DICHLORVOS

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

STCC NUMBER

4921537 - dichlorvos mixture, dry (agricultural insecticides, other than liquid)
4921536 - dichlorvos (insecticides, other than agricultural, not elsewhere classified)
4921535 - dichlorvos (agricultural insecticide, not elsewhere classified, other than liquid)
4921534 - dichlorvos (agricultural insecticide, not elsewhere classified, liquid)

DESIGNATIONS

BEILSTEIN HANDBOOK REFERENCE:4-01-00-02063
BEILSTEIN REFERENCE NUMBER:1709141
NSC NUMBER:6738

MOLECULAR FORMULA

C4-H7-Cl2-O4-P

ERG GUIDE NUMBER

152-SUBSTANCES - TOXIC (COMBUSTIBLE)

SYNONYM REFERENCE

(Budavari, 2000; CHRIS , 2002; EPA, 1990; HSDB , 2002; (IARC, 1991); Lewis, 2000; OHM/TADS , 2002; RTECS , 2002)

USES/FORMS/SOURCES

USES

Dichlorvos is used as an acaricide/insecticide and fumigant for the control of household, public health and stored-product insect pests, and as a 'disinsectant' in airplanes. It is also used for veterinary applications, including the control of ecto- and endoparasites of domestic animals; for example, as an anti-helmintic for swine and dogs or as a worming agent (Hartley & Kidd, 1990a; ACGIH, 1991a; Hathaway et al, 1996a; ITI, 1995; Lewis, 1998; Ashford, 1994; Hayes & Laws, 1991a; Howard, 1991a).
DDVP PEST STRIPS: From 2000 to 2013, 31 cases of acute illness caused by dichlorvos-impregnated resin strips (DDVP pest strips; available in the US as 16 g, 65 g, and 80 g sizes) were identified in the US (n=24) and Canada (n=7). Neurologic (eg, headache), respiratory (eg, dyspnea), and gastrointestinal (eg, nausea) effects were reported in 68%, 55%, and 42% of cases, respectively (Tsai et al, 2014).

FORMS

Dichlorvos is commercially available as emulsifiable concentrations, soluble concentrates, aerosols, wettable powders, oil-based concentrates, sprays, resin strips, flea collars, and baits (OHM/TADS, 2002; HSDB, 2002).

SOURCES

Dichlorvos is an anti-acetylcholinesterase organophosphate insecticide. Chemically it is O,O-dimethyl-O-2,2-dichlorovinyl phosphate; it is the breakdown product of trichlorfon (Hayes & Laws, 1991; Grant, 1993).
Dichlorvos is produced from the Perkow reaction of trimethyl phosphite and chloral; it is also generated from the dehydrochlorination and rearrangement of trichlorfon (Ashford, 1994).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

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

USES: Dichlorvos is available in the United States as a technical grade product used as a fumigant and insecticide. It may also be available in other countries.

TOXICOLOGY: Because dichlorvos is an organic ester of phosphoric acid, it does not require metabolism to an active form and may produce rapid onset of symptoms. Due to its rapid metabolic detoxification, dichlorvos has an unusually wide margin between inhibition of serum cholinesterase and onset of clinical effects; recovery is also rapid relative to other organophosphates. In general, 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 develop.

EPIDEMIOLOGY: Exposure is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.

WITH POISONING/EXPOSURE

MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy has been reported in a small number of patients following intentional or inadvertent exposure to dichlorvos. It may rarely develop 6 to 21 days following exposure. 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

The following are symptoms due to organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for dichlorvos, but could potentially occur in individual cases.
TOXICOLOGY: Because dichlorvos is an organic ester of phosphoric acid, it does not require metabolism to an active form and may produce rapid onset of symptoms. Due to its rapid metabolic detoxification, dichlorvos has an unusually wide margin between inhibition of serum cholinesterase and onset of clinical effects; recovery is also rapid relative to other organophosphates. In general, 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 develop.
EPIDEMIOLOGY: Exposure is common, but serious toxicity is unusual in the US. 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 the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy has been reported in a small number of patients following intentional or inadvertent exposure to dichlorvos. It may rarely develop 6 to 21 days following exposure. 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.

Dichlorvos is a very toxic poison by ingestion, inhalation, and eye or dermal contact (AAR, 1998; Lewis, 1996). The most common route of exposure is spillage on the skin, followed by rapid absorption through the skin. Inhalation is the second most common route; oral exposure is usually only by accident or suicide (Clayton & Clayton, 1993).

The following general symptoms of the anticholinesterase activity of organophosphates may occur after exposure to dichlorvos.

MUSCARINIC EFFECTS (PARASYMPATHETIC): Bradycardia, hypotension, bronchospasm, bronchorrhea, salivation, lacrimation, diaphoresis, urinary incontinence, vomiting, diarrhea, miosis.
NICOTINIC EFFECTS (SYMPATHETIC/MOTOR): Tachycardia, hypertension, fasciculations, muscle cramps, mydriasis, weakness, respiratory paralysis.
CENTRAL EFFECTS: CNS depression, agitation, confusion, restlessness, anxiety, headache, psychosis, delirium, coma, seizures.

Signs and symptoms of organophosphate poisoning also include the following:

Eye irritation, ocular pain, blurring of distant vision, and loss of accommodation (Budavari, 1996; Hathaway et al, 1996; ITI, 1995; Hall & Rumack, 1992)
Giddiness, slurring of speech, disorientation, drowsiness, and vertigo (Budavari, 1996; Hathaway et al, 1996; Hall & Rumack, 1992; Hayes & Laws, 1991)
Cardiac arrhythmias, up to complete heart block, and a sensation of tightness in the chest, excess respiratory mucus, difficulty in breathing, Cheyne-Stokes respiration, pulmonary edema, oronasal frothing, cyanosis, pulmonary rales and rhonchi (Budavari, 1996; Hathaway et al, 1996; ITI, 1995; Hall & Rumack, 1992)
Nausea and abdominal cramps (Hathaway et al, 1996)
Skin irritation and allergic contact dermatitis (ACGIH, 1991; Budavari, 1996)
Loss of muscle coordination, random jerking movements, profound weakness, muscle twitching (Hathaway et al, 1996; ITI, 1995; Hall & Rumack, 1992)

Dichlorvos depletes glycogen stores by stimulating glycogen phosphorylase and inhibiting glycogen synthesis (HSDB , 2000). Rats developed hyperglycemia and abnormal glucose tolerance tests (preventable by insulin) after being given a dose of dichlorvos equal to half the LD50 dose (Hayes & Laws, 1991).

Dichlorvos exposure symptoms have a remarkably rapid onset and recovery. Because dichlorvos is an organic ester of phosphoric acid, it does not require metabolism to an active form and may produce rapid onset of symptoms. Because of its rapid metabolic detoxification, dichlorvos has an unusually wide margin between inhibition of serum cholinesterase and onset of clinical effects (Hayes & Laws, 1991).

Respiratory paralysis is the most serious consequence of the paralytic symptoms resulting from dichlorvos exposure. Acute respiratory insufficiency, due to any combination of depression of the respiratory center, respiratory paralysis, apnea, bronchospasm, ARDS, or increased bronchial secretions, is the main cause of death in many acute organophosphate poisonings (Lerman & Gutman, 1988; Hathaway et al, 1996; Kecik et al, 1993; Uzyurt et al, 1992; Sittig, 1991; Anon, 1984) .

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

Some organophosphates can induce a delayed combined sensory-motor peripheral polyneuropathy. Based on a review of the literature, dichlorvos has produced delayed peripheral neuropathy following intentional and inadvertent exposures in some cases (Lotti & Moretto, 2005).

CHRONIC CLINICAL EFFECTS

CHOLINESTERASE

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

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, has occurred in persons occupationally exposed to mevinphos and phosphamidon residues on leaves of agricultural crops (Whorton & Obrinsky, 1983; Midtling et al, 1985).

One worker chronically exposed to dichlorvos developed persistent irritant contact dermatitis (Hathaway et al, 1996).

Acute or chronic exposure to organophosphates may impair concentration and induce confusion and drowsiness and may be a factor in plane crashes by agricultural pilots doing crop-dusting (Levin & Rodnitzky, 1976).

CASE SERIES: A case-control study of 100 adult patients given neuropsychological testing at least 3 months after acute organophosphate poisoning reported subtle effects that could not be detected by clinical exam or EEG. Although patients had worse scores on neuropsychological tests than control subjects, they were still within the normal range (Savage et al, 1988).

A series of 16 organophosphate-poisoned individuals had abnormal single-photon-emission tomography scans, with parietal perfusion deficits. One case involved dichlorvos alone (Yilmazlar & Ozyurt, 1997).

Impaired memory is a chief 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).

Psychosis and a variety of other personality and behavioral disorders have been ascribed to exposure to organophosphates (Joubert & Joubert, 1988; Conyers & Goldsmith, 1971; Dille & Smith, 1964; Gershon & Shaw, 1961) . These problems are more common with chronic exposure.

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).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

PREHOSPITAL DECONTAMINATION

INGESTION: Prehospital gastrointestinal decontamination is NOT recommended because of the potential for early coma or seizures and aspiration.
DERMAL: Remove contaminated clothing. Wash skin thoroughly with soap and water. Systemic toxicity can result from dermal exposure.
OCULAR: Copious eye irrigation.

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 depends on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975).

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

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

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

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

SMALL SPILL DECONTAMINