PHORATE

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.

MOLECULAR FORMULA

C7-H17-O2-P-S3

ERG GUIDE NUMBER

152-SUBSTANCES - TOXIC (COMBUSTIBLE)

SYNONYM REFERENCE

(EPA, 1985; RTECS , 1990)

USES/FORMS/SOURCES

USES

PHORATE (O,O-diethyl S-(2-(ethylthio)ethyl) ester of phosphorodithioic acid) is used as a systemic and contact insecticide and acaricide (HSDB). THIMET is a common synonym. Phorate is permitted in the feed and drinking water of animals and/or for the treatment of food-producing animals (Sax, 1984).

FORMS

PHORATE (O,O-diethyl S-(2-(ethylthio)ethyl) ester of phosphorodithioic acid) is a clear-liquid organophosphorus pesticide (HSDB). It is stable at room temperature, but decomposes fairly rapidly in the environment (EOSH, 1982).
Like PARATHION, phorate is a cholinesterase inhibitor and is more toxic than parathion (HSDB). The probable oral lethal dose for humans is less than 5 mg/kg or a taste (less than 7 drops for a 150-pound person) (HSDB). The metabolites of phorate are considered at least as toxic as the parent compound (HSDB).
There are no controlled studies of phorate poisoning in humans from which a no-effect dose could be determined (HSDB).
The ACGIH has established a Biological Exposure Index (BEI) for organophosphate cholinesterase inhibitors. Refer to the BIOMONITORING section for more information.

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

Phorate is an organophosphate compound. The following are symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for phorate, but could potentially occur in individual cases.

USES: Phorate (O,O-diethyl S-(2-(ethylthio) ethyl) ester of phosphorodithioic acid) is an organophosphate insecticide and acaricide.

TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop.

EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US; exposure is rare.

WITH POISONING/EXPOSURE

MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to phorate. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete.
CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Contact with molten substance may cause severe burns to skin and eyes.
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

SUMMARY

Phorate is an organophosphate compound. The following are symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for phorate, but could potentially occur in individual cases.
TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop.
EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US; exposure is rare.

EXPOSURE

MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to phorate. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete.
CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

ACID BASE

METABOLIC ACIDOSIS: Metabolic acidosis has occurred in several cases of severe poisoning (Hui, 1983; Meller et al, 1981; Moore & James, 1981).

CARDIOVASCULAR

BRADYCARDIA: Bradycardia and hypotension have occurred following moderate to severe poisoning (Ganendran, 1974) with one study reporting hypotension (systolic blood pressure less than 90 mmHg) in 20% of patients and a heart rate of less than 60 beats per minute in 21% of patients (Bardin et al, 1987a). Bradycardia was a frequent finding in a group of chronically exposed phorate pesticide formulators (Kashyap et al, 1984).
CARDIAC DYSRHYTHMIAS: Cardiac dysrhythmias and conduction defects have been reported in patients with severe organophosphate poisoning (Wren et al, 1981; Kiss & Fazekas, 1982). ECG abnormalities may include: sinus bradycardia, A-V dissociation, idioventricular rhythms, multiform premature ventricular extrasystoles, polymorphic ventricular tachycardia, prolongation of the PR, QRS, and QT intervals, and "torsade de pointes" polymorphous ventricular dysrhythmias (Brill et al, 1984; Ludomirsky et al, 1982).
TACHYCARDIA: Tachycardia is a common adverse effect following exposure (Zwiener & Ginsburg, 1988a), and in one study, a heart rate of greater than 100 beats/minute was reported in 49% of patients (Bardin et al, 1987a).
MYOCARDITIS: Protracted toxic myocarditis has been suspected (Wren et al, 1981; Kiss & Fazekas, 1982).
INCREASED BLOOD PRESSURE: Increases in blood pressure can occur as a result of the nicotinic effects of organophosphate poisoning (Lund & Monteagudo, 1986).

DERMATOLOGIC

DIAPHORESIS: Profuse sweating may occur as one of the muscarinic signs of organophosphate poisoning (Ganendran, 1974).
DERMATITIS: Dermal sensitization has occurred with some organophosphates following skin exposure (Milby et al, 1964). In general, organophosphates can react with proteins and are potential haptens for allergic reactions.

ENDOCRINE

HYPERGLYCEMIA: Hyperglycemia can occur following severe poisoning (Namba, 1972).
GLYCOSURIA: Glycosuria (without ketosis) can occur following severe poisoning (Namba, 1972).

GASTROINTESTINAL

Nausea, vomiting, diarrhea, abdominal cramps and hypersalivation are common muscarinic signs of organophosphate poisoning (Bardin et al, 1987a). Gastrointestinal complaints were a frequent finding in a group of chronically exposed phorate formulators (Kashyap et al, 1984).
FECAL INCONTINENCE: Fecal incontinence occurs in severe poisoning (Hayes, 1965).

GENITOURINARY

URINARY INCONTINENCE: Involuntary urination can occur in more severe poisonings, and changes in urinary frequency may also become evident (Done, 1979).

HEENT

MIOSIS: Intense miosis is a typical manifestation, and is useful diagnostically, but is not always present following exposure. In one study, miosis occurred in 50/61 patients (82%) (Bardin et al, 1987a).
MYDRIASIS: Even with the probable occurrence of miosis, mydriasis can occur in severely poisoned individuals (Dixon, 1957).
BLURRED VISION: Lacrimation and blurred vision are commonly present, and blurred vision may persist for several months (Milby, 1971; Whorton & Obrinsky, 1983).
PHOTOPHOBIA: Photophobia, sometimes persisting for several months, has occurred in persons occupationally exposed to mevinphos and phosphamidon residues on leaves of agricultural crops (Whorton & Obrinsky, 1983; Midtling et al, 1985).
EXCESSIVE SALIVATION: Excessive salivation, a muscarinic effect, has occurred following exposure. In one study, it was reported in more than 50% of patients (Bardin et al, 1987a).

HEMATOLOGIC

CHOLINESTERASE INHIBITION: Organophosphate poisoning can lead to inhibition of plasma pseudocholinesterase or erythrocyte acetylcholinesterase, or both (Namba, 1972).
PROTHROMBIN TIME ABNORMALITIES: Alterations in prothrombin time (shortened or prolonged), and increased or decreased factor VII levels have been described, but clinically significant bleeding or hypercoagulability are rare (Von Kaulla & Holmes, 1961).
BLEEDING: Tendency to bleeding, probably related to platelet dysfunction, may occur (Ziemen, 1984).

IMMUNOLOGIC

DERMAL SENSITIZATION: Dermal sensitization to some organophosphates has been reported following skin exposure (Milby et al, 1964), although a majority have not been adequately evaluated for this activity (Coye, 1984).

MUSCULOSKELETAL

FASCICULATIONS: Fasciculations (muscle twitching) occur commonly. Fasciculations were present in 33/61 patients (54%) in one study (Bardin et al, 1987a; HSDB , 1998).
MUSCLE WEAKNESS: Muscle weakness occurs commonly (Bardin et al, 1987a; HSDB , 1998).
PARALYSIS: Muscle paralysis can occasionally supervene following exposure (Done, 1979).

NEUROLOGIC

The earliest manifestations of poisoning are often referable to the central nervous system (CNS): giddiness, uneasiness, restlessness, anxiety and tremulousness (Morgan, 1993; Grob & Garlick, 1950). The initial CNS effects are commonly followed by headache, ataxia, drowsiness, difficulty in concentrating, mental confusion, and slurred speech (Grob & Garlick, 1950; Sittig, 1991).
SEIZURE: Seizure may be an early symptom after a significant exposure (Joy, 1982), with children appearing to be more susceptible to seizures than adults (Zwiener & Ginsburg, 1988). Additionally, EEG changes following mild organophosphate poisoning have appeared similar to interictal EEG's of temporal lobe epileptics (Brown, 1971).
DISTURBED CONSCIOUSNESS: Changes in mental cognition can occur following exposure. In one study, more than 50% of patients in one study had a disturbed level of consciousness. Five of 61 patients were confused; 16/61 were confused and unable to sit or stand; 16/61 were stuporous without reaction to speech (Bardin et al, 1987a).
COMA: In severe poisonings, coma can supervene. Rarely, generalized convulsions can follow (Grob & Garlick, 1950).
PARALYSIS: Type II neurological effects involving paralysis can appear from 12 to 72 hours following exposure. The paralysis is unresponsive to atropine and may be due to excess acetylcholine at nicotinic receptors. Paralytic signs include: inability to lift the neck or sit up, ophthalmoparesis, slow eye movement, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis and death (Wadia et al, 1987). In rare cases, paralysis of the diaphragm has occurred (Rivett & Potgieter, 1987).
DELAYED NEUROTOXICITY/SECONDARY PERIPHERAL NEUROPATHY: Delayed neurotoxicity, appears to be a rare complication (Wadia et al, 1987). Typically, it appears 6 to 21 days after acute exposure and can involve progressive distal weakness and ataxia in the lower limbs. Flaccid paralysis, spasticity, ataxia, or quadriplegia may ensue (Cherniack, 1988). Recovery requires weeks to months, and the recovery may never be complete (Done, 1979a).
There seems to be no relationship between the severity of acute cholinergic effects and delayed neurotoxicity (Cherniack, 1986).
ATAXIA: Following acute bromophos exposure, a cerebellar disorder manifested as ataxia developed approximately 5 weeks after acute exposure with no acute cholinergic effects and no other delayed neuropathy evident (Michotte et al, 1989).
DYSKINESIA: Dyskinesias can result following exposure to organophosphates. Case reports identified multiple forms dyskinesia including choreoathetosis (ceaseless jerky, sinuous, involuntary movements) (Joubert et al, 1984), opisthotonos (type of spasm where the head and heels are drawn backward while the trunk is forward) (Smith, 1977), and opsoclonus (rapid, uncontrolled eye movements) (Pullicino & Aquilina, 1989).

PSYCHIATRIC

PSYCHOSIS: Psychosis and a variety of other personality and behavioral disorders have been described from exposure to organophosphates (Conyers & Goldsmith, 1971; Joubert & Joubert, 1988). These effects are more common with chronic exposure. Organophosphates may exacerbate psychotic symptoms in persons with preexisting schizophrenic tendencies; it is not clear if these symptoms can be induced by organophosphates in the absence of preexisting abnormality (Levin & Rodnitzky, 1976).
ANXIETY: Anxiety and/or irritability have frequently occurred in persons exposed to organophosphates (Levin & Rodnitzky, 1976).
IMPAIRED CONCENTRATION: Acute or chronic exposure to organophosphates may impair concentration and induce confusion and drowsiness and may be a factor in plane crashes by agricultural pilots doing cropdusting (Levin & Rodnitzky, 1976).
REDUCED COGNITION: Persons with other signs of organophosphate poisoning have shown reduced cognitive efficiency and slowness of thought related to the degree of cholinesterase inhibition (Levin & Rodnitzky, 1976).
IMPAIRED MEMORY: Impaired memory is a major CNS effect of organophosphate exposure and may occur in the absence of other overt clinical signs. It has been found in workers chronically exposed to organophosphates (Levin & Rodnitzky, 1976).
SPEECH IMPAIRMENT: Slowed speech, problems in finding words, slurring, intermittent pauses, and perseveration have been seen in persons who have other clinical signs of organophosphate poisoning (Levin & Rodnitzky, 1976).
DEPRESSION: Depression, correlated with the severity of cholinesterase inhibition, has occurred in cases of acute organophosphate poisoning (Levin & Rodnitzky, 1976).

RESPIRATORY

Increased bronchial secretions, bronchospasm, chest tightness, heartburn, and dyspnea occur in severe and moderately severe organophosphate poisonings (Hayes, 1965).
PULMONARY EDEMA: Acute lung injury can occur as a manifestation of severe organophosphate poisoning (Chhabra & Sepaha, 1970; Morgan, 1993).
ASTHMA EXACERBATION: Asthma exacerbations may occur after the inhalation of nontoxic amounts of some organophosphates in sensitive patients with preexisting asthma (Bryant, 1985). Bronchospasms following exposure may be a pharmacologic effect from the muscarinic activity of organophosphates (Lund & Monteagudo, 1986).
TACHYPNEA: Tachypnea (increased respiratory rate) has been reported following exposure with one study reporting a respiratory rate greater than 30 breaths per minute in 39% of patients (Bardin et al, 1987a).
RESPIRATORY FAILURE: Acute respiratory insufficiency, due to any combination of depression of the respiratory center, respiratory paralysis, bronchospasm or increased bronchial secretions, is the main cause of death in many acute organophosphate poisonings (Lerman & Gutman, 1988; Anon, 1984; Morgan, 1993).
PNEUMONITIS: Aspiration of commercial organophosphate preparations which contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986).

VITAL SIGNS

FEVER: Fever occurred in a 5-year-old boy who had ingested a small amount of a mixture of parathion, diazinon and chlordane; it persisted for two days (DePalma et al, 1970).

CHRONIC CLINICAL EFFECTS

Repeated exposures to phorate may produce cumulative effects. A 2-week exposure to phorate in 40 male formulators resulted in toxicity in 60%. GI symptoms and decreased heart rate were more prominent than neurological symptoms. A significant depression in plasma cholinesterase levels was observed at the end of the first week (55%) and even more by the end of the second week (71%) compared with pre-exposure values (HSDB). Pesticide formulators had lower plasma cholinesterase levels during phorate formulation than during disulfoton formulation (Brokopp, 1981).

A 45-year-old farmer with a history of polycystic renal disease developed an episode of gross hematuria accompanied by hypertension and requiring dialysis. Symptoms of organophosphate poisoning associated with dialysis occurred in two separate episodes following the initial treatment. Phorate was found in the water supply and in blood samples from other members of the family who had organophosphate poisoning symptoms (Benson, 1970).

Rats given various doses of phorate showed decreased liver cholinesterase activity after 1 month and reduced red blood cell activity after 2 months of continuous exposure (Doroshenko, 1973).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

ORAL EXPOSURE

Prehospital gastrointestinal decontamination is NOT recommended because of the potential for early coma or seizures and aspiration.

DERMAL EXPOSURE

Remove contaminated clothing. Wash skin thoroughly with soap and water.

EYE EXPOSURE

Copious eye irrigation.

INHALATION EXPOSURE

Immediately assess airway and respiratory function. Administer oxygen.

PERSONNEL PROTECTION

Universal precautions should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids.
Vomiting containing organophosphates should be placed in a closed impervious container for proper disposal.

DECONTAMINATION OF SPILLS/SUMMARY

A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975).

NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).

Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975a).
Chlorine-active compounds such as sodium hypochlorite (household bleach) or calcium hypochlorite (bleaching powder, chlorinated lime) may also be used to detoxify organophosphate spills (EPA, 1975a).

In some instances, a combination of an alkaline substance with a chlorine-active compound may be used (Pesticide User's Guide, 1976).

While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED.

SMALL SPILL DECONTAMINATION

Three cups of Arm & Hammer washing soda (sodium carbonate) or Arm & Hammer baking soda (sodium bicarbonate) may be combined with one-half cup of household bleach and added to a plastic bucket of water. The washing soda is more alkaline and may be more efficacious, if available. Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978).

Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 1975a).
NOTE: Do NOT use a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent. Call the National Pesticide Telecommunications Network for further assistance at 1-800-858-7378 or on the web at http://nptn.orst.edu.

LARGE SPILL DECONTAMINATION

Sprinkle or spray the area with a mixture of one gallon of sodium hypochlorite (bleach) mixed with one gallon of water. Then spread calcium hydroxide (hydrated or slaked lime) liberally over the area and allow to stand for at least one hour (Pesticide User's Guide, 1976). Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978).
Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination.

NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.

FURTHER CONTACT INFORMATION

For further information contact the National Pesticide Telecommunications Network at 1-800-858-7378 or contact on the web at http://nptn.orst.edu.
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378.
The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675.
CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.

ANTIDOTES

SUMMARY: Atropine is used to antagonize muscarinic effects. Oximes (pralidoxime in the US, or obidoxime in some other countries) are used to reverse neuromuscular blockade. Use of oximes is usually indicated for patients with moderate to severe toxicity.
AUTOINJECTORS

INDICATION: Atropine-containing autoinjectors are used for the initial treatment of poisoning by organophosphate nerve agents and organophosphate or carbamate insecticides (Prod Info DuoDote(R) intramuscular injection solution, 2011; Prod Info ATROPEN(R) IM injection, 2005). Pralidoxime use following carbamate exposure may not be indicated.
NOTE: The safety and efficacy of MARK I kit (Note: the MARK I autoinjector kit was last produced by Meridian Medical Technologies, Columbia, MD in 2008. This product may still be available in some locations.), ATNAA, or DuoDote(R) has not been established in children. All of these autoinjectors contain benzyl alcohol as a preservative (Prod Info DuoDote(R) intramuscular injection solution, 2011; Prod Info ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, 2002). Since the AtroPen(R) comes in different strengths, certain dose units have been approved for use in children (Prod Info ATROPEN(R) IM injection, 2005).
The AtroPen(R) autoinjector (atropine sulfate; Meridian Medical Technologies, Inc, Columbia, MD) delivers a dose of atropine in a self-contained unit. There are 4 AtroPen(R) strengths: AtroPen(R) 0.25 mg in 0.3 mL of solution (dispenses 0.21 mg of atropine base; equivalent to 0.25 mg of atropine sulfate), AtroPen(R) 0.5 mg in 0.7 mL of solution (dispenses 0.42 mg of atropine base; equivalent to 0.5 mg of atropine sulfate), Atropen(R) 1 mg in 0.7 mL of solution (dispenses 0.84 mg of atropine base; equivalent to 1 mg of atropine sulfate), and AtroPen(R) 2 mg in 0.7 mL of solution (dispenses 1.67 mg of atropine base; equivalent to 2 mg of atropine sulfate) (Prod Info ATROPEN(R) IM injection, 2005).

AtroPen(R): DOSE: ADULT AND CHILDREN OVER 10 YEARS OF AGE: Mild symptoms, in cases where exposure is known or suspected: Inject one 2 mg AtroPen(R) (green pen) into the outer thigh as soon as symptoms appear; pralidoxime chloride may also be required. Severe symptoms: Inject one 2 mg AtroPen(R) (green pen) into the outer thigh as soon as symptoms appear, administer 2 additional 2 mg AtroPen(R) doses in rapid succession 10 min after receiving the first dose; pralidoxime chloride and/or an anticonvulsant may also be required, patients should be closely monitored for at least 48 to 72 hr. PEDIATRIC: Mild symptoms, in cases where exposure is known or suspected: dose for infants less than 7 kg (generally less than 6 months of age) = 0.25 mg (yellow pen), dose for children 7 to 18 kg (generally 6 months to 4 years of age) = 0.5 mg (blue pen), dose for children 18 to 41 kg (generally 4 to 10 years of age) = 1 mg (dark red pen), dose for children over 41 kg = 2 mg (green pen): inject one AtroPen(R) into the outer thigh as soon as symptoms appear; pralidoxime chloride may also be required. Severe symptoms: Administer 2 additional AtroPen(R) doses (see above) in rapid succession 10 min after receiving the first dose; pralidoxime chloride and/or an anticonvulsant may also be required, patients should be closely monitored for at least 48 to 72 hr (Prod Info ATROPEN(R) IM injection, 2005).
If pralidoxime is required, pralidoxime prefilled autoinjector delivers 600 mg IM (adult dosing); may repeat every 15 minutes up to 3 injections if symptoms persist. The safety and efficacy of pralidoxime auto-injector for use in nerve agent poisoning have not been established in pediatric patients (Prod Info pralidoxime chloride intramuscular auto-imjector solution, 2003)

ATNAA (Antidote Treatment Nerve Agent Autoinjector, Meridian Medical Technologies, Columbia, Maryland) is currently used by the US military and provides atropine injection and pralidoxime chloride injection in a single needle. Each self-contained unit dispenses 2.1 mg of atropine in 0.7 mL and 600 mg of pralidoxime chloride in 2 mL via intramuscular injection (Prod Info ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, 2002).

ATNAA: DOSE: ADULT: One ATNAA into the lateral thigh muscle or buttocks. Wait 10 to 15 minutes for effect (Prod Info ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, 2002).

MARK I: This device (Meridian Medical Technologies, Columbia, Maryland) was used by the US military. (Note: the MARK I autoinjector kit was last produced by Meridian Medical Technologies, Columbia, MD in 2008. This product may still be available in some locations.) Each kit contains two autoinjectors: an atropine and a pralidoxime autoinjector. The atropine autoinjector delivers 2.1 mg of atropine in 0.7 mL via intramuscular injection. The pralidoxime autoinjector delivers 600 mg pralidoxime chloride in 2 mL via intramuscular injection (Prod Info DUODOTE(TM) IM injection, 2006).
DuoDote(R) is a dual chambered device (Meridian Medical Technologies, Columbia, Maryland) that delivers 2.1 mg of atropine in 0.7 mL and 600 mg of pralidoxime chloride in 2 mL sequentially using a single needle for use in a civilian or community setting. It should be administered by Emergency Medical Services personnel who have been trained to recognize and treat nerve agent or insecticide intoxication (Prod Info DuoDote(R) intramuscular injection solution, 2011).
DuoDote(R): DOSE: ADULT: Two or more mild symptoms, initial dose, 1 injector (atropine 2.1 mg/pralidoxime chloride 600 mg) IM into the mid-lateral thigh, wait 10 to 15 minutes for effect; subsequent doses, if at any time severe symptoms develop, administer 2 additional injectors in rapid succession IM into the mid-lateral thigh and immediately seek definitive medical care; MAX 3 doses unless definitive medical care is available (Prod Info DuoDote(R) intramuscular injection solution, 2011).
Therapeutic plasma concentrations of pralidoxime exceeding 4 mcg/mL were achieved within 4 to 8 minutes after injection (Sidell & Groff, 1974).
DIAZEPAM Autoinjector (Meridian Medical Technologies): Contains 10 mg of diazepam in 2 mL for intramuscular injection for seizure control (Prod Info diazepam autoinjector IM injection solution, 2005).
These devices are designed for initial field treatment. Although autoinjector doses may be adequate for nerve agent exposures, ORGANOPHOSPHATE exposures may require additional atropine or pralidoxime doses in the hospital setting that exceed those in the available autoinjectors.
For medical questions concerning Meridian products, you can call 1-800-438-1985. For general product information, call 1-800-638-8093.

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (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.

FIRST AID

ORAL EXPOSURE

Prehospital gastrointestinal decontamination is NOT recommended because of the potential for early coma or seizures and aspiration.

DERMAL EXPOSURE

Remove contaminated clothing. Wash skin thoroughly with soap and water.

EYE EXPOSURE

Copious eye irrigation.

INHALATION EXPOSURE

Immediately assess airway and respiratory function. Administer oxygen.

PERSONNEL PROTECTION

Universal precautions should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids.
Vomiting containing organophosphates should be placed in a closed impervious container for proper disposal.

DECONTAMINATION OF SPILLS/SUMMARY

A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975).

NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).

Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975a).
Chlorine-active compounds such as sodium hypochlorite (household bleach) or calcium hypochlorite (bleaching powder, chlorinated lime) may also be used to detoxify organophosphate spills (EPA, 1975a).

In some instances, a combination of an alkaline substance with a chlorine-active compound may be used (Pesticide User's Guide, 1976).

While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED.

SMALL SPILL DECONTAMINATION

Three cups of Arm & Hammer washing soda (sodium carbonate) or Arm & Hammer baking soda (sodium bicarbonate) may be combined with one-half cup of household bleach and added to a plastic bucket of water. The washing soda is more alkaline and may be more efficacious, if available. Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978).

Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 1975a).
NOTE: Do NOT use a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent. Call the National Pesticide Telecommunications Network for further assistance at 1-800-858-7378 or on the web at http://nptn.orst.edu.

LARGE SPILL DECONTAMINATION

Sprinkle or spray the area with a mixture of one gallon of sodium hypochlorite (bleach) mixed with one gallon of water. Then spread calcium hydroxide (hydrated or slaked lime) liberally over the area and allow to stand for at least one hour (Pesticide User's Guide, 1976). Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978).
Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination.

NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.

FURTHER CONTACT INFORMATION

For further information contact the National Pesticide Telecommunications Network at 1-800-858-7378 or contact on the web at http://nptn.orst.edu.
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378.
The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675.
CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.

ANTIDOTES

SUMMARY: Atropine is used to antagonize muscarinic effects. Oximes (pralidoxime in the US, or obidoxime in some other countries) are used to reverse neuromuscular blockade. Use of oximes is usually indicated for patients with moderate to severe toxicity.
AUTOINJECTORS

INDICATION: Atropine-containing autoinjectors are used for the initial treatment of poisoning by organophosphate nerve agents and organophosphate or carbamate insecticides (Prod Info DuoDote(R) intramuscular injection solution, 2011; Prod Info ATROPEN(R) IM injection, 2005). Pralidoxime use following carbamate exposure may not be indicated.
NOTE: The safety and efficacy of MARK I kit (Note: the MARK I autoinjector kit was last produced by Meridian Medical Technologies, Columbia, MD in 2008. This product may still be available in some locations.), ATNAA, or DuoDote(R) has not been established in children. All of these autoinjectors contain benzyl alcohol as a preservative (Prod Info DuoDote(R) intramuscular injection solution, 2011; Prod Info ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, 2002). Since the AtroPen(R) comes in different strengths, certain dose units have been approved for use in children (Prod Info ATROPEN(R) IM injection, 2005).
The AtroPen(R) autoinjector (atropine sulfate; Meridian Medical Technologies, Inc, Columbia, MD) delivers a dose of atropine in a self-contained unit. There are 4 AtroPen(R) strengths: AtroPen(R) 0.25 mg in 0.3 mL of solution (dispenses 0.21 mg of atropine base; equivalent to 0.25 mg of atropine sulfate), AtroPen(R) 0.5 mg in 0.7 mL of solution (dispenses 0.42 mg of atropine base; equivalent to 0.5 mg of atropine sulfate), Atropen(R) 1 mg in 0.7 mL of solution (dispenses 0.84 mg of atropine base; equivalent to 1 mg of atropine sulfate), and AtroPen(R) 2 mg in 0.7 mL of solution (dispenses 1.67 mg of atropine base; equivalent to 2 mg of atropine sulfate) (Prod Info ATROPEN(R) IM injection, 2005).

AtroPen(R): DOSE: ADULT AND CHILDREN OVER 10 YEARS OF AGE: Mild symptoms, in cases where exposure is known or suspected: Inject one 2 mg AtroPen(R) (green pen) into the outer thigh as soon as symptoms appear; pralidoxime chloride may also be required. Severe symptoms: Inject one 2 mg AtroPen(R) (green pen) into the outer thigh as soon as symptoms appear, administer 2 additional 2 mg AtroPen(R) doses in rapid succession 10 min after receiving the first dose; pralidoxime chloride and/or an anticonvulsant may also be required, patients should be closely monitored for at least 48 to 72 hr. PEDIATRIC: Mild symptoms, in cases where exposure is known or suspected: dose for infants less than 7 kg (generally less than 6 months of age) = 0.25 mg (yellow pen), dose for children 7 to 18 kg (generally 6 months to 4 years of age) = 0.5 mg (blue pen), dose for children 18 to 41 kg (generally 4 to 10 years of age) = 1 mg (dark red pen), dose for children over 41 kg = 2 mg (green pen): inject one AtroPen(R) into the outer thigh as soon as symptoms appear; pralidoxime chloride may also be required. Severe symptoms: Administer 2 additional AtroPen(R) doses (see above) in rapid succession 10 min after receiving the first dose; pralidoxime chloride and/or an anticonvulsant may also be required, patients should be closely monitored for at least 48 to 72 hr (Prod Info ATROPEN(R) IM injection, 2005).
If pralidoxime is required, pralidoxime prefilled autoinjector delivers 600 mg IM (adult dosing); may repeat every 15 minutes up to 3 injections if symptoms persist. The safety and efficacy of pralidoxime auto-injector for use in nerve agent poisoning have not been established in pediatric patients (Prod Info pralidoxime chloride intramuscular auto-imjector solution, 2003)

ATNAA (Antidote Treatment Nerve Agent Autoinjector, Meridian Medical Technologies, Columbia, Maryland) is currently used by the US military and provides atropine injection and pralidoxime chloride injection in a single needle. Each self-contained unit dispenses 2.1 mg of atropine in 0.7 mL and 600 mg of pralidoxime chloride in 2 mL via intramuscular injection (Prod Info ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, 2002).

ATNAA: DOSE: ADULT: One ATNAA into the lateral thigh muscle or buttocks. Wait 10 to 15 minutes for effect (Prod Info ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, 2002).

MARK I: This device (Meridian Medical Technologies, Columbia, Maryland) was used by the US military. (Note: the MARK I autoinjector kit was last produced by Meridian Medical Technologies, Columbia, MD in 2008. This product may still be available in some locations.) Each kit contains two autoinjectors: an atropine and a pralidoxime autoinjector. The atropine autoinjector delivers 2.1 mg of atropine in 0.7 mL via intramuscular injection. The pralidoxime autoinjector delivers 600 mg pralidoxime chloride in 2 mL via intramuscular injection (Prod Info DUODOTE(TM) IM injection, 2006).
DuoDote(R) is a dual chambered device (Meridian Medical Technologies, Columbia, Maryland) that delivers 2.1 mg of atropine in 0.7 mL and 600 mg of pralidoxime chloride in 2 mL sequentially using a single needle for use in a civilian or community setting. It should be administered by Emergency Medical Services personnel who have been trained to recognize and treat nerve agent or insecticide intoxication (Prod Info DuoDote(R) intramuscular injection solution, 2011).
DuoDote(R): DOSE: ADULT: Two or more mild symptoms, initial dose, 1 injector (atropine 2.1 mg/pralidoxime chloride 600 mg) IM into the mid-lateral thigh, wait 10 to 15 minutes for effect; subsequent doses, if at any time severe symptoms develop, administer 2 additional injectors in rapid succession IM into the mid-lateral thigh and immediately seek definitive medical care; MAX 3 doses unless definitive medical care is available (Prod Info DuoDote(R) intramuscular injection solution, 2011).
Therapeutic plasma concentrations of pralidoxime exceeding 4 mcg/mL were achieved within 4 to 8 minutes after injection (Sidell & Groff, 1974).
DIAZEPAM Autoinjector (Meridian Medical Technologies): Contains 10 mg of diazepam in 2 mL for intramuscular injection for seizure control (Prod Info diazepam autoinjector IM injection solution, 2005).
These devices are designed for initial field treatment. Although autoinjector doses may be adequate for nerve agent exposures, ORGANOPHOSPHATE exposures may require additional atropine or pralidoxime doses in the hospital setting that exceed those in the available autoinjectors.
For medical questions concerning Meridian products, you can call 1-800-438-1985. For general product information, call 1-800-638-8093.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

GENERAL/SUMMARY

The minimum lethal human dose to this agent has not been delineated.
The actual lethal dose of an organophosphate can vary widely and depends strongly on the route and rate of exposure and on the aggressiveness of the treatment used.

MAXIMUM TOLERATED EXPOSURE

The World Health Organization (WHO) has classified phorate as pesticide class Ia (Extremely hazardous) (World Health Organization, 2006).

GENERAL/SUMMARY

No-effect levels for daily dosing based on cholinesterase inhibition: Rats (0.05 to 0.15 mg/kg/day); Dogs (0.01 to 0.05 mg/kg/day) (ACGIH, 1991).
Extrapolating the above for a human daily no-effect dose: 0.03 to 0.1 mg/kg/day, or 2.1 to 7 mg/day for a 70 kg human.

PEDIATRIC

Note that CHILDREN MAY EXHIBIT DIFFERENT PREDOMINANT SIGNS of organophosphate poisoning from adults. In a study on 25 children poisoned by organophosphate or carbamate compounds, the major symptoms in most of them were CNS depression, stupor, flaccidity, dyspnea, and coma. Other classical signs of organophosphate poisoning, such as miosis, fasciculations, bradycardia, excessive salivation and lacrimation, and gastrointestinal symptoms, were infrequent (Sofer et al, 1989).
Children tend to be more sensitive to organophosphates than adults (Zwiener & Ginsburg, 1988).

OCCUPATIONAL

Three workers at a pesticide-formulating plant developed symptoms of organophosphate poisoning associated with each worker wearing a uniform that was contaminated with 76 percent parathion and then laundered. The uniform had been laundered three times before the third worker wore it and he still developed nausea, vomiting, and red cell cholinesterase activity of 75 percent of normal (Clifford & Nies, 1989).

Carcinogenicity Ratings for CAS298-02-2 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Phorate

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.

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: Phorate
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 IRIS

EPA Risk Assessment Values for CAS298-02-2 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

References: RTECS, 2003
- LC50- (INHALATION)RAT:
- LD50- (INTRAPERITONEAL)GERBIL:
- LD50- (SKIN)GUINEA_PIG:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)RABBIT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (INTRAVENOUS)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- TDLo- (INTRAPERITONEAL)GERBIL:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS298-02-2 (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.

Adopted Value

Phorate

TLV:

TLV-TWA: 0.05 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: BEI(A), IFV, Skin
Definitions:

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.
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.
IFV: Inhalable fraction and vapor.
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.

TLV Basis - Critical Effect(s): Cholinesterase inhib
Molecular Weight: 260.40

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS298-02-2 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS298-02-2 (National Institute for Occupational Safety and Health, 2007):

Listed as: Phorate
REL:

TWA: 0.05 mg/m(3)
STEL: 0.2 mg/m(3)
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: [skin]

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.

Note(s):

IDLH: Not Listed

OSHA PEL Values for CAS298-02-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS298-02-2 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS298-02-2 (U.S. Environmental Protection Agency, 2010):

Listed as: Phorate
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information:
Listed as: Phosphorodithioic acid, O,O-diethyl S-[(ethylthio)methyl] ester
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS298-02-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS298-02-2 (U.S. Environmental Protection Agency, 2010b):

Listed as: Phorate
P or U series number: P094
Footnote:
Listed as: Phosphorodithioic acid, O,O-diethyl S-[(ethylthio)methyl] ester
P or U series number: P094
Footnote:
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS298-02-2 (U.S. Environmental Protection Agency, 2010):

Listed as: Phorate
Reportable Quantity, in pounds: 10

Only the statutory or final RQ is shown. For more information, see 40 CFR table 302.4.

Threshold Planning Quantity, in pounds:

10
Amount necessary to be covered by this standard. See 40 CFR 355.30.

Note(s): Not Listed

EPA SARA Title III, Community Right-to-Know for CAS298-02-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS298-02-2 (49 CFR 172.101 - App. B, 2005):

Listed as Phorate
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS298-02-2 (EPA, 2005):

Not Listed

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS298-02-2 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

It is recommended that the product's temperature not exceed 25 to 30 degrees C, and be kept away from sources of heat, free flames or spark-generating equipment.

STORAGE

ROOM/CABINET RECOMMENDATIONS

Storage areas must be located at suitable distance from inhabited buildings, animal shelters, and food stores; moreover, they must be inaccessible to unauthorized persons, children, and domestic animals (HSDB , 1990).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (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.

Wear full protective clothing when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).

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.

Any contaminated clothing should be discarded as hazardous waste. Repeated laundering may not remove organophosphate from clothing (Clifford & Nies, 1989).

DECONTAMINATION: Remove contaminated clothing. Wash the skin, including the hair, beneath the nails, groin, and umbilical area, three times.

A single washing with soap and water can remove up to 80 to 92 percent of an organophosphate on the skin if done immediately (Fredriksson, 1961). If delayed, the same procedure may remove only 50 to 70 percent.
Following a soap and water wash, a second wash with 95 percent ethanol will leave only about a 5 to 10 percent organophosphate residue (Fredriksson, 1961).
The best results of skin decontamination are achieved with a thorough soap and water wash, followed by a 95 percent ethanol wash, followed by a second soap and water wash (Fredriksson, 1961).
Tincture of green soap contains 30 percent ethanol, and has been recommended for dermal decontamination of organophosphate exposures.

LEATHER: Leather absorbs organophosphates and is extremely difficult to decontaminate. Rescuers should not wear leather items that are not completely covered by rubber or impervious plastic. Contaminated leather items may need to be disposed of by incineration.

RESPIRATORY PROTECTION

Wear a self-contained positive pressure breathing apparatus when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).

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 298-02-2.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- Combustible material: may burn but does not ignite readily.
- Containers may explode when heated.
- Runoff may pollute waterways.
- Substance may be transported in a molten form.
When heated to decomposition, Phorate releases highly toxic fumes of oxides of carbon, phosphorus, and sulfur (Sax & Lewis, 1989).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS298-02-2 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (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 152 (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 CAS298-02-2 (NFPA, 2002):

Not Listed

Choose an extinguishing agent suitable for fires in surrounding material (AAR, 1987).

Water may be used in flooding quantities as fog (AAR, 1987).

COMBUSTION TOXICITY

When heated to decomposition, phorate releases highly toxic fumes of oxides of carbon, phosphorus, and sulfur (Sax & Lewis, 1989).

DUST/VAPOR HAZARD

When heated to decomposition, phorate releases highly toxic fumes of oxides of carbon, phosphorus, and sulfur (Sax & Lewis, 1989).

REACTIVITY HAZARD

When heated to decomposition, phorate releases highly toxic fumes of oxides of phosphorus and sulfur (Lewis, 1996).

Most organophosphate pesticides degrade relatively rapidly in the environment; a notable exception is LEPTOPHOS, which is lipophilic (Abou-Donia, 1983).

All organophosphate esters undergo hydrolysis in water; generally the water-soluble products of hydrolysis are less toxic than the parent compound (Minton & Murray, 1988).

EVACUATION PROCEDURES

SUMMARY

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 152 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (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 152 (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:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

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.

Downwind evacuation should be considered if this material is involved in a fire or if a large discharge has occurred (AAR, 1987).

AIHA ERPG Values for CAS298-02-2 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS298-02-2 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Phorate
TEEL-0 (units = mg/m3): 0.04
TEEL-1 (units = mg/m3): 0.04
TEEL-2 (units = mg/m3): 0.04
TEEL-3 (units = mg/m3): 0.12
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 CAS298-02-2 (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):

Listed as: Phorate
Proposed Value:

AEGL-1

10 min exposure:

ppm:
mg/m3: Not recommended due to insufficient data

30 min exposure:

ppm:
mg/m3: Not recommended due to insufficient data

1 hr exposure:

ppm:
mg/m3: Not recommended due to insufficient data

4 hr exposure:

ppm:
mg/m3: Not recommended due to insufficient data

8 hr exposure:

ppm:
mg/m3: Not recommended due to insufficient data

Definitions:

AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.

Listed as: Phorate
Proposed Value:

AEGL-2

10 min exposure:

ppm:
mg/m3: 0.073 mg/m(3)

30 min exposure:

ppm:
mg/m3: 0.05 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 0.04 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 0.01 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.005 mg/m(3)

Definitions:

AEGL-2 is the airborne concentration 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.

Listed as: Phorate
Proposed Value:

AEGL-3

10 min exposure:

ppm:
mg/m3: 0.22 mg/m(3)

30 min exposure:

ppm:
mg/m3: 0.15 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 0.12 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 0.031 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.015 mg/m(3)

Definitions:

AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.

NIOSH IDLH Values for CAS298-02-2 (National Institute for Occupational Safety and Health, 2007):

Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area).
- 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 152 (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.
DECONTAMINATION OF SPILLS
- A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1975a; EPA, 1978).
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required.
Water spray may be used to reduce or knock down vapors (AAR, 1987).

SMALL LEAK/SPILL

Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and an approved respirator. Get fire-fighting equipment ready. Contain any liquid spill around the edge and absorb with Zorb-All(R), soil, sweeping compound, sawdust, dry sand or similar material. Dispose of absorbed or dry material in disposible containers (EPA, 1975; Ford, 1989).
Scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R), or similar material. Re-absorb scrubbing liquid and dispose as above (Ford, 1989). Several washes may be required for decontamination (EPA, 1978).

LARGE LEAK/SPILL

Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and approved personal protection equipment. Get fire-fighting equipment ready (Ford, 1989).
Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime, lime or lime water when in dilute solutions), and calcium carbonate (crushed limestone) may be used for detoxification (EPA, 1975a).
- In general it would be preferable to detoxify spilled material before absorbing for disposal whenever possible.
Contain any liquid spill around the edge and absorb with Zorb-All(R), soil, sweeping compound, sawdust, dry sand or similar material. Dispose of absorbed or dry material in disposible containers (EPA, 1975; Ford, 1989).
- Containers should be sealed to prevent further decontamination.
After the bulk of the material has been removed, further decontaminate spoiled surfaces with alkaline treatment as described above, or with concentrated alkaline detergent. Absorb and dispose of waste water as described above.
Water spray may be used to reduce or knock down vapors (AAR, 1987).
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. Consult the local Emergency Response Committee for guidance.

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

ENVIRONMENTAL EXPOSURE

Phorate is introduced to the environment through its direct application as a pesticide on numerous crop species (HSDB, 2004).

OCCUPATIONAL EXPOSURE

Workers may be exposed to phorate through its production, application, and as a residue on plants, clothing, and equipment (HSDB, 2004).

GENERAL POPULATION EXPOSURE

Phorate has been detected in surface waters. The general population may be exposed to phorate through drinking water and as a residue in or on food crops. It may also be carried from the workplace to the home on clothing and equipment, creating a source of exposure for persons associated with phorate workers (HSDB, 2004).

ENVIRONMENTAL FATE AND KINETICS

Vapor phase phorate degrades through reaction with photochemically-produced hydroxyl radicals; the reaction half-life is estimated to be 1.5 hours, based on the calculated rate constant of 2.5 x 10(-10) cm(3)/molecule/sec at 25 degrees C (HSDB, 2004).
Laboratory data indicates rapid photolysis (half-life <30 minutes) will occur for atmospheric phorate under midsummer sunlight conditions (HSDB, 2004).
- Photolysis effectively eliminated phorate in solution and from an exposed glass surface using ultraviolet light with wavelength >290 nm. The rate constant for elimination of phorate from a methanol-water (60:40) solution was 4.9 X 10(-5)/s, while the half-life of phorate as a thin film on glass was 5 hours (Sharma & Gupta, 1994).

WATER

SURFACE WATER
- Phorate is expected to volatilize from water surfaces, based on its estimated Henry's Law constant of 4.37 x 10(-6) atm-m(3)/mole. Volatilization half-lives have been estimated at 14 days for a model river (1 m deep, flowing 1 m/sec, wind velocity of 0.5 m/sec), 105 days for a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec), and 810 days for a model pond (with adsorption to sediment taken into consideration) (HSDB, 2004).
- Adsorption to suspended solids and sediment will inhibit phorate's volatilization from water surfaces. Studies have shown presence of sediment in the water column to decrease phorate volatilization(HSDB, 2004).
- Phorate will hydrolyze; by-products include diethyl disulfide, hydrogen sulfide, and formaldehyde under alkaline conditions (HSDB, 2004).
- Photolysis effectively eliminated phorate in solution and from an exposed glass surface using ultraviolet light with wavelength >290 nm. The rate constant for elimination of phorate from a methanol-water (60:40) solution was 4.9 X 10(-5)/s, while the half-life of phorate as a thin film on glass was 5 hours (Sharma & Gupta, 1994).

SOIL

TERRESTRIAL
- Based on an organic carbon partition coefficient (Koc) of 543 - 3200, phorate is predicted to have low to moderate mobility in soils. This adsorption to soils will attenuate phorate's volatilization, which is expected to occur from moist, but not dry, soil surfaces (HSDB, 2004).
- In soils, phorate is oxidized to the sulfoxide and sulfone and their phosphorothioate analogues, which are subsequently hydrolyzed. The sulfone may persist under certain conditions (Tomlin, 2000).
- A study was conducted to investigate the persistence of insecticides after seasonal (spring and fall) applications to silt loam soil over a 4 year period. Phorate did not accumulate from one year to the next, and its residue represented less than 0.2% of the compound applied after 5 years (Talekar, 1983).
- When labeled phorate was applied to soils the initial loss by volatilization was as great as 24% within one hour. After that little or no additional volatilization occurred (HSDB , 1990).
- Photolysis half-life for phorate in soil has been calculated at 1.8 days (HSDB, 2004).

ABIOTIC DEGRADATION

When released to the atmosphere, phorate is expected to exist solely as a vapor in the ambient air, where it degrades rapidly through photolysis and reaction with photochemically-produced hydroxyl radicals (HSDB, 2004).

In soils, phorate adsorbs relatively strongly to soils, resulting in low to slight mobility. Some volatilization from moist soil surfaces will occur, but is not expected from dry soil surfaces due to phorate's low vapor pressure. Biodegradation studies indicate phorate will also be removed from soils through biodegradation (HSDB, 2004).

In aquatic environments, phorate is expected to volatilize slowly from water surfaces, though this is attenuated by its adsorption to suspended solids and sediments. It will also be hydrolyzed and undergo photolysis in sunlight conditions. Bioconcentration by aquatic organisms is expected to be moderate (HSDB, 2004).

BIODEGRADATION

Biodegradation rates of phorate in various soil types were measured as follows (HSDB, 2004):
Soil Type Half-Life
sandy loam 7 days
silty clay loam 9 days
clay loam 8 days

Microbial degradation of phorate in loam soil, sandy soil, and muck soil resulted in formation of phorate sulfone and phorate sulfoxide by-products. The by-products were present at the lowest amounts in sandy soil (HSDB, 2004).

Calculated biodegradation half-lives for phorate in soils range from 5 to 68 days (HSDB, 2004).

The effects of malathion and phorate at concentrations from 10 to 300 mcg/g on the microbial population of an agricultural soil were studied. Nitrifying bacteria and fungal population were not affected by the insecticides, while the total bacteria populations were significantly reduced (Gonzalezlopez et al, 1993).

BIOACCUMULATION

FISH

Bioconcentration in fish is expected to be moderate (HSDB, 2004).

BIOCONCENTRATION FACTOR

A bioconcentration factor (BCF) of 90 has been determined for phorate in sheepshead minnows after 28 days of exposure to the chemical (HSDB, 2004).
The blue-green algae, Anabaena sp., had the following BCF values (HSDB, 2004):
BCF phorate dose concentration
3 2.5 mcg/mL
6 5 mcg/mL
12 10 mcg/mL
The blue-green algae, Anabaena fertilissima, had the following BCF values (HSDB, 2004):
phorate dose concentration BCF time to maximum bioconcentration
2.5 mcg/mL 8 16 hours
5 mcg/mL 12 16 hours
10 mcg/mL 11 32 hours
BCF for phorate in vegetation = 0.020 (HSDB, 2004)

ENVIRONMENTAL TOXICITY

FISH

LC50 - BLUEGILL (Lepomis macrochirus), 1.0 g: 2.0 mcg/L for 96H -- static bioassay, no aeration, at 15 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 1.5 - 2.5 mcg/L) (HSDB, 2004)
LC50 - CHANNEL CATFISH (Ictalarus punctatus), 1.0 g: 280 mcg/L for 96H -- static bioassay, no aeration, at 15 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 115 - 680 mcg/L) (HSDB, 2004)
LC50 - CUTTHROAT TROUT (Salmo clarki), 1.0 g: 6.0 mcg/L for 96H -- static bioassay, no aeration, at 12 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 5.2 - 6.8 mcg/L) (HSDB, 2004)
LC50 - LARGEMOUTH BASS (Micropterus salmoides), 0.9 g: 5.0 mcg/L for 96H -- static bioassay, no aeration, at 15 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 4.7 - 5.4 mcg/L) (HSDB, 2004)
LC50 - NORTHERN PIKE (Esox lucius), 0.7 g: 110 mcg/L for 96H -- static bioassay, no aeration, at 15 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 90 - 130 mcg/L) (HSDB, 2004)
LC50 - RAINBOW TROUT (Salmo gairdneri), 1.2 g: 13 mcg/L for 96H -- static bioassay, no aeration, at 12 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 11 - 16 mcg/L) (HSDB, 2004)
LC50 - SHEEPSHEAD MINNOW (Cyprinodon variegatus): 1.3 mcg/L for 96H (Verschueren, 2001)
LC50 - SILVERSIDE (Menidia beryllina): 0.33 mcg/L for 96H (Verschueren, 2001)

CRUSTACEAN

EC50 - BRINE SHRIMP (Artemia sp.): >50 mg/L for 24H (Verschueren, 2001)
LC50 - CRAYFISH (Orconectes nais): 50 mcg/L for 96H -- conditions of bioassay not given (HSDB, 2004)
LC50 - FRESHWATER SHRIMP (Gammarus lacustris): 9 mcg/L for 96H (Verschueren, 2001)
LC50 - SCUD (Gammarus fasciatus), mature: 4 mcg/L for 96H -- static bioassay, no aeration, at 15 degrees C, pH 7.2 - 7.5, water hardness of 40-50 mg/L as calcium carbonate, alkalinity of 30-35 mg/L (95% confidence limit 2 - 6 mcg/L) (HSDB, 2004)
LC50 - SCUD (Gammarus fasciatus): 0.60 mcg/L for 96H (Verschueren, 2001)

ZOOPLANKTON

EC50 - ROTIFER (Brachionus plicatilis): >50 mg/L for 24H (Verschueren, 2001)

BIRD

LC50 - (ORAL) BOBWHITE (Colinus virginianus), 14 days old: 373 ppm for 5D -- in diet (95% confidence limit 115 - 680 ppm) (HSDB, 2004)
LD50 - (ORAL) CHUKAR (Alectoris chukar), 3 months old: 12.8 mg/kg -- (95% confidence limit 3.20 - 51.2 mg/kg) (HSDB, 2004)
LD50 - (ORAL) GRACKLE: 1.3 mg/kg (HSDB, 2004)
LC50 - (ORAL) JAPANESE QUAIL (Coturnix coturnix), 17 days old: 200 ppm for 5D -- in diet (HSDB, 2004)
LC50 - (ORAL) MALLARD (Anas platyrhynchos), 10 days old: 248 ppm for 5D -- in diet (95% confidence limit 198 - 306 ppm) (HSDB, 2004)
LD50 - (ORAL) MALLARD (Anas platyrhynchos), 3-4 months old, female: 0.616 mg/kg -- (95% confidence limit 0.367 - 1.03 mg/kg) (HSDB, 2004)
LD50 - (ORAL) PHEASANT (Phastanus colchicus), 3-4 months old: 7.12 mg/kg -- (95% confidence limit 4.94 - 10.3 mg/kg) (HSDB, 2004)
LD50 - (ORAL) REDWING BLACKBIRD: 1.0 mg/kg (HSDB, 2004)
LC50 - (ORAL) RING-NECKED PHEASANT, 10 days old: 441 ppm for 5D -- in diet (95% confidence limit 381 - 510 ppm) (HSDB, 2004)
LD50 - (ORAL) STARLING: 7.5 mg/kg (HSDB, 2004)

AMPHIBIAN

LD50 - (ORAL) BULLFROG (Rana catesbeiana): 85.2 mg/kg -- (95% confidence limit 59.3 - 122 mg/kg) (HSDB, 2004)

INSECT

LC50 - STONEFLY (Pteronarcys californica), second year class: 4 mcg/L for 96H -- static bioassay, no aeration, pH 7.2 - 7.5, water hardness of 40 - 50 mg/L as calcium carbonate, alkalinity of 30 - 35 mg/L, at 15 degrees C, (95% confidence limit 2 - 6 mcg/L) (HSDB, 2004)
LD50 - HONEYBEE: 0.32 mcg/bee -- acute contact (HSDB, 2004)

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

260.39 (Lewis, 1996)

DESCRIPTION/PHYSICAL STATE

Phorate is a clear, mobile liquid with an objectionable, skunk-like odor (Budavari, 1996; Lewis, 1996; Sittig, 1991; EPA, 1988; ACGIH, 1991; HSDB , 1998).

SHELF LIFE

Stable at room temperature (Budavari, 1996)
Has a half-life of 2 hours in aqueous solution at pH 8 and at 70 degrees C; much more stable in acid medium (HSDB , 1998).
Oxidizable in air (Sunshine, 1969)

VAPOR PRESSURE

8.4 X 10(-4) mmHg (at 20 degrees C) (Budavari, 1989)

0.002 mmHg (at 21 degrees C) (ACGIH, 1986)

DENSITY

TEMPERATURE AND/OR PRESSURE NOT LISTED

1.156 (Budavari, 1996)

FREEZING/MELTING POINT

MELTING POINT

-42.9 degrees C; -45 degrees F (Spencer, 1982)

BOILING POINT

75-78 degrees C (at 0.1 mmHg) (Budavari, 1989)

118-120 degrees C (at 0.8 mmHg) (Budavari, 1989)

125-127 degrees C (at 2.0 mmHg) (Budavari, 1989)

257-261 degrees F (at 2.0 mmHg) ( EPA, 1985)

FLASH POINT

160 degrees C (Tagliabue open cup) (EPA, 1988)

SOLUBILITY

IN WATER

50 ppm (Budavari, 1996)
Insoluble in water (ACGIH, 1991)
17.9 +/- 2.2 mg of 99 percent pure phorate dissolves in one liter of water at 20 degrees C (HSDB , 1998).

IN ORGANIC SOLVENTS

Miscible with carbon tetrachloride, dibutyl phthalate, methyl cellosolve, dioxane, xylene and vegetable oils (ACGIH, 1991) Budavari, 1996)
Soluble in ethanol, ether, aromatic hydrocarbons (Sunshine, 1969).
Very soluble in aliphatic hydrocarbons (Sunshine, 1969).

HENRY'S CONSTANT

5.47 X 10(-6) atm-m(3)/mole (Ehrenfeld et al, 1986)

OTHER/PHYSICAL

INDEX OF REFRACTION

1.5329 (at 25 degrees C) (Budavari, 1996)

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