyl phosphate in a manufacturing facility with air concentrations of tricresyl phosphate ranging from 0.27 milligram per cubic meter to 0.67 milligram per cubic meter, some symptoms of hypoesthesia, decreased vibratory sense, sluggish reflexes, nausea, heartburn, and emesis were noted (Tabershaw & Kleinfeld, 1957; Tabershaw & Kleinfeld, 1957).
    1) Decreased activities of plasma pseudocholinesterase were also noted, but did not correlate with either degree of exposure or symptoms (Tabershaw & Kleinfeld, 1957; Tabershaw & Kleinfeld, 1957).
    2) These workers were also exposed to phosphorus oxychloride which may have been responsible for some of the recorded symptomatology (Tabershaw & Kleinfeld, 1957; Tabershaw & Kleinfeld, 1957).
    f) Men exposed over a period of several months at 1.5 milligrams per cubic meter of commercial hydraulic fluid (21 percent triorthocresyl phosphate activity) showed no physical or neurologic abnormalities (ACGIH, 1986).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) Blood levels of TOCP are not generally available and have not been correlated with degree of toxicity.
    b) Plasma pseudocholinesterase levels have been noted to be decreased to as low as 70% of normal in exposed individuals, but these levels do not correlate with either the severity of symptoms or the degree of exposure (Hathaway, 1996).
    c) TOCP inhibits neurotoxic esterase (NTE) which is found in circulating lymphocytes as well as nervous tissue (Hayes & Laws, 1991; Lotti et al, 1983).
    1) Assays of NTE in circulating lymphocytes have correlated well with exposure to the neurotoxic agents DEF and merphos (Lotti et al, 1983).
    2) NTE assays are, however, not currently readily available for monitoring of either exposed workers or patients with acute poisoning, and the relationship between NTE levels and degree of symptomatology has not yet been demonstrated.

Workplace Standards

    A) ACGIH TLV Values for CAS78-30-8 (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) Triorthocresyl phosphate
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI(A), Skin
    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.
    b) BEI(A): The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational. Substances identified as Acetylcholinesterase Inhibiting Pesticides are part of this notation.
    c) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Cholinesterase inhib
    d) Molecular Weight: 368.37
    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 CAS78-30-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Triorthocresyl phosphate
    2) REL:
    a) TWA: 0.1 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 40 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS78-30-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Triorthocresyl 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: Triorthocresyl 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 CAS78-30-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Triorthocresyl phosphate
    2) Table Z-1 for Triorthocresyl 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: 0.1
    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) References: ACGIH, 1986 RTECS, 1999
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 1960 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 900 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 2500 mg/kg
    4) LD50- (ORAL)RAT:
    a) 1160 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Although TOCP inhibits plasma pseudocholinesterase, this is thought to be only an incidental finding and not the neurotoxic mechanism (Gosselin et al, 1984).
    B) The CBDP metabolite is a potent esterase inhibitor and is also a more potent producer of axonal damage in experimental animals than TOCP (Gosselin et al, 1984). There are major differences in susceptibility to TOCP-induced neuropathy among various animal species, and it may be that the ability to metabolize TOCP to this cyclic saligen phosphate metabolite is the determinant of these susceptibility differences (Hayes & Laws, 1991).
    C) Inhibition of a neurotoxic esterase (NTE) may be responsible for the peripheral neuropathy seen in TOCP poisoning (Hayes & Laws, 1991; Stumpf et al, 1989).
    1) Neither carbamylation nor sulfation of neurotoxic esterase cause axonal damage, while phosphorylation does produce axonopathy (Gosselin et al, 1984).
    2) In one in vitro experiment, TOCP did not inhibit neurotoxic esterase unless there was prior metabolic activation by liver microsomes, suggesting that the CBDP metabolite was responsible (Sprague & Castles, 1985).
    3) Neurotoxic esterase activity was maximally inhibited (46%) in ferrets which received 1,000 mg/kg TOTP dermally and which subsequently presented with ataxia, partial paresis, and axonal degeneration of the lateral funiculus and fasciculus grascilis on autopsy (Stumpf et al, 1989).
    D) TOCP produces a delayed onset peripheral neuropathy of the "dying back" or "distal axonopathy" type (Snyder, 1987; Hayes & Laws, 1991).
    1) This involves Wallerian degeneration beginning at the portion of the nerve most distal from the cell body and extending a varying distance proximally (Hayes & Laws, 1991). Myelin degeneration may be seen as a secondary effect (Hayes & Laws, 1991).
    2) 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 & Laws, 1991). 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 & Laws, 1991).
    3) Neurotoxicity of TOCP apparently involves its activation with hydroxylation of a ring methyl group by the liver cytochrome P-450 system. The activated compound then cyclizes to form the saligenin cyclic phosphate (CBDP) by intramolecular transphosphorylation with liberation of one aryl group (Eto, 1969).
    E) TOCP-induced neuropathy is associated with dose-dependent decreased phosphofructokinase activity (Hernandez et al, 1989).
    F) Hens given tri-ortho-tolyl phosphate (TOTP) at an oral dose of 360 mg/kg had increased activity of calcium-activated neutral protease (CANP or calpain), an enzyme responsible for degradation of axonal and muscle cytoskeletal elements. The increase in CANP activity in the brain occurred within 4 days and that in the gastrocnemius muscle and sciatic nerve was noted within 2 days of administration (El-Fawal et al, 1990).
    G) In TOCP intoxicated hens aggregations of phosphorylated neurofilaments develop in the spinal cord and peripheral nerve axons prior to the onset of axonal degeneration (Jensen et al, 1992).

