TOCP AND RELATED AGENTS
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
TOCP o-CRESYL PHOSPHATE PHOSFLEX 179-C PHOSPHORIC ACID, TRI-o-CRESYL ESTER PHOSPHORIC ACID, TRI-o-TOLYL ESTER PHOSPHORIC ACID, TRIS(2-METHYLPHENYL) ESTER TOFK o-TOLYL PHOSPHATE TOTP TRICRESYL PHOSPHATE TRI-o-CRESYL PHOSPHATE TRI-ortho-CRESYL PHOSPHATE o-TRIKRESYLPHOSPHATE (German) TRI 2-METHYLPHENYL PHOSPHATE TRIORTHOCRESYL PHOSPHATE TRIS(o-CRESYL)-PHOSPHATE TRIS(o-METHYLPHENYL)PHOSPHATE TRIS(o-TOLYL)-PHOSPHATE TRI-o-TOLYL PHOSPHATE TRI-2-TOLYL PHOSPHATE TROJKREZYLU FOSFORAN (Polish)
IDENTIFIERS
SYNONYM REFERENCE
- (RTECS , 1999; Lewis, 1996)
USES/FORMS/SOURCES
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). 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. 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). A pure motor neuropathy has been described in two patients, one exposed to Dipterex and one exposed to Divipan (Vasilescu & Florescu, 1980).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- 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.
A pre-paralytic phase occurs in some patients, manifesting with diarrhea, conjunctivitis, laryngitis, rhinitis, pharyngitis, distal extremity paresthesias, and cramping calf pain. 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.
- PERMANENT SEQUELAE - Some patients make an apparent full recovery while others remain with more or less severe disability.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
- TOCP is the most toxic of the three isomers of tricresyl phosphate (tri-ortho-cresyl phosphate, tri-meta-cresyl phosphate (TMCP or tri-m-cresyl phosphate), and tri-para-cresyl phosphate (TPCP or tri-p-cresyl phosphate) in decreasing order of toxicity) (Sittig, 1985; Clayton & Clayton, 1994). It is the only isomer which produces delayed peripheral neuropathy (ILO, 1983).
- TOCP can be toxic by the oral, inhalation, or dermal exposure routes without signs of irritation (Hathaway et al, 1991). Dermal exposure may be as important as inhalation in occupational settings (ACGIH, 1992).
- There have been over 10,000 cases of human poisonings involving ingestion of contaminated cooking oil, flour, or Jamaican ginger extract (Hathaway et al, 1991; (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; Clayton & Clayton, 1994; Hayes & Laws, 1991). The lethal human oral dose of TOCP is about 1 g/kg; doses of 6 to 7 mg/kg have produced serious paralysis (Hathaway et al, 1991).
- TOCP is not irritating to the skin (Hathaway et al, 1991). A single accidental splash contact with TOCP does not produce corneal burns (Grant, 1986).
- The major toxicity of TOCP is a delayed peripheral polyneuropathy of a Wallerian-type "dying back" or "peripheral axonopathy" variety, originating distally and eventually involving demyelination of the axon (Gosselin et al, 1984; Hayes & Laws, 1991) Hathaway et al, 1991; (Clayton & Clayton, 1994).
- TOCP poisoning is characterized by early nausea, vomiting, diarrhea, and abdominal pain, with no signs and symptoms of anticholinesterase poisoning (Aring, 1942; Gosselin et al, 1984; Namba et al, 1971). Early GI signs then clear, followed by an 8- to 35-day asymptomatic latent period.
- A pre-paralytic phase occurs in some patients, with diarrhea, conjunctivitis, laryngitis, rhinitis, pharyngitis, distal extremity paresthesias, and cramping calf pain (Namba et al, 1971). Part of the pre-paralytic phase may include a feverish feeling, despite a normal body temperature (Gosselin et al, 1984). Non-tender, symmetrical swelling of the parotid glands has been described in some cases of TOCP poisoning (Plunkett, 1976; Susser & Stein, 1957). Eye inflammation lasting about 24 to 36 hours may occur during the pre-paralytic phase in about a third of cases (Namba et al, 1971).
- After a symptom-free period lasting 8 to 35 days, patients may develop sharp pains in the calf muscles. Some may have numbness and tingling in the feet and hands, but sensory deficits are minor compared to the effects on the motor nerves (Hathaway et al, 1991; (Clayton & Clayton, 1994).
- Flaccid paralysis begins in the feet and toes ("foot-drop") after a few hours, and in the hands and wrists over approximately another 10 days (Clayton & Clayton, 1994). This flaccid paralysis has signs of a lower motor neuron lesion, and involves muscle wasting (Namba et al, 1971). Paralysis peaks in intensity over a period of 2 to 3 months, then variably resolves.
- 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).
- Spasticity of the lower extremities may develop after flaccid paralysis. 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). Residual gait disorders have been called "Jake Walk," after the popular name of the Jamaican ginger extract ("Ginger Jake") responsible for many cases of poisoning (Hathaway et al, 1991).
- The prognosis is often favorable with a low mortality, but there have been fatalities. Autopsy of 6 human cases revealed demyelination of nerve cells and involvement of the anterior horn cells (Hathaway et al, 1991).
- Histopathologic findings in cases of human poisonings have shown axonal degeneration in peripheral nerves and degenerative changes in the anterior horn cells and pyramidal tracts (Hathaway et al, 1991; (Inoue et al, 1988).
- A metabolite is thought to be responsible for the delayed neurotoxic effects. 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). It may exert its effects by phosphorylation of cellular proteins, including calcium/calmodulin kinase II and cytoskeletal proteins (Abou Donia, 1993). The TOCP metabolite appears to bind to the same sites inhibited by DIISOPROPYLFLUOROPHOSPHATE, another inducer of delayed neurotoxicity, in chicken spinal cords (Konno et al, 1994).
- Similar delayed neuropathies have been produced by TOCP in experimental and domestic animals. 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 the cyclic saligen phosphate metabolite is the determinant of these susceptibility differences (Hayes & Laws, 1991). Strain differences have also been seen in rats, with Long-Evans being the most sensitive (Carrington & Abou Donia, 1988). A standard assay for delayed neurotoxicity uses atropinized hens, one of the most sensitive species (Luttrell et al, 1988).
CHRONIC CLINICAL EFFECTS
- TOCP is an insidious occupational poison because months of exposure can occur before any symptoms develop. In one case, a man was exposed for 5 months before anorexia, nausea, and leg aches developed; he eventually developed permanent paralysis (Clayton & Clayton, 1994).
- Workers with an average of 8.9 years exposure to TOCP (ranging from 0.27 to 0.67 mg/m(3)) developed hypoesthesia, decreased vibratory sense, sluggish reflexes, nausea, heartburn, and emesis. These workers were also exposed to phosphorus oxychloride, which may have been responsible for some of the symptoms (Tabershaw & Kleinfeld, 1957; Tabershaw & Kleinfeld, 1957).
- Men exposed over a period of several months to 1.5 mg/m(3) of commercial hydraulic fluid containing 21% TOCP showed no physical or neurologic abnormalities (ACGIH, 1992).
- One case of allergic contact dermatitis to TOCP has been reported (Norris & Storrs, 1990). Respiratory sensitization may be expected after repeated inhalation exposure.
- Rats are relatively resistant to the neurotoxic effects of TOCP. Rats given TOCP by gavage at doses up to 100 mg/kg/day for 63 days did not develop delayed neurotoxicity (Somkuti et al, 1988).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance;give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
GENERAL The following information is for Organophosphate Compounds in general. Severe toxicity may develop rapidly following exposure or may be delayed by 12 hours or more. Rapid removal from toxic environments, decontamination procedures, and specific therapy if required are essential. First responders, emergency medical, and emergency department personnel should take proper precautions (wear rubber gowns, rubber aprons, rubber gloves, etc) when treating patients with organophosphate poisoning to avoid contamination. Emesis containing organophosphates should be placed in closed impervious containers for proper disposal.
INHALATION EXPOSURE 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. If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests. Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
DERMAL EXPOSURE Systemic effects can occur from dermal exposure to organophosphates. 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). Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
EYE EXPOSURE 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. Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
ORAL/PARENTERAL EXPOSURE Inducing emesis is contraindicated because of possible early onset of respiratory depression and seizures. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION 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). 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. 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).
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. Suction oral secretions. ATROPINE THERAPY: If symptomatic from organophosphate poisoning, administer IV atropine until lung fields are clear to auscultation. Adult - 2 to 5 mg every 10 to 15 minutes; Child - 0.05 mg/kg every 10 to 15 minutes. Atropinization may be required for hours to days depending on severity. PRALIDOXIME (PROTOPAM, 2-PAM) - Severe organophosphate poisoning, characterized by profound weakness and respiratory depression, should also be treated with 2-PAM. Adult - 1 to 2 g IV at 0.5 g per min; Child - 25 to 50 mg/kg over 5 to 30 minutes; may repeat in one hour and every 6 to 12 hours if muscle weakness is not relieved or if patient is comatose. Continuous Infusion (Controversial) - Adult - 500 mg/hr. Pralidoxime may need to be administered over several days. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response. CONTRAINDICATIONS - Succinylcholine and other cholinergic agents are contraindicated.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
MAXIMUM TOLERATED EXPOSURE
PEDIATRIC OCCUPATIONAL 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). 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). 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). 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). 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). 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). 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).
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).
- Carcinogenicity Ratings for CAS78-30-8 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Triorthocresyl phosphate EPA (U.S. Environmental Protection Agency, 2011): Not Listed 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 NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Triorthocresyl phosphate MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS78-30-8 (U.S. Environmental Protection Agency, 2011):
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS78-30-8 (American Conference of Governmental Industrial Hygienists, 2010):
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.
- AIHA WEEL Values for CAS78-30-8 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS78-30-8 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS78-30-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS78-30-8 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS78-30-8 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS78-30-8 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS78-30-8 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS78-30-8 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS78-30-8 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS78-30-8 (49 CFR 172.101 - App. B, 2005):
Listed as Tricresyl phosphate (less than 1% ortho-isomer) Severe Marine Pollutant: No Listed as Tricresyl phosphate with more than 3 percent ortho isomer Severe Marine Pollutant: Yes Listed as Tricresyl phosphate, not less than 1% ortho-isomer but not more than 3% orthoisomer Severe Marine Pollutant: Yes
- EPA TSCA Inventory for CAS78-30-8 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 2574 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN2574 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS78-30-8 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Most TOCP poisoning cases have resulted from the ingestion of adulterated cooking oil, flour, or ginger extract (Gosselin et al, 1984). Poisoning has also occurred following dermal or inhalation exposure (ACGIH, 1986). Preventive measures include keeping the material out of all substances intended for human consumption and workplace preventive measures such as engineering controls, respiratory protection, and wearing of impervious gloves and other protective clothing to preclude dermal exposure. Modern production methods which seek to keep TOCP concentrations at less than 1% of the total tricresyl phosphate isomer mixture (Gosselin et al, 1984) may also help reduce exposure.
STORAGE
- ROOM/CABINET RECOMMENDATIONS
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 78-30-8.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Containers may explode when heated. Runoff may pollute waterways.
TOCP is combustible in heat or flames (Lewis, 1992).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS78-30-8 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material. Use water spray or fog; do not use straight streams.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS78-30-8 (NFPA, 2002):
- Carbon dioxide and dry chemical are the appropriate fire-fighting chemicals. For large fires use water spray; fog or foam may be used but may cause frothing (CHRIS , 1992; Lewis, 1992).
EXPLOSION HAZARD
- TOCP is not an explosion hazard.
DUST/VAPOR HAZARD
- TOCP is not volatile, but it may be easily absorbed through the skin (ACGIH, 1986; ITI, 1988).
- The heated liquid would release toxic vapors (Clayton & Clayton, 1982).
- Toxic gases including oxides of phosphorous would be released during a fire (Lewis, 1992).
REACTIVITY HAZARD
- TOCP will react with oxidizers (Lewis, 1992).
- The heated liquid would release toxic vapors (Clayton & Clayton, 1982).
- Toxic gases including oxides of phosphorous would be released during a fire (Lewis, 1992).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas.
- AIHA ERPG Values for CAS78-30-8 (AIHA, 2006):
- DOE TEEL Values for CAS78-30-8 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Tri-o-tolyl phosphate (Triorthocresyl phosphate) TEEL-0 (units = ppm): 0.1 TEEL-1 (units = ppm): 0.3 TEEL-2 (units = ppm): 0.6 TEEL-3 (units = ppm): 40 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS78-30-8 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS78-30-8 (National Institute for Occupational Safety and Health, 2007):
IDLH: 40 mg/m3 Note(s): Not Listed
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
TOCP will sink in water (CHRIS , 1992). For very small spills, absorb with paper towels and dispose by burning in a furnace (ITI, 1988). Adsorb the spilled material with sand or similar noncombustible adsorbent such as crushed limestone (ITI, 1988). Hazardous Waste Disposal: Incinerate with afterburner and alkaline scrubber. Place in open furnace and add equal parts of sand and crushed limestone; use a combustible solvent to ignite (ITI, 1988).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Air: Workers exposed to aryl phosphates in concentrations ranging from 0.2 to 3.4 mg/m(3) exhibited some cholinesterase inhibition, but no correlation existed between these reduced levels and gastrointestinal and neurological symptoms (Hathaway et al, 1991).
- Water: While the effect of low concentrations of TOCP on aquatic life is unknown, this agent may be dangerous if it enters water intakes. Therefore, local health and wildlife officials and operators of water intakes in the vicinity should be notified of water spills (CHRIS , 1992).
- Water: TOCP sinks in water (CHRIS , 1992).
- Soil: Pollution hazard is not established at the time of this review.
ENVIRONMENTAL FATE AND KINETICS
ENVIRONMENTAL TOXICITY
- No data is available (CHRIS , 1992).
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- TOCP is a colorless to pale yellow, odorless, oily liquid (ACGIH, 1986).
VAPOR PRESSURE
- 10 mmHg (at 200 degrees C) (HSDB , 1999)
- 0.00002 mmHg (at 77 degrees F) (NIOSH , 1999)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
DENSITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
BOILING POINT
- TOCP will boil and slightly decompose at 410 degrees C (Lewis, 1996).
FLASH POINT
- 225 degrees C; 437 degrees F (NFPA, 1997)
AUTOIGNITION TEMPERATURE
- 385 degrees C; 725 degrees F (NFPA, 1991; Lewis, 1996)
EXPLOSIVE LIMITS
SOLUBILITY
This compound is very soluble in common solvents, thinners and vegetable oils including; alcohol, benzene, ether, carbon tetrachloride, toluene, and acetic acid (Budavari, 1996; HSDB , 1999; Lewis, 1997).
SPECTRAL CONSTANTS
OTHER/PHYSICAL
- NUCLEAR MAGNETIC RESONANCE
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