DEMETON-S-METHYL

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

MOLECULAR FORMULA

C6-H15-O3-P-S2

ERG GUIDE NUMBER

152-SUBSTANCES - TOXIC (COMBUSTIBLE)

SYNONYM REFERENCE

(RTECS , 1999)

USES/FORMS/SOURCES

USES

Demeton-S-methyl is used as an insecticide (Morgan, 1989; EPA, 1985).

FORMS

Demeton-S-methyl is an organophosphate compound. It is a colorless to pale yellow oily liquid with an unpleasant, garlic-like odor (HSDB, 2003). It is soluble in polar organic solvents and sparingly soluble in water (HSDB, 2003).

SOURCES

Demeton-S-methyl is made by the reaction of beta-hydroxyethyl sulfide with O,O-dimethyl hydrogen phosphorothioate; by alkylation of O,O-dimethyl-thiophosphoric acid with 2-(ethylmercapto)-ethyl chloride; or by a process involving alcohol chlorination, hydrolysis, and dehydrochlorination using 2-ethylthioethanol and O,O-dimethyl phosphorochlorothioate (HSDB, 2003).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

The following are symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for demeton-S-methyl, but could potentially occur in individual cases.

USES: Demeton-S-methyl, an organophosphate compound, formerly used as an insecticide is no longer available for use in the United States. It may be available for use in other countries.

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. Organophosphates are a 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.
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 inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, 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 demeton-S-methyl. 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 (i.e., secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

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

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Contact with molten substance may cause severe burns to skin and eyes.
Avoid any skin contact.
Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases.
Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

ACUTE CLINICAL EFFECTS

SUMMARY

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. Organophosphates are a common source of severe poisoning in developing countries.
MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to development of delayed peripheral neuropathy. Manifestations can include inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, 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 demeton-S-methyl. 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 (i.e., secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

ACID-BASE

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

CARDIOVASCULAR

HYPOTENSIVE EPISODE: Bradycardia and hypotension occur following moderate to severe poisoning (Ganendran, 1974). Hypotension (systolic blood pressure less than 90 mmHg) occurred in 20% of patients in one study.
CONDUCTION DISORDER OF THE HEART: Cardiac dysrhythmias and conduction defects have been reported in patients with severe organophosphate poisoning (Wren et al, 1981; Kiss & Fazekas, 1982; Chhabra & Sepaha, 1970).

ECG abnormalities may include sinus bradycardia, A-V dissociation, idioventricular rhythms, multiform premature ventricular extrasystoles, polymorphic ventricular tachycardia, prolongation of the PR, QRS, and QT intervals, "Torsade de Pointes" polymorphous ventricular dysrhythmias (Brill et al, 1984; Ludomirsky et al, 1982), and tachycardia (Zwiener & Ginsburg, 1988).

DERMATOLOGIC

DERMATITIS: Dermal sensitization has occurred with some organophosphates following skin exposure (Milby et al, 1964).

ENDOCRINE

HYPERGLYCEMIA: In severe poisoning hyperglycemia and glycosuria (without ketosis) are present (Namba, 1972).

GASTROINTESTINAL

NAUSEA, VOMITING and DIARRHEA: Nausea, vomiting, diarrhea, abdominal cramps and hypersalivation are common muscarinic signs of organophosphate poisoning (Bardin et al, 1987).
INCONTINENCE OF FECES: Fecal incontinence occurs in severe poisoning (Hayes, 1965).
PANCREATITIS: Acute pancreatitis has been reported following the ingestion of parathion, malathion, difonate, coumafos, diazanon, and mevinphos and also following dermal exposure to dimethoate (Hsiao et al, 1996).

GENITOURINARY

URINARY INCONTINENCE: Incontinence and frequency may be observed in cases of severe toxicity (Done, 1979).

HEENT

EYES

MIOSIS: Intense miosis is a typical manifestation of organophosphate poisoning; however, pupils may be normal or dilated (Bardin et al, 1987) Morgan, 1993).
MYDRIASIS: Severely poisoned individuals may exhibit mydriasis (dilatation of the pupils) (Dixon, 1957).
BLURRED VISION: Lacrimation and blurred vision are commonly present; blurred vision may persist for several months (Milby, 1971; Whorton & Obrinsky, 1983).
DECREASED VISUAL ACUITY: Fenthion has been reported to produce macular lesions in chronically exposed patients, some resulting in compromised vision (Misra et al, 1985).
PHOTOPHOBIA: Sometimes persisting for several months, photophobia has occurred in persons occupationally exposed to mevinphos and phosphamidon residues on leaves of agricultural crops (Whorton & Obrinsky, 1983; Midtling et al, 1985).

THROAT

SALIVATION: Greater than 50% of patients in one study experienced excessive salivation (Bardin et al, 1987).

HEMATOLOGIC

DEFICIENCY OF CHOLINESTERASE: The hallmark of organophosphate poisoning is the inhibition of plasma pseudocholinesterase and/or erythrocyte acetylcholinesterase (Namba, 1972).
COAGULATION DISORDER: Alterations in prothrombin time (shortened or prolonged), and increased or decreased factor VII levels have been described, but clinically significant bleeding or hypercoagulability are rare (Von Kaulla & Holmes, 1961).

MUSCULOSKELETAL

MUSCLE WEAKNESS: Muscle weakness, fatigability and fasciculations occur commonly (Bardin et al, 1987).

NEUROLOGIC

COMA: In severe poisoning coma is common (Grob & Garlick, 1950; Sittig, 1991; Grob & Garlick, 1950a).
PARALYSIS: So-called Type II neurological effects involve paralysis appearing from 12 to 72 hours after exposure; this paralysis is unresponsive to atropine and may be due to excess acetylcholine at nicotinic receptors (Wadia et al, 1987). Paralytic signs include inability to lift the neck or sit up, ophthalmoparesis, slow eye movement, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis and death (Wadia et al, 1987).
SEIZURE: Seizures may be an early symptom after a significant exposure (Joy, 1982). Children may be more susceptible to seizures than adults (Zwiener & Ginsburg, 1988).
ANXIETY: The earliest manifestations of organophosphate poisoning often include central nervous system effects. Symptoms include giddiness, uneasiness, restlessness, anxiety, and tremulousness (Grob & Garlick, 1950).
STUPOR: Confusion and stupor have been observed in severe poisonings (Grob & Garlick, 1950a).
ATAXIA: Initial central nervous system effects are commonly followed by headache, ataxia, drowsiness difficulty in concentrating, mental confusion, and slurred speech (Grob & Garlick, 1950a).
DISTURBANCE IN THINKING: Persons with other signs of organophosphate poisoning have shown reduced cognitive efficiency and slowness of thought related to the degree of cholinesterase inhibition (Levin & Rodnitzky, 1976).

PSYCHIATRIC

PSYCHOTIC DISORDER: Psychosis and a variety of other personality and behavioral disorders have been described from exposure to organophosphates (Dille & Smith, 1964; Conyers & Goldsmith, 1971; Joubert & Joubert, 1988).
AMNESIA: Impaired memory is a major CNS effect of organophosphate exposure and may occur in the absence of other overt clinical signs; it has been found in workers chronically exposed to organophosphates (Levin & Rodnitzky, 1976).
DISTURBANCE IN SPEECH: Slowed speech, problems in finding words, slurring, intermittent pauses, and perseveration have been seen in persons who have other clinical signs of organophosphate poisoning (Levin & Rodnitzky, 1976).
DEPRESSIVE DISORDER: Depression, correlated with the severity of cholinesterase inhibition, has occurred in cases of acute organophosphate poisoning; this finding is consistent with the theory of affective disorders being the result of cholinergic predominance in the central nervous system (Levin & Rodnitzky, 1976).

RESPIRATORY

RESPIRATORY FAILURE: Acute respiratory insufficiency, due to any combination of depression of the respiratory center, respiratory paralysis, bronchospasm or increased bronchial secretions, is the main cause of death in many acute organophosphate poisonings (Lerman & Gutman, 1988; Anon, 1984).
ACUTE LUNG INJURY: Noncardiogenic pulmonary edema is a manifestation of severe organophosphate poisoning (Chhabra & Sepaha, 1970).
DYSPNEA: Increased bronchial secretions, bronchospasm, chest tightness, heartburn, and dyspnea occur in severe and moderately severe organophosphate poisonings (Hayes, 1965).

CHRONIC CLINICAL EFFECTS

At the time of this review, no studies were found on chronic demeton-S-methyl exposure in humans or experimental animals.

In general, chronic exposure to organophosphates can lead to cumulative depression of cholinesterase levels until a critical lack of activity causes symptoms of organophosphate poisoning to appear, in a pattern similar to that of acute poisoning (Coye et al, 1986). The level of chronic exposure which can be tolerated depends on the rate of uptake and degradation of the organophosphate in the body in relation to its potency in inhibiting acetylcholinesterase, and the rate of the individual's replenishment of acetylcholinesterase activity.

-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, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a).

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, 1975aa).
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, 1975aa).

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, 1978a).

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, 1975aa).
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, 1978a).
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, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a).

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, 1975aa).
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, 1975aa).

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, 1978a).

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, 1975aa).
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, 1978a).
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

SUMMARY

The actual lethal dose of an organophosphate can vary widely and depends strongly on the route and rate of exposure and on the aggressiveness of the treatment used.

MAXIMUM TOLERATED EXPOSURE

PESTICIDE CLASSIFICATION

The World Health Organization (WHO) has classified demeton-S-methyl, technical grade, as pesticide class 1B (highly hazardous) (World Health Organization, 2006).

PEDIATRIC

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

OCCUPATIONAL

Fifteen workers (13 farm workers, 2 agricultural pilots) developed mild to moderate cholinergic symptoms which lasted from one day to several weeks after dermal and possibly inhalation exposure to demeton-S-methyl (Smith, 1977).
An agricultural pilot developed serious cholinergic poisoning after being drenched with demeton-S-methyl when a spray tank ruptured during an airplane crash (Kipling & Cruickshank, 1985).
Approximately one week after demeton-S-methyl was sprayed on cotton in a region of Egypt, 673 occupational cases, including 3 deaths, were reported (Hayes & Laws, 1991).

CASE REPORTS

Following ingestion of one to two mouthfuls of a 25% demeton-S-methyl solution, a 31-year-old woman developed severe cholinergic poisoning that required 30 days to fully resolve (Barr, 1966).
Fatalities are reported following ingestion of 15 mL demeton-S-methyl in a 65-year-old male who died of pulmonary embolism 4 days after exposure and also following ingestion of between 50 and 500 mg/kg in a patient who died of cardiovascular collapse 83 hours after exposure (HSDB , 1999).

Carcinogenicity Ratings for CAS919-86-8 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Demeton-S-methyl

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

EPA (U.S. Environmental Protection Agency, 2011): Not Listed
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
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 CAS919-86-8 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

References: EPA, 1985 Lewis, 1996 RTECS, 1999
- LC50- (INHALATION)RAT:
- LD50- (INTRAPERITONEAL)GUINEA_PIG:
- LD50- (ORAL)GUINEA_PIG:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (INTRAVENOUS)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LDLo- (INTRAVENOUS)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS919-86-8 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

Demeton-S-methyl

TLV:

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

Notations and Endnotes:

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

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
BEI(A): The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational. Substances identified as Acetylcholinesterase Inhibiting Pesticides are part of this notation.
IFV: Inhalable fraction and vapor.
SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.

TLV Basis - Critical Effect(s): Cholinesterase inhib
Molecular Weight: 230.3

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

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

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

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

AIHA WEEL Values for CAS919-86-8 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS919-86-8 (National Institute for Occupational Safety and Health, 2007):

Not Listed

OSHA PEL Values for CAS919-86-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS919-86-8 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS919-86-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS919-86-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS919-86-8 (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 CAS919-86-8 (U.S. Environmental Protection Agency, 2010):

Listed as: Demeton-S-Methyl
Reportable Quantity, in pounds: 500

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

Threshold Planning Quantity, in pounds:

500
Amount necessary to be covered by this standard. See 40 CFR 355.30.

Note(s): Not Listed

EPA SARA Title III, Community Right-to-Know for CAS919-86-8 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS919-86-8 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS919-86-8 (EPA, 2005):

Listed as: Phosphorothioic acid, S-[2-(ethylthio)ethyl] O,O-dimethyl ester

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 CAS919-86-8 (NFPA, 2002):

Not Listed

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

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

First responders, emergency medical, and emergency department personnel should take proper precautions (wear rubber gowns, rubber aprons, rubber gloves, etc) when treating patients with organophosphate poisoning to avoid contamination. Emesis containing organophosphates should be placed in closed impervious containers for proper disposal.

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

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

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

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

RESPIRATORY PROTECTION

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

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 919-86-8.

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

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

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

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS919-86-8 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

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

Dry chemical, CO2 or water spray.

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

Water spray, fog or regular foam.
Move containers from fire area if you can do it without risk.
Dike fire control water for later disposal; do not scatter the material.
Use water spray or fog; do not use straight streams.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers.
Cool containers with flooding quantities of water until well after fire is out.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.
For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

NFPA Extinguishing Methods for CAS919-86-8 (NFPA, 2002):

Not Listed

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

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

COMBUSTION TOXICITY

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

DUST/VAPOR HAZARD

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

REACTIVITY HAZARD

When heated to decomposition, demeton-S-methyl releases highly toxic fumes of oxides of phosphorus and sulfur (Lewis, 1996).

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 CAS919-86-8 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS919-86-8 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Demeton-s-methyl
TEEL-0 (units = mg/m3): 0.05
TEEL-1 (units = mg/m3): 0.15
TEEL-2 (units = mg/m3): 5
TEEL-3 (units = mg/m3): 200
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS919-86-8 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS919-86-8 (National Institute for Occupational Safety and Health, 2007):

Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area).
- Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.
- Stop leak if you can do it without risk.
- Prevent entry into waterways, sewers, basements or confined areas.
- Cover with plastic sheet to prevent spreading.
- Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers.
- DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
DECONTAMINATION OF SPILLS
- A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978).
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required.
Water spray may be used to reduce or knock down vapors (AAR, 1987).

SMALL LEAK/SPILL

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

LARGE LEAK/SPILL

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

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

POLLUTION SOURCES

Demeton-S-methyl is released directly to the environment through its application as an insecticide and acaricide (HSDB, 2004; IPCS, 1997).

The main metabolites of demeton-S-methyl, oxydemeton-methyl and demeton-S-methylsulfone, are also commercial pesticides and are similar to demeton-S-methyl in their mechanism of action and toxicological profiles (IPCS, 1997).

Spray drift from arable applications or top fruit, air-assisted applications may result in pollution of local bodies of water, presenting a risk to aquatic organisms (IPCS, 1997).
Demeton-S-methyl does not occur naturally in the environment (IPCS, 1997).

OCCUPATIONAL EXPOSURE

Workers may be exposed to demeton-S-methyl during its manufacture, packaging, mixing, and spraying applications. The most common exposure routes are dermal and inhalation (HSDB, 2004; IPCS, 1997).

GENERAL POPULATION EXPOSURE

The general population is exposed to demeton-S-methyl by ingesting food crops containing residues of the chemical. However, very little information is available on actual dietary exposure levels (HSDB, 2004; IPCS, 1997).

TERRESTRIAL ORGANISMS

Vertebrates are exposed to demeton-S-methyl by grazing on vegetation treated with the chemical and/or consumption of contaminated insects (IPCS, 1997).

ENVIRONMENTAL FATE AND KINETICS

If released to the atmosphere, demeton-S-methyl will exist both in vapor and particulate phases in the ambient air. Modeling based on gas/particle partitioning of semivolatile organic compounds and its vapor pressure of 3.0 x 10(-4) mmHg (at 20 degrees C) indicates this will occur (HSDB, 2004).
- Vapor-phase demeton-S-methyl is degraded through reaction with photochemically-produced hydroxyl radicals, with a rate constant for this reaction estimated at 4.7 x 10(-11) cm(3)/molecule-sec (at 25 degrees C). This corresponds to a reaction half-life of approximately 8 hours (assuming a hydroxyl radical concentration of 5 x 10(5) radicals/cm(3)) (HSDB, 2004).
- Particulate-phase demeton-S-methyl may be removed from the atmosphere by both dry and wet deposition (HSDB, 2004).

WATER

SURFACE WATER
- Demeton-S-methyl is not expected to adsorb to sediment or suspended solids in water, based on its estimated organic carbon-water partition coefficient (Koc) value of 85. An average organic matter-water partition coefficient (Kom) of 18 was measured in pond sediments (HSDB, 2004).
- It may undergo slow hydrolysis (HSDB, 2004).
- The primary degradation reactions are demethylation in acidic media and hydrolysis of the phosphorus-ester bond in basic media (IPCS, 1997).
- Oxidation to the sulfoxide and sulfone may occur (HSDB, 2004).
- Demeton-S-methyl is not expected to volatilize from water surfaces, based on its estimated Henry's Law constant of 2.7 x 10(-8) atm-m(3)/mole (HSDB, 2004).
- Direct photolysis is not expected to occur because demeton-S-methyl does not absorb light at wavelengths of 237 or greater. Irradiation of aquatic solutions of demeton-S-methyl (3.6 - 3.7 mg/L) for 8 hours did not result in photodegradation. However, when solutions of demeton-S-methyl were fortified with humic matter (10 mg/L) and irradiated for 8 hours, a half-live of 8 hours was measured, indicating that sensitized or indirect photolysis may occur (IPCS, 1997).

SOIL

TERRESTRIAL
- An estimated organic carbon-water partition coefficient (Koc) value of 85 indicates that demeton-S-methyl will have high mobility in soil (HSDB, 2004).
- Biodegradation is the major fate process of demeton-S-methyl in soil (IPCS, 1997).
- It may also undergo slow hydrolysis or oxidation to the sulfoxide and sulfone (HSDB, 2004).
- Volatilization of demeton-S-methyl from moist soil and dry soil surfaces is not expected to be significant, based on an estimated Henry's Law constant of 2.7 x 10(-8) atm-m(3)/mole and a measured vapor pressure of 3.0 x 10(-4) mmHg, respectively (HSDB, 2004).

ABIOTIC DEGRADATION

Demeton-S-methyl is not persistent in the environment, and is degraded through a number of mechanisms (IPCS, 1997).

Demeton-S-methyl is degraded in the atmosphere through photooxidation and may be removed by wet and dry deposition (HSDB, 2004).
It is biodegraded in soils, and may also undergo slow hydrolysis or oxidation (IPCS, 1997).
Photolysis is not expected to be a significant degradation process for demeton-S-methyl (IPCS, 1997).

BIODEGRADATION

Biodegradation is the major fate process for demeton-S-methyl in soil (IPCS, 1997).

Reported biodegradation half-lives for demeton-S-methyl vary greatly, ranging from 4 hours to 26 days (estimated) (HSDB, 2004; IPCS, 1997).

Biodegradation of demeton-S-methyl was tested under aerobic conditions with several species of microorganisms (Nocardia, Arthrobacter, Corynebacter, Brevibacterium, Bacillus, Pseudomonas), all of which were able to degrade the compound. After 14 days of incubation, the amount of demeton-S-methyl degraded ranged from 65% (A. roseoparaffineus) to 99% (P. putida) (IPCS, 1997).

Biodegradation half-lives for demeton-S-methyl in two standardized soils, non-sterile and sterile, were approximately 8 hours and 70 hours, respectively (IPCS, 1997).

Based on limited data taken from a soil study, demeton-S-methyl is expected to biodegrade in water (HSDB, 2004).

BIOACCUMULATION

FISH

No data are available on bioaccumulation of demeton-S-methyl in fish. However, the probability of bioaccumulation in fish is expected to be low, based on the log Pow of 1.3 (IPCS, 1997).

BIOCONCENTRATION FACTOR

Demeton-S-methyl is not expected to bioconcentrate in aquatic organisms, based on its estimated bioconcentration factor (BCF) of 4 (calculated using a measured log Kow of 1.02) (HSDB, 2004).

ENVIRONMENTAL TOXICITY

AQUATIC ORGANISMS

VERTEBRATES

FISH

LC50 - CARP (Cyprinus carpio), 6 cm/1.6 g: 40 - 60 mg/L -- 28.1% active ingredient; 18 degrees C (IPCS, 1997)
LC50 - FISH (Cirrhana mrigala), 51 ± 3 mg: 1.45 mg/L -- 20 degrees C (IPCS, 1997)
LC50 - GOLDEN ORFE (Leucuscus idus melamotus), 6.4 ± 0.6 cm/2.5 ± 0.6 g: 23.2 mg/L -- 27.3% active ingredient; 21 ± 2 degrees C (IPCS, 1997)
LC50 - GOLDEN ORFE (Leucuscus idus melamotus), 6.0 ± 7.5 cm/2.5 - 4.2 g: 43 mg/L -- 52.7% active ingredient; 21 degrees C (IPCS, 1997)
LC50 - GOLDFISH (Carassius auratus), 6 cm/1.5 g: 20 - 40 mg/L -- 28.1% active ingredient; 18 degrees C (IPCS, 1997)
LC50 - PEARL ROACH (Scardinius erythrophthalmus), 6 cm/1.3 g: 30 - 40 mg/L -- 18 degrees C (IPCS, 1997)
LC50 - RAINBOW TROUT (Onchorhyncus mykiss), 6.4 ± 1.0 cm/3.0 ± 0.6 g: 0.59 mg/L -- 69.5% active ingredient; 15 ± 2 degrees C (IPCS, 1997)
LC50 - RAINBOW TROUT (Onchorhyncus mykiss), 4.0 - 5.5 cm/1.0 - 1.5 g: 4.5 mg/L -- 52.7% active ingredient; 16 degrees C (IPCS, 1997)
LC50 - RAINBOW TROUT (Onchorhyncus mykiss), 6.9 ± 1.1 cm/3.5 ± 1.6 g: 5.44 mg/L -- 27.3% active ingredient; 15 ± 2 degrees C (IPCS, 1997)

INVERTEBRATES

ALGAE

EC50 - GREEN ALGA (Scenedesmus subspicatus): 8 mg/L for 96H -- for increase of biomass; 97.3% technical purity; (at pH 7.8 - 8.5; 23 degrees C) (IPCS, 1997)
EC50 - GREEN ALGA (Scenedesmus subspicatus): 13 mg/L for 96H -- for increase of biomass; pre-solution xylene; 53.7% active ingredient; (at pH 7.7 - 8.5; 22 degrees C) (IPCS, 1997)
EC50 - GREEN ALGA (Scenedesmus subspicatus): 22 mg/L for 96H -- for affected growth rate; 97.3% technical purity; pH 7.8 - 8.5; 23 degrees C (IPCS, 1997)
EC50 - GREEN ALGA (Scenedesmus subspicatus): 37 mg/L for 96H -- for increase of biomass; EC formulation; 27.3% active ingredient; (at pH 7.6 - 10.4; 23 degrees C) (IPCS, 1997)
EC50 - GREEN ALGA (Scenedesmus subspicatus): 37 mg/L for 96H -- for affected growth rate; pre-solution xylene; 53.7% active ingredient; (at pH 7.7 - 8.5; 22 degrees C) (IPCS, 1997)
EC50 - GREEN ALGA (Scenedesmus subspicatus): >100 mg/L for 96H -- for affected growth rate; EC formulation; 27.3% active ingredient; (at pH 7.6 - 10.4; 23 degrees C) (IPCS, 1997)
LOEC - GREEN ALGA (Scenedesmus subspicatus): 3 mg/L for 96H -- for increase of biomass; 97.3% technical purity; (at pH 7.8 - 8.5; 23 degrees C) (IPCS, 1997)
LOEC - GREEN ALGA (Scenedesmus subspicatus): 10 mg/L for 96H -- for increase of biomass; pre-solution xylene; 53.7% active ingredient; (at pH 7.7 - 8.5; 22 degrees C) (IPCS, 1997)
LOEC - GREEN ALGA (Scenedesmus subspicatus): 32 mg/L for 96H -- for increase of biomass; EC formulation; 27.3% active ingredient; (at pH 7.6 - 10.4; 23 degrees C) (IPCS, 1997)
NOEC - GREEN ALGA (Scenedesmus subspicatus): 1 mg/L for 96H -- for increase of biomass; 97.3% technical purity; (at pH 7.8 - 8.5; 23 degrees C) (IPCS, 1997)
NOEC - GREEN ALGA (Scenedesmus subspicatus): 1 mg/L for 96H -- for increase of biomass; pre-solution xylene; 53.7% active ingredient; (at pH 7.7 - 8.5; 22 degrees C) (IPCS, 1997)
NOEC - GREEN ALGA (Scenedesmus subspicatus): 18 mg/L for 96H -- for increase of biomass; EC formulation; 27.3% active ingredient; (at pH 7.6 - 10.4; 23 degrees C) (IPCS, 1997)

MOLLUSCS AND CRUSTACEANS

LC50 - CLAM (Donax cuneatus): 0.0064 mg/L for 96H -- commercial formulation (at 25-28.5 degrees C) (IPCS, 1997)
LC50 - MOLLUSC (Paphia laterisulca): 0.0042 mg/L for 96H -- commercial formulation (IPCS, 1997)
LC50 - PRAWN (Macrobrachium lamerrii): 1.3 mg/L for 72H -- commercial formulation; (at 27 ± 2 degrees C) (IPCS, 1997)
LC50 - WATER FLEA (Daphnia magna): 0.022 mg/L for 48H -- pre-solution in xylene (53.7%) (at 20 ± 1 degrees C) (IPCS, 1997)
LC50 - WATER FLEA (Daphnia magna): 0.023 mg/L for 48H -- technical (96.7%) (at 20 ± 1 degrees C) (IPCS, 1997)
LC50 - WATER FLEA (Daphnia magna): >0.1 mg/L for 24H -- technical (96.7%) (at 20 ± 1 degrees C) (IPCS, 1997)
LC50 - WATER FLEA (Daphnia magna): >0.1 mg/L for 24H -- pre-solution in xylene (53.7%) (at 20 ± 1 degrees C) (IPCS, 1997)
LOEC - WATER FLEA (Daphnia magna): 11.7 mcg/L -- 27.3% emulsifiable concentrate, equivalent to 3.1 mcg/L active ingredient (IPCS, 1997)
NOEC - WATER FLEA (Daphnia magna): 3.7 mcg/L -- of a 27.3% emulsifiable concentrate, equivalent to 1 mcg/L active ingredient (IPCS, 1997)
NOEC - WATER FLEA (Daphnia magna): >= 6.5 mcg/L (active ingredient) for 21D -- for reproduction (IPCS, 1997)
TC - WATER FLEA (Daphnia magna): 10 mcg/L (active ingredient) (IPCS, 1997)

TERRESTRIAL ORGANISMS

BIRDS

LD50 - (ORAL) CANARY (Serinus canarius): 10 - 20 mg/kg -- 99.7% pure (IPCS, 1997)
LD50 - (ORAL) JAPANESE QUAIL (Coturnix japonica): 44 - 50 mg/kg -- 99.7% pure; Cremephor EL as vehicle (IPCS, 1997)

LD50 - (CONTACT) BEE (Apidae sp.): 0.60 mcg/bee (IPCS, 1997)

Demeton-S-methyl has high acute toxicity to aquatic invertebrates and is toxic to fish and birds (IPCS, 1997).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

230.30

DESCRIPTION/PHYSICAL STATE

Demeton-S-methyl is a pale yellow oily liquid (EPA, 1985; Lewis, 1996).

DENSITY

OTHER TEMPERATURE AND/OR PRESSURE

LIQUID: 1.207 g/mL (at 20 degrees C) (EPA, 1985; Budavari, 1996)
LIQUID: 1.21 g/mL (at 20 degrees C) (Lewis, 1996)

BOILING POINT

89 degrees C (at 0.15 mmHg)

192 degrees F (at 0.15 mmHg) (EPA, 1985)

SOLUBILITY

IN WATER

3300 ppm (at room temperature) (EPA, 1985; Budavari, 1996)
Demeton-S-methyl is slightly soluble in water (Lewis, 1996)

IN ORGANIC SOLVENTS

soluble in most organic solvents (Budavari, 1996)

OTHER/PHYSICAL

INDEX OF REFRACTION

1.5065 (at 25 degrees C) (Budavari, 1996)

-REFERENCES

GENERAL BIBLIOGRAPHY

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40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.

49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.

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65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.

67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.

68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.

69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.

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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.

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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.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

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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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

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

Product Information: ATNAA ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR intramuscular injection solution, atropine pralidoxime chloride intramuscular injection solution. Meridian Medical Technologies, Inc (per Manufacturer), Columbia, MD, 2002.

Product Information: DUODOTE(TM) IM injection, atropine, pralidoxime chloride IM injection. Meridian Medical Technologies,Inc, Columbia, MD, 2006.

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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