Physicochemical

Physical Characteristics

    A) TOCP is a colorless to pale yellow, odorless, oily liquid (ACGIH, 1986).

Molecular Weight

    A) 368.39

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Decreased sperm motility and disorganization of the seminiferous epithelium were noted in TOCP-treated birds (Somkuti et al, 1987).
    B) Chicken orally treated with 100 mg/kg TOCP for 18 days developed ataxia on day 7 and paralysis on day 15 of treatment (Somkuti et al, 1988).
    C) After an acute dose of TOCP, domestic chickens appear normal for 10 to 14 days after which they stop laying eggs and display an increasing clumsiness of gait. By the 15th to 20th day posttreatment, they become severely paralyzed in the legs and the wings are weakened. At higher doses, complete paralysis is followed by death (Snyder, 1987).
    11.1.2) BOVINE/CATTLE
    A) Cattle consuming molasses contaminated with TOCP for 15 days developed diarrhea, restlessness, and stiffness terminating in paraplegia. Postmortem showed patchy pneumonia, degenerative changes in liver and kidney, and demyelination of spinal cords and nerves (Clarke & Clarke, 1975).
    11.1.6) FELINE/CAT
    A) Cats exposed to TOCP had extensive damage to the myelin sheath and Schwann cells secondary to the destructive lesion in the axons (Johnson, 1969).
    11.1.12) RODENT
    A) Male Fischer 344 rats showed no consistent neurobehavioral changes or evidence of neuropathological damage in nervous tissues following treatment with 10 to 100 mg of TOCP given daily for a period of 64 days (Snyder, 1987; Somkuti et al, 1988).
    B) No teratogenicity was demonstrated as specifically attributable to TOCP compared to control groups among Long-Evans rats (Tocco et al, 1987).
    11.1.13) OTHER
    A) OTHER
    1) All 16 rabbits given at least 6 g TOCP/kg body weight developed anorexia, salivation, diarrhea, trembling, and paralysis on the 3rd or 4th day posttreatment (Snyder, 1987).

