ACEPHATE

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.

STCC NUMBER

4921674

DESIGNATIONS

IMO CLASSIFICATION:3.2 - Organophosphorus pesticides, liquid flammable, toxic, NOS, flashpoint less than 23 degrees C
IMO CLASSIFICATION:6.1 - Organophosphorus pesticides, liquid toxic, NOS; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint between 23 degrees C and 61 degrees C; Organophosphorus pesticides, solid, toxic, NOS

MOLECULAR FORMULA

C4-H10-N-O3-P-S

ERG GUIDE NUMBER

152-SUBSTANCES - TOXIC (COMBUSTIBLE)

SYNONYM REFERENCE

(EPA, 1990; EXTOXNET, 1995; Hartley & Kidd, 1990; HSDB , 2001; Lewis, 2000; RTECS , 2001)

USES/FORMS/SOURCES

USES

Acephate is used as a contact and systemic insecticide against many beetle varieties, crickets, moths, worms, aphids and other chewing and sucking insects. It controls parasites in goats, sheep, hogs, horses, chickens and cattle. Acephate is used on lawns, turf, pastures and rangeland, and is also acceptable for indoor houseplants. Agricultural crops such as beans, cotton, bell peppers, lettuce and celery can also to treated with this insecticide (Clayton & Clayton, 1993a; EPA, 1990a; HSDB, 2002; Lewis, 1998)
Acephate is also used in food-processing plants (EPA, 1990a).

FORMS

Acephate is available in various forms (EPA, 1990a; Hartley & Kidd, 1990a; HSDB, 2002; Sine, 1987a; Thompson, 1987):

75% soluble powder
25% soluble powder
50% wettable powder
2% dust
technical product (80-90% pure)
encapsulated and various granular forms
pressurized liquid
a cartridge
soluble liquid and solid concentrates
75% suspension
0-25% pressurized spray

O,O-dimethylphosphoramidothioate, methylthioacetate (MTA) and O,O,S-trimethylphosphorothioate have been identified as impurities in commercial-grade acephate. Impurities are present in small amounts (EPA, 1990a; Mallipudi et al, 1979; Umetsu et al, 1977).

SOURCES

Acephate is manufactured by the "acetylation of O,O-dimethyl phosphoroamdothiate followed by isomerization" or by combining acetic anhydride with methamidophos (Ashford, 1994; HSDB, 2002).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

Acephate is an organophosphate compound. The following are signs and 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 acephate, but could potentially occur in individual cases.

USES: Acephate is used as an insecticide and registered for use by the US Environmental Protection Agency for a variety of fruit and vegetable crops, in food handling establishments, ornamental plants, and for use in and around the home. It is both a contact and systemic insecticide.

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. Common source of severe poisoning in developing countries.

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. Based on animal studies in rats, acephate is a relatively weak cholinesterase inhibitor when given orally; it was approximately six orders of magnitude weaker.
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 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 acephate. 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

The hallmark of organophosphate poisoning is inhibition of plasma pseudocholinesterase and erythrocyte acetylcholinesterase; acephate inhibits both (Ames et al, 1989; Maroni et al, 1990; Namba, 1972). However, acephate is a relatively weak cholinesterase inhibitor (Hussain et al, 1985).

The earliest manifestations of poisoning are often referable to the central nervous system, with giddiness, uneasiness, restlessness, anxiety and tremulousness. These initial effects are commonly followed by headache, ataxia, drowsiness, difficulty in concentrating, mental confusion and slurred speech (Grob & Garlick, 1950).

A disturbed level of consciousness also occurs, including confusion, inability to sit or stand, and stupor without reaction to speech (Bardin et al, 1987). Seizures may be an early symptom after a substantial exposure; children may be more susceptible to seizures than adults (Joy, 1982; Zwiener & Ginsburg, 1988). In severe poisoning, coma supervenes, rarely followed by generalized seizures; deep tendon reflexes are weak or absent (Grob & Garlick, 1950).
Acute or chronic exposure to organophosphates may impair concentration and produce confusion and drowsiness, reduced cognitive efficiency and slowness of thought, slowed speech, problems in finding words, slurring, intermittent pauses and perseveration (Levin & Rodnitzky, 1976).
So-called Type II neurological effects involve paralysis appearing from 12 to 72 hours after exposure; paralytic signs include inability to lift the neck or sit up, ophthalmoparesis, slow eye movement, facial weakness, difficulty swallowing, limb weakness (mainly proximal), areflexia, respiratory paralysis and death (Wadia et al, 1987).
Delayed neurotoxicity, an apparently rare complication, appears 6 to 21 days after acute exposure. Initial flaccidity, arm and leg weakness, and a shuffling gait are followed by spasticity, hypertonicity, hyperreflexia, clonus and abnormal reflexes; quadriplegia may occur (Bingham et al, 2001; Cherniack, 1988; Wadia et al, 1987). Severe cases progress to complete paralysis, impaired respiration and death (Cavanagh, 1963; Johnson, 1975). Recovery requires weeks to months, and may never be complete (Done, 1979).

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).

Chest tightness, dyspnea, tachypnea, increased bronchial secretions, bronchospasm, rhonchi or crepitations, and acute pulmonary edema can occur in severe organophosphate poisonings (Bardin et al, 1987; Chhabra & Sepaha, 1970; Hayes, 1965). Asthma may occur after the inhalation of nontoxic amounts of some organophosphates in sensitive patients with pre-existing asthma (Bryant, 1985)
Aspiration of commercial organophosphate preparations that contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986).

Bradycardia and hypotension occur after moderate to severe poisoning (Bardin et al, 1987; Ganendran, 1974). However, tachycardia is also common (Zweiner & Ginsburg, 1988). Moreover, hypertension can occur as a nicotinic effect of organophosphate poisoning (Lund & Monteagudo, 1986). Cardiac arrhythmias and conduction defects have been reported in patients with severe organophosphate poisoning (Wren et al, 1981; Kiss & Fazekas, 1982; Chhabra & Sepaha, 1970).

Nausea, vomiting, diarrhea, abdominal cramps and hypersalivation are common muscarinic signs of organophosphate poisoning (Bardin et al, 1987). Fecal incontinence occurs in severe poisoning (Hayes, 1965). Acute pancreatitis has been reported after exposure to some organophosphates; ileus may be the only symptom of pancreatitis in these cases (Hsiao et al, 1996) Lankisch et al, 1990).

Intense miosis (a muscarinic sign) is typical manifestation but is not invariably present; severely poisoned individuals may demonstrate mydriasis (Dixon, 1957). Lacrimation and blurred vision commonly occur; blurred vision may persist for several months (Milby, 1971; Whorton & Obrinsky, 1983). Photophobia, sometimes persisting for several months, has occurred after occupational exposure (Whorton & Obrinsky, 1983; Midtling et al, 1985).

Profuse sweating may occur as one of the muscarinic signs of organophosphate poisoning (Bardin et al, 1987; Ganendran, 1974). Pallor is also sometimes noted (Done, 1979). Muscle weakness, fatigability and fasciculations occur commonly; muscle paralysis occasionally supervenes (Bardin et al, 1987; Done, 1979). Involuntary urination occurs in the more severe poisonings; urinary frequency may also be evident (Done, 1979).

Metabolic acidosis has occurred in several cases of severe poisoning (Hui, 1983; Meller et al, 1981; Moore & James, 1981). Hyperglycemia and glycosuria (without ketosis) may also be present in severe poisoning (Namba, 1972).

Some signs and symptoms of acute organophosphate poisoning can persist for days to months, based on experience with parathion. These include fatigue, ocular symptoms, EEG abnormalities, gastrointestinal complaints, excessive dreams, and intolerance to exposure to organophosphates (ILO, 1983).

Delayed effects may be most pronounced with highly lipid-soluble organophosphates, such as fenthion, or the phosphorothioates, such as chlorpyrifos. After an initial period of apparent recovery, clinical effects may reoccur for up to several weeks after an acute exposure (Minton & Murray, 1988).

Children may have different signs and symptoms of organophosphate poisoning than adults. The chief signs and symptoms of organophosphate poisoning in children are central nervous system depression, stupor, flaccidity, dyspnea and coma. Other classical signs of organophosphate poisoning were not seen frequently in one study of organophosphate-poisoned children (Sofer et al, 1989).

CHRONIC CLINICAL EFFECTS

In general, chronic organophosphate exposure can lead to cumulative depression of cholinesterase levels until a critical lack of activity causes signs and symptoms of organophosphate poisoning to appear, in a pattern similar to that of acute poisoning (Coye et al, 1986).

Psychosis and a variety of other personality and behavioral disorders have been described after exposure to organophosphates; these problems are more common with chronic exposure (Dille & Smith, 1964; Gershon & Shaw, 1961; Conyers & Goldsmith, 1971; Joubert & Joubert, 1988). Organophosphates may exacerbate psychotic symptoms in people with pre-existing schizophrenic tendencies; it is not evident if these symptoms can be induced by organophosphates in the absence of pre-existing abnormality (Levin & Rodnitzky, 1976).

Impaired memory is a principal central nervous system 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).

In a comprehensive review of the literature regarding the neurological sequelae of organophosphate poisoning, the UK Department of Health, Committee on Toxicity of Chemical in Food, Consumer Products, and the Environment, Working Group on Organophosphates, concluded as follows (Anon, 1999):

"The balance of evidence supports the view that neuropsychological abnormalities can occur as a long-term complication of acute (organophosphate) poisoning, particularly if the poisoning is severe. Such abnormalities have been most evident in neuropsychological tests involving sustained attention and speeded flexible cognitive processing. Current evidence suggests that long-term memory is not affected."
Delayed peripheral neuropathy is recognized as a known complication of organophosphate poisoning. Moreover, organophosphates that do not inhibit the neurotoxic esterase can also give rise to sequelae, although these are usually subclinical and recognized only with neurodiagnostic testing.
"The limited evidence available does not allow any firm conclusions to be drawn regarding the risk of developing psychiatric illness in the long term as a consequence of acute poisoning."
The current evidence is not sufficient to support the occurrence of neuropsychological abnormalities, peripheral neuropathy or psychiatric illness after prolonged, low-level exposure to organophosphates.

-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

ADULT

Insufficient data are available to accurately determine potential risk to humans (EPA, 1990).
Acephate is considered a moderately toxic organophosphate insecticide (Lewis, 1998; Morgan, 1993).
The occurrence of poisoning is partially dependent on the rate of absorption through inhalation, skin penetration and/or ingestion (Morgan, 1993).

MAXIMUM TOLERATED EXPOSURE

SUMMARY

The World Health Organization (WHO) has classified acephate, technical grade, as pesticide class III (slightly hazardous) (World Health Organization, 2006).

ANIMAL DATA

Acephate has a relatively low toxicity to laboratory animals when they are exposed through oral, inhalation, and dermal routes (EPA, 1990).
The no-effect dietary level for rats and dogs was 10 ppm in a 90-day study (Clayton & Clayton, 1993; HSDB , 2002).
Rats and dogs exposed to 100 ppm chronically over a two-year period showed no gross or histologic changes except for slight growth depression in the rats. Cholinesterase levels were slightly depressed in the dogs at 100 ppm, but the rats experienced slight to moderate cholinesterase inhibition at 30 ppm. Acephate proved to be non-mutagenic, non-carcinogenic and non-teratogenic in this study (Clayton & Clayton, 1993; Hartley & Kidd, 1990; HSDB , 2002).
Rats were given 1 or 10 mg/kg/day for 15 weeks by intubation. Brain cholinesterase was not affected at either dose. Rats given 1 mg/kg/day did not show a decrease in plasma or erythrocyte cholinesterase, whereas those given 10 mg/kg/day did (Singh & Drewes, 1987).
Mice given 25 ppm acephate for 5 days showed 22 percent inhibition of brain acetylcholinesterase. A dose of 100 ppm produced 42 percent inhibition, and 400 ppm produced 57 percent inhibition (Rattner & Michael, 1985).
A chronic diet of acephate at 0.25 mg/kg to rats was the lowest effect level based on the RBC, brain, and inhibited cholinesterase activity in plasma (EPA, 1990).
Acephate that had been stored for 3 to 6 months was less toxic to mice than fresh acephate (Umetsu et al, 1977).

Carcinogenicity Ratings for CAS30560-19-1 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
EPA (U.S. Environmental Protection Agency, 2011): C ; Listed as: Acephate

C : Possible human carcinogen.

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
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 CAS30560-19-1 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor: 8.7x10(-3) per mg/kg-day
RfD: 4x10(-3) mg/kg-day

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk: 2.5x10(-4) per mg/L

TOXICITY VALUES

Clayton & Clayton, 1993 HSDB, 2002 Lewis, 2000 Rattner & Hoffman, 1984 RTECS, 2002 Zinkl et al, 1981
- LC50- (INHALATION)RAT:
- LCLo- (INHALATION)MOUSE:
- LD50- (ORAL)CHICKEN:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)RABBIT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LDLo- (ORAL)DOG:
- TDLo- (INTRAPERITONEAL)MOUSE:
- TDLo- (ORAL)MOUSE:
- TDLo- (ORAL)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS30560-19-1 (American Conference of Governmental Industrial Hygienists, 2010):

Not Listed

AIHA WEEL Values for CAS30560-19-1 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS30560-19-1 (National Institute for Occupational Safety and Health, 2007):

Not Listed

OSHA PEL Values for CAS30560-19-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS30560-19-1 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS30560-19-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS30560-19-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS30560-19-1 (U.S. Environmental Protection Agency, 2010b):

Not Listed
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 CAS30560-19-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS30560-19-1 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Acephate (Acetylphosphoramidothioic acid O,S-dimethyl ester)
Effective Date for Reporting Under 40 CFR 372.30: 1/1/95
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS30560-19-1 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS30560-19-1 (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 CAS30560-19-1 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

HANDLING

Acephate is a relatively stable, non-corrosive material (Clayton & Clayton, 1993; Hartley & Kidd, 1990).

Solid and liquid organophosphorus pesticides may be transported in a molten form (HSDB , 2001).

STORAGE

CONTAINER

Keep container closed when not in use (HSDB , 2001).
Leak-proof containers must be labeled, indicating the degree of toxicity, how to use the chemical, and precautions to take during application (HSDB , 2001).

ROOM/CABINET RECOMMENDATIONS

Store acephate in a cool, dry area (Clayton & Clayton, 1993; HSDB , 2001).
Do not transport, or store acephate beside, or above food items (HSDB , 2001).
Storage areas should be fitted with secure locks (HSDB , 2001).
Floors should be impervious and kept clear. If it is necessary to repackage, adequate lighting should be available (HSDB , 2001).

-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 chemical clothing when working in the vicinity of spills, leaks, or when fighting fires (AAR, 2000).

Structural firefighter's protective clothing is ineffective for spill incidents (HSDB , 2001).
Overalls of polyvinyl chloride, or a tight material are recommended (HSDB , 2001).
In addition to standard chemical protective garments, signalmen for aerial dusting should also wear a hat and cape made of polyvinyl chloride or a water-repellant material (HSDB , 2001).
Wear rubber or neoprene gloves, and rubber boots (EPA, 1975a; Ford, 1989; HSDB , 2001).

DECONTAMINATION:

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

Contaminated clothing should be segregated and soaked in a calcium carbonate solution for several hours before washing. Repeated laundering may not remove organophosphate from clothing. Any clothing that can not be decontaminated, should be discarded as hazardous waste (Clifford & Nies, 1989; HSDB , 2001).

EYE/FACE PROTECTION

Goggles are recommended for eye protection (HSDB , 2001).

RESPIRATORY PROTECTION

Wear a gas mask, self-contained positive pressure breathing apparatus, or a respirator with an activated-carbon gas filter cartridge when working in the vicinity of spills, leaks, or when fighting fires (AAR, 2000; HSDB , 2001).

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 30560-19-1.

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.
Organophosphorus pesticides do not readily ignite, but it is combustible adn considered highly flammable, depending on the carriet used to mix with the pesticide (AAR, 2000; HSDB , 2001).
Some liquid organophosphorus pesticides have a low flash point (HSDB , 2001).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS30560-19-1 (NFPA, 2002):

Not Listed

INITIATING OR CONTRIBUTING PROPERTIES

Solid organophosphorus pesticides consist of two or more solid materials, or liquid absorded in a dry carrier. Depending on the carrier used, the mixture may, or may not be water-soluble or combustible (AAR, 2000).
Flammable liquid organophosphorus pesticides are produced from a liquid, or solid that has been dissolved in a liquid carrier that is emulsifiable in water. The flash point is below 73 degrees F (AAR, 2000).
Vapors may form explosive mixtures with air (HSDB , 2001).
Water spray can knock down vapors, but may not prevent ignition in closed areas (AAR, 2000; HSDB , 2001).

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 CAS30560-19-1 (NFPA, 2002):

Not Listed

Since a solid, organophosphorus pesticide does not burn, or burns with difficulty, choose an extinguishing agent suitable for the type of surrounding fire (AAR, 2000).

Water may be used in flooding quantities as fog; however, solid streams of water may be ineffective in putting the fire out except in cases when the fire is from a solid organophosphorus pesticide (AAR, 2000).

Alcohol-resistant foams, carbon dioxide, and dry chemicals are recommended for small liquid organophosphorus pesticide fires (AAR, 2000; HSDB , 2001).

Fog, water spray (do not use straight streams), and alcohol-resistant foam are appropriate extinguishing agents for large fires (HSDB , 2001).

COMBUSTION TOXICITY

When heated to decomposition, acephate releases toxic fumes of oxides of nitrogen, phosphorus, and sulfur (Lewis, 2000).

EXPLOSION HAZARD

Heat from fires may cause containers to explode (HSDB , 2001).

DUST/VAPOR HAZARD

Avoid beathing the dust or fumes from the burning material. When heated to decomposition, acephate releases toxic fumes of oxides of nitrogen, phosphorus, and sulfur (AAR, 2000; HSDB , 2001; Lewis, 2000).

Organophosphorus vapors can cause dizziness and suffocation (HSDB , 2001).

Water spray can knock down vapors, but may not prevent ignition in closed areas (AAR, 2000; HSDB , 2001).

REACTIVITY HAZARD

Oxides of nitrogen, phosphorus, and sulfur are produced when acephate is heated to decomposition (Lewis, 2000).

Vapors of organophosphorus pesticides may form explosive mixtures with air (HSDB , 2002).

The primary hazard is the flammability of the carrier mixed with liquid organophosphorus pesticides (HSDB , 2002).

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 CAS30560-19-1 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS30560-19-1 (U.S. Department of Energy, Office of Emergency Management, 2010):

Not Listed

AEGL Values for CAS30560-19-1 (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):

Not Listed

NIOSH IDLH Values for CAS30560-19-1 (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.

SMALL LEAK/SPILL

All personnel handling the spill must wear encapsulating, vapor, and chemical protective clothing. (AAR, 2000; HSDB , 2001).
Isolate and ventilate the area. Eliminate ignition sources, and get fire-fighting equipment ready (Ford, 1989; HSDB , 2001).
If packages are damaged or leaking, contact the Pesticide Safety Team Network at 800-424-9300 (HSDB , 2001).
Absorb with Zorb-All(R), sweeping compound, sawdust, dry earth or sand, or any other non-combustible material. Transfer absorbed or dry material to containers, taking precautions to keep water out of the containers (EPA, 1975a; Ford, 1989; HSDB , 2001).
Scrub the spilled area with a concentrated detergent such as TIDE(R), ALL(R), or a similar product. Re-absorb scrubbing liquid and dispose as above. Several washes may be required for decontamination (EPA, 1978; Ford, 1989).

LARGE LEAK/SPILL

All personnel handling the spill must wear encapsulating, vapor, and chemical protective clothing (AAR, 2000; HSDB , 2001).
Isolate and ventilate the area. Eliminate ignition sources, and get fire-fighting equipment ready (Ford, 1989; HSDB , 2001).
If packages are damaged or leaking, contact the Pesticide Safety Team Network at 800-424-9300 (HSDB , 2001).
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. The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1975; EPA, 1978).
Land spills can be treated 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), calcium carbonate (limestone), fly ash, commercial sorbents, or cement powder (AAR, 2000; EPA, 1975a).
Contain the liquid spill using a plastic sheet, if necessary. Absorb with Zorb-All(R), sweeping compound, sawdust, dry earth or sand, or any other non-combustible material. Transfer absorbed or dry material to containers, taking precautions to keep water out of the containers (EPA, 1975a; Ford, 1989; HSDB , 2001).
Scrub the spilled area with concentrated detergent such as TIDE(R) , ALL(R), or similar product. Re-absorb scrubbing liquid and dispose as above (Ford, 1989). Several washes may be required for decontamination (EPA, 1978).
Water spray may be used to reduce or knock down vapors (AAR, 2000).

WASTE TREATMENT OPTIONS

CHEMICAL TREATMENT

Combustible containers from organic or metallo-organic pesticides should be incinerated in appropriate facilities, or placed in specific landfills. Exceptions include organic mercury, cadmium, lead, or arsenic compounds (HSDB , 2001).
Non-combustible containers from organic or metallo-organic pesticides must be triple rinsed. If the containers are in good condition, they may be returned to the manufacturer for reuse, if it is permissible under the US DOT regulations. Containers that can not be reused should be punctured, and transported to a scrap metal facility for recycling, disposal, or burial in an appropriate landfill (HSDB , 2001).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Artificial Sources: Acephate's use as an insecticide releases the compound directly to the soil environment through applications (usually spraying) to protect crops and seeds(1). HSDB 2003 Aceohate has been used as an insecticide, and therefore has been released to the environment through typical applications (HSDB, 2003).

ENVIRONMENTAL FATE AND KINETICS

In an ambient atmosphere, acephate can exist in both particulate and vapor-phases (HSDB , 2001).
It rapidly degrades in the vapor-phase when it reacts to photochemically produced hydroxyl radicals. The estimated half-life is 6 hours (HSDB , 2001).
Acephate can be physically removed from the atmosphere as the particles settle (HSDB , 2001).
Acephate's water-solubility properties make it possible for the chemical to be physically removed by rainfall or dissolved in clouds (HSDB , 2001).

WATER

SURFACE WATER
- Degradation studies show acephate degrades by an aquatic hydrolysis, or microbial process (HSDB , 2001).
- Acephate is relatively stable to hydrolysis, but the hydrolysis rate increases as the pH level increases (Hartley & Kidd, 1990; HSDB , 2001).
- Some studies have shown that acephate degrades more rapidly in non-sterile creek water as compared to sterilized creek water (HSDB , 2001).
- Acephate degrades more rapidly in alkaline water than in acidic water (HSDB , 2001).
- Its leaching properties make ground water contamination a potential hazard (Hartley & Kidd, 1990).
- Direct photolysis, bioconcentration, adsorption to sediment, and aquatic volatilization are not considered to be important environmental fate processes (HSDB , 2001).
- During a hydrolysis study, there was not a significant volatilization measurement from water to air (HSDB , 2001).

SOIL

TERRESTRIAL
- Acephate degrades by aquatic hydrolysis, or a microbial process (HSDB , 2001).
- Acephate dissipates rapidly in soil, but persists longer in anaerobic conditions (Hartley & Kidd, 1990; HSDB , 2001).
- Most soils have a half-life of 0.5-4 days. Organic muck soils have half-lives of 6-13 days (HSDB , 2001).
- Acephate is mobile in most soils except when the chemical has aged, and then it is virtually immobile in sandy loam soil (Hartly & Kidd, 1990).
- Alkaline soils degrade more rapidly than acidic soils (HSDB , 2001).

OTHER

OTHER
- Acephate has residual systemic activity in plants for 10 to 15 days after application (Clayton & Clayton, 1993; Hartley & Kidd, 1990).
- Acephate was taken up by the cones of white spruce and partially converted to its principal metabolite, methamidophos. Both chemicals persisted longer in water than in soils, and acephate was more resistant to microbial attack than methamidophos (Sundaram, 1993).

ABIOTIC DEGRADATION

Over a 20 day period, the hydrolysis of acephate was measured in buffered distilled water and findings showed as the pH and temperature increased, the hydrolysis rate increased.At 20 degrees C, the percentage of initial acephate that hydrolyzed ranged from 2.4 percent at pH 4.0 to 22.1 percent at pH 8.2. At 30 degrees C, 4.5 percent acephate hydrolyzed at pH 4.0, and 82.2 percent hydrolyzed at pH 8.2 (HSDB , 2001).

By-products of acephate hydrolysis at 37 degrees C are O,S-dimethyl phosphorothiolate, a major hydrolysis product; methamidophos; and O-methylacetyl phosphoramidothiolate (HSDB , 2001).

Acephate is not altered by photodegradation (HSDB , 2001).

"The rate constant for the vapor-phase reaction of acephate with photochemically produced hydroxyl radicals has been estimated to be 6.8X10(-11) cm(3)/molecule-sec at 25 degrees C which corresponds to an atmospheric half-life of about 6 hours at an atmospheric concentration of 5X10(+5) hydroxyl radicals per cm(3)" (HSDB , 2001).

BIODEGRADATION

Acephate can degrade in the soil and water through microbial degradation (HSDB , 2001).

BIOACCUMULATION

FISH

It is not expected to bioconcentrate in aquatic organisms. A study showed acephate did not bioaccumulate in clams, crabs, daphnia, diatoms, fish, and snails (EPA; 1990; (HSDB , 2001).

PLANTS

AQUATIC
- In an ecosystem study, acephate did not bioaccumulate in algae (HSDB , 2001).
- In an ecosystem study, acephate did not bioaccumulate in elodea, or carrot plants (EPA, 1990; HSDB , 2001).

MAMMALS

Animal metabolism data available reveals a large percentage of the chemical is rapidly eliminated from the body through the urine (EPA, 1990).

BIOCONCENTRATION FACTOR

The bioconcentration factor is estimated to be 0.1-0.3 (HSDB , 2001).

ENVIRONMENTAL TOXICITY

LC50 - (WATER) GRAMMARUS PSEUDOLIMNAEUS, mature: >50 mcg/L for 96H (at 12 degrees C) (HSDB , 2001)

LC50 - (WATER) RAINBOW TROUT (salmo gairdneri): 1100 mcg/L for 96H (at 10 degrees C) (HSDB , 2001)

LC50 - (WATER) FATHEAD MINNOW (pimephales promelas): >1000 mcg/L for 96H (at 20 degrees C) (HSDB , 2001)

LC50 - (WATER) BLUEGILL (lepomis machrochirus): >1000 mcg/L for 96H (at 20 degrees C) (HSDB , 2001)

LC50 - (WATER) COTURNIX: 3275 ppm for 5 D (HSDB , 2001)

LC50 - (WATER) BLUEGILL SUNFISH: 2050 mg/L for 96H (Hartley & Kidd, 1990)

LC50 - (WATER) RAINBOW TROUT: > 1000 mg/L for 96H (Hartley & Kidd, 1990)

LC50 - (WATER) CHANNEL CATFISH: 2230 mg/L for 96H (Hartley & Kidd, 1990)

LC50 - (WATER) GOLDFISH: 9550 mg/L for 96H (Hartley & Kidd, 1990)

Acephate is practically nontoxic to freshwater fish and freshwater invertebrates, moderately toxic to avian species, and highly toxic to honey bees (EPA, 1990).

The acephate bait was shown to be an economical and safe technique for destroying bee swarms (Williams et al, 1992).

Acephate bait in wax paper envelopes in concentrations of 150, 500, 1,500 and 4,500 ppm eliminated bee swarms, and most queens of Africanized local hives within one day. Worker bee mortality in traps ranged from 18% (150 ppm) to 73% (4,500 ppm) of the original population (Williams et al, 1992).

Symptoms of acute oral intoxication of mallards are: ataxia, jerkiness, imbalance, mild spasms in legs and feet, intermittent tremors, immobility, and spread wings (Lewis, 1998).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

183.16

DESCRIPTION/PHYSICAL STATE

Acephate, technical grade, is water-soluble, colorless crystals, or it can also be found as a white crystalline solid or powder. The odor is described as a strong, pungent, mercaptan-type or rotten-cabbage smell (Clayton & Clayton, 1993; Hartley & Kidd, 1990; HSDB , 2002; Lewis, 1998).

VAPOR PRESSURE

1.7x10(-6) mmHg (at 24 degrees C) (Clayton & Clayton, 1993)

1.7x10(-6) mmHg (at 25 degrees C) (HSDB , 2001)

0.226 mPa (at 24 degrees C) (Hartley & Kidd, 1990)

SPECIFIC GRAVITY

TEMPERATURE AND/OR PRESSURE NOT LISTED

1.35 (Clayton & Clayton, 1993; HSDB , 2002)

FREEZING/MELTING POINT

MELTING POINT

82-89 degrees C (97% technical) (EPA, 1990; Sine, 1987)
82-89 degrees C (technical grade 80-90% pure) (HSDB, 2001)
64-68 degrees C (impure) (Budavari, 2000)
72-80 degrees C (Lewis, 1998)
65 degrees C (Lewis, 1997)
93 degrees C (Hartley & Kidd, 1990a)
86.9-91 degrees C (Clayton & Clayton, 1993a)

FLASH POINT

below 73 degrees F - organophosphorus pesticides, liquid (AAR, 2000)

SOLUBILITY

IN WATER

790 g/L (at 20 degrees C) (Hartley & Kidd, 1990; Sine, 1987)
650 g/L (technical grade 80-90%; room temperature) (HSDB , 2002)
818,000 mg/L (at 25 degrees C) (HSDB , 2002)
High solubility (65%) (EPA, 1990)

IN ORGANIC SOLVENTS

HEXANE: 0.1 g/L (at 20 degrees C) (Hartley & Kidd, 1990)
BENZENE: 16 g/L (at 20 degrees C) (Hartley & Kidd, 1990)
KEROSENE: <1% (Clayton & Clayton, 1993)
XYLENE: < 10% (Clayton & Clayton, 1993)

OTHER

AROMATIC SOLVENTS: < 50 g/L (technical grade 80-90%; room temperature) (HSDB , 2002)
ACETONE:151 g/L (at 20 degrees C) (Hartley & Kidd, 1990)
ACETONE: >100 g/L (technical grade 80-90%; room temperature) (HSDB , 2002)
ETHANOL: > 100 g/L (at 20 degrees C) (Hartley & Kidd, 1990)
ETHANOL: > 100 g/L (technical grade 80-90%; room temperature) (HSDB , 2002)
ETHYL ACETATE: 35 g/L (at 20 degrees C) (Hartley & Kidd, 1990)

OCTANOL/WATER PARTITION COEFFICIENT

log Kow= -0.85 (measured) (HSDB , 2001)

HENRY'S CONSTANT

5.0 x 10(-13) atm-cu m/mole (estimated) (HSDB , 2001)

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

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Product Information: ATROPEN(R) IM injection, atropine IM injection. Meridian Medical Technologies, Inc (per manufacturer), Columbia, MD, 2005.

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Product Information: DUONEB(R) inhalation solution, ipratropium bromide albuterol sulfate inhalation solution. Dey, Napa, CA, 2005.

Product Information: DuoDote(R) intramuscular injection solution, atropine and pralidoxime chloride intramuscular injection solution. Meridian Medical Technologies(TM), Inc. (per Manufacturer), Columbia, MD, 2011.

Product Information: Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, isoproterenol HCl intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection. Hospira, Inc. (per FDA), Lake Forest, IL, 2013.

Product Information: PRALIDOXIME CHLORIDE intramuscular injection, pralidoxime chloride intramuscular injection. Meridian Medical Technologies, Inc. (per DailyMed), Columbia, MD, 2003.

Product Information: PROTOPAM(R) CHLORIDE injection, pralidoxime chloride injection. Baxter Healthcare Corporation, Deerfield, IL, 2006.

Product Information: PROTOPAM(R) Chloride injection, pralidoxime chloride injection. Baxter Healthcare Corporation, Deerfield, IL, 2010.

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Product Information: diazepam autoinjector IM injection solution, diazepam autoinjector IM injection solution. Meridian Medical Technologies Inc, Columbia, MD, 2005.

Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.

Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.

Product Information: magnesium sulfate heptahydrate IV, IM injection, solution, magnesium sulfate heptahydrate IV, IM injection, solution. Hospira, Inc. (per DailyMed), Lake Forest, IL, 2009.

Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.

Product Information: pralidoxime chloride intramuscular auto-imjector solution, pralidoxime chloride intramuscular auto-imjector solution. Meridian Medical Technologies, Inc. (per manufacturer), Columbia, MD, 2003.

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