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) ACGIH: Documentation of the Threshold Limit Values, 5th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1986.
    14) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    15) Abou-Donia MB, Suwita E, & Nomeir AA: Absorption, distribution, and elimination of a single oral dose of [14C]tri-o-cresyl phosphate in hens. Toxicol 1990; 61:13-25.
    16) Abou-Donia MB, Trofatter LP, & Graham DG: Electromyographic, neuropathologic, and functional correlates in the cat as a result of tri-o-cresyl phosphate delayed neurotoxicity. Toxicol Appl Pharmacol 1986; 83:126-141.
    17) Ahmed AE, Jacob S, & Soliman S: Whole-body autoradiographic disposition, elimination and placental transport of [14C]tri-o-cresyl phosphate in mice. J Appl Toxicol 1993; 13:259-267.
    18) Ahmed MM & Glees P: Neurotoxicity of tricresyl phosphate (TCP) in slow loris (Nycticebus coucang coucang). Acta Neuropathol 1971; 19:94-98.
    19) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    20) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    21) Aring CD: The systemic nervous affinity of triorthocresyl phosphate (Jamaica Ginger Palsy). Brain 1942; 65:34-37.
    22) Barrett DS & Oehme FW: The effect of a single oral dose of tri-o-cresyl phosphate on neurotoxic esterase and acetylcholinesterase activities in the central nervous system, erythrocytes and plasma. Vet Human Toxicol 1994; 36:1-4.
    23) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996.
    24) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    25) Burka LT & Chapin RE: Toxicokinetics of (14)C-saligenin cyclic-o-tolyl phosphate in anesthetized male F-344 rats. Reprod Toxicol 1993; 7:81-86.
    26) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 1992; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    27) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires January/31/1999; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    28) Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
    29) Carlton BD, Basaran AH, & Mezza LE: Examination of the reproductive effects of tricresyl phosphate administered to Long-Evans rats. Toxicology 1987; 46:321-328.
    30) Chapin RE, Phelps JL, & Burka LT: The effects of tri-o-cresyl phosphate and metabolites on rat Sertoli cell function in primary culture. Toxicol Appl Pharmacol 1991; 108:194-204.
    31) Chapin RE, Phelps JL, & Somkuti SG: The interaction of Sertoli and Leydig cells in the testicular toxicity of tri-o-cresyl phosphate. Toxicol Appl Pharmacol 1990; 104:483-495.
    32) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    33) Clarke EG & Clarke ML: Veterinary Toxicology, Williams & Wilkins Co, Baltimore, MD, 1975.
    34) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2, Toxicology, 3rd ed, John Wiley & Sons, New York, NY, 1982.
    35) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Volume 2D, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994, pp 3063-3075.
    36) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    37) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    38) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    39) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    40) El-Fawal HA, Correll L, & Gay L: Protease activity in brain, nerve, and muscle of hens given neuropathy-inducing organophosphates and a calcium channel blocker. Toxicol Appl Pharmacol 1990; 103:133-142.
    41) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    42) Eto M: Specificity and mechanism in the action of saligenin cyclic phoshorus esters. Residue Rev 1969; 25:187-200.
    43) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    44) Fathy FA & Bursian SJ: The effect of triorthocresyl phosphate, a delayed neurotoxin, on the testes of young broilers. Toxicol Lett 1991; 56:7-12.
    45) Goldstein DA, McGuigan MA, & Ripley BD: Acute tricresylphosphate intoxication in childhood. Human Toxicol 1988; 7:179-182.
    46) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    47) Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, Williams & Wilkins, Baltimore, MD, 1984, pp II-302-III-388-393.
    48) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    49) Grant WM: Toxicology of the Eye, 3rd ed, Charles C. Thomas, Springfield, IL, 1986, pp 942-944.
    50) Grant WM: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    51) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    52) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1999; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    53) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    54) Hayes WJ Jr & Laws ER Jr: Handbook of Pesticide Toxicology, Volume 2, Academic Press, Inc, San Diego, CA, 1991, pp 957-972.
    55) Hernandez AF, Pla A, & Villanueva E: Decreased phosphofructokinase activity during the development of triorthocresyl-phosphate-induced delayed neuropathy. Toxicol Letters 1989; 49:35-40.
    56) Hunter D, Perry KMA, & Evans RB: Toxic polyneuritis arising during the manufacture of tricresyl phosphate. Br J Ind Med 1944; 1:227-231.
    57) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    58) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    59) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    60) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    61) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    62) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    63) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    64) ILO: Encyclopaedia of Occupational Health and Safety, 3rd ed, Vol 2. Parmeggiani L (Ed), International Labour Organization, Geneva, Switzerland, 1983, pp 2217.
    65) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1988, pp 540-541.
    66) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1995.
    67) Inoue N, Fujishiro K, & Mori K: Triorthocresyl phosphate poisoning--a review of human cases. Sangyo Ika Daigaku Zasshi 1988; 10:433-442.
    68) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    69) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    70) Jensen KF, Lapadula DM, & Knoth Anderson J: Anomalous phosphorylated neurofilament aggregations in central and peripheral axons of hens treated with tri-ortho-cresyl phosphate (TOCP). J Neuroscience Research 1992; 33:455-460.
    71) Johnson MK: Delayed neurotoxic action of some organophosphorus compounds. Br Med Bull 1969; 25:231-235.
    72) Konno N, Suzuki N, & Horiguchi H: Characterization of high-affinity binding sites for diisopropylfluorophospahte (DFP) from chicken spinal cord membranes. Biochem Pharmacol 1994; 48:2073-2079.
    73) Lewis RJ: Dangerous Properties of Industrial Materials, 8th ed, Van Nostrand Reinhold Company, New York, NY, 1992, pp 3427.
    74) Lewis RJ: Hawley's Condensed Chemical Dictionary, 13th ed, John Wiley & Sons, Inc, New York, NY, 1997.
    75) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 9th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    76) Litau VG: Data for the characterization of skin resorption of tricresylphosphate in mixture with adipic acid. Gig Tr Prof Zabol 1975; 9:58-59.
    77) Lotti M, Becker CE, & Aminoff MJ: Occupational exposure to the cotton defoliants DEF and Merphos. J Occup Med 1983; 25:517-522.
    78) Luttrell WE, Pleban PA, & Olajos EJ: Effect of acute tri-o-tolyl phosphate exposure on 2', 3'-cyclic nucleotide 3'-phosphohydrolase activity in hen neural tissues. Neurotoxicology 1988; 9:539-544.
    79) Mele JM & Jensh RP: Teratogenic effects of orally administered tri-o-cresyl phosphate on Wistar albino rats. Teratology 1977; 15:32A.
    80) Morgan JP & Tulloss TC: The jake walk blues: A toxicologic tragedy mirrored in American popular music. Ann Intern Med 1976; 85:804-808.
    81) Morgan JP: The Jamaica ginger paralysis. JAMA 1982; 248:1864-1867.
    82) NFPA: Fire Protection Guide to Hazardous Materials, 10th ed, National Fire Protection Association, Quincy, MA, 1991, pp 325M-88.
    83) NFPA: Fire Protection Guide to Hazardous Materials, 12th ed, National Fire Protection Association, Quincy, MA, 1997.
    84) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    85) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1999; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    86) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    87) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    88) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    89) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    90) Namba T, Nolte CT, & Jackrel J: Poisoning due to organophosphate insecticides: Acute and chronic manifestations. Am J Med 1971; 50:475-492.
    91) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    92) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    93) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    94) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    95) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    96) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    97) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    98) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    99) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    100) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    101) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    102) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    103) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    104) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    105) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    106) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    107) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    108) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    109) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    110) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    111) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    112) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    113) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    114) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    115) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    116) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    166) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    167) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    168) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    169) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    170) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    171) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    172) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    173) Norris P & Storrs FJ: Allergic contact dermatitis to adhesive bandages. Dermatol Clin 1990; 8:147-152.
    174) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    175) Pellin M, Vicedo JL, & Vilanova E: Sensitivity to tri-o-cresylphosphate neurotoxicity on n-hexane exposed hens as a model of simultaneous hexacarbon solvent and organophosphorus occupational intoxication. Arch Toxicol 1987; 59:311-318.
    176) Plunkett ER: Handbook of Industrial Toxicology, Chemical Publishing Company, Inc, New York, NY, 1976, pp 421-423.
    177) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    178) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1999; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    179) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    180) Sarkar JK: Outbreaks of paralytic disease in West Bengal due to tricresyl phosphate poisoning. J Ind Med Assoc 1974; 63:359-361.
    181) Schardein JL: Chemically Induced Birth Defects, Marcel Dekker, Inc, New York, NY, 1993.
    182) Senanayake N & Jeyaratnam J: Toxic polyneuropathy due to gingili oil contaminated with tri-cresyl phosphate affecting adolescent girls in Sri Lanka. Lancet 1981; 1:88-89.
    183) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2nd ed, Noyes Publications, Park Ridge, NJ, 1985.
    184) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.
    185) Smith HV & Spalding JMK: Outbreak of paralysis in Morocco due to ortho-cresyl phosphate poisoning. Lancet 1959; 2:1019-1021.
    186) Snyder R: Ethel Browning's Toxicity and Metabolism of Industrial Solvents, 2nd ed, Hydrocarbons, 1, Elsevier, New York, NY, 1987.
    187) Somkuti SG, Lapadula DM, & Chapin RE: Light and electron microscopic evidence of tri-o-cresyl phosphate (TOCP)-mediated testicular toxicity in Fischer 344 rats. Toxicol Appl Pharmacol 1991; 107:35-46.
    188) Somkuti SG, Lapadula DM, & Chapin RE: Testicular toxicity following oral administration of tri-o-cresyl phosphate (TOCP) in roosters. Toxicol Letters 1987; 37:279-290.
    189) Somkuti SG, Lapadula DM, & Chapin RE: Time course of the tri-o-cresyl phosphate-induced testicular lesion in F-344 rats: enzymatic, hormonal, and sperm parameter studies. Toxicol Appl Pharmacol 1987a; 89:64-72.
    190) Somkuti SG, Tilson HA, & Brown HR: Lack of delayed neurotoxic effect after tri-o-cresyl phosphate treatment in male Fischer 344 rats: biochemical, neurobehavioral, and neuropathological studies. Fundam Appl Toxicol 1988; 10:199-205.
    191) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    192) Srivastava AK, Das M, & Khanna SK: An outbreak of tricresyl phosphate poisoning in Calcutta, India (letter). Fd Chem Toxic 1990; 28:303-304.
    193) Stumpf AM, Tanaka D Jr, & Aulerich RJ: Delayed neurotoxic effects of tri-o-tolyl phosphate in the European ferret. J Toxicol Environ Health 1989; 26:61-73.
    194) Susser M & Stein Z: An outbreak of tri-ortho-cresyl phosphate (T.O.C.P.) poisoning in Durban. Br J Ind Med 1957; 14:111-120.
    195) Tabershaw IR & Kleinfeld M: Manufacture of tricresyl phosphate and other alkyl phenyl phosphates: An industrial hygiene study. II. Clinical effects of tricresyl phosphate. AMA Arch Ind Health 1957; 15:541-544.
    196) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.
    197) Tocco DR, Randall JL, & York RG: Evaluation of the teratogenic effects of tri-ortho-cresyl phosphate in the Long-Evans hooded rat. Fundam Appl Toxicol 1987; 8:291-297.
    198) Tosi L, Righetti C, & Adami L: October 1942: a strange epidemic paralysis in Saval, Verona, Italy. Revision and diagnosis 50 years later of tri-ortho-cresyl phosphate poisoning. J Neurology, Neurosurg & Psychiatry 1994; 57:810-813.
    199) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    200) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    201) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    202) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    203) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    204) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    205) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    206) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    207) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    208) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    209) Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.
    210) Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.
    211) Varghese RG, Bursian SJ, & Tobias C: Organophosphorus-induced delayed neurotoxicity: a comparative study of the effects of tri-ortho-tolyl phosphate and triphenyl phosphite on the central nervous system of the Japanese quail. Neurotoxicology 1995; 16:45-54.
    212) Vasilescu C & Florescu A: Clinical and electrophysiological study of neuropathy after organophosphorus compounds poisoning. Arch Toxicol 1980; 43:305-315.
    213) Vora DD, Dastur DK, & Braganca BM: Toxic polyneuritis in Bombay due to ortho-cresyl-phosphate poisoning. J Neurol Neurosurg Psychiatr 1962; 25:234-242.
    214) Wang D, Tao Y, & Li Z: Toxic polyneuropathy due to flour contaminated with tricresyl phosphate in China (letter). Clin Toxicol 1995; 33:373-374.
    215) Woolf AD: Ginger Jake and the blues: a tragic story of poisoning. Vet Human Toxicol 1995; 37:252-254.
    216) Yuasa R, Kaneko Z, & Kikui M: Clinicopathological findings of sequelae of triorthocresylphosphate poisoning. Clin Neurol (Tokyo) 1970; 10:170-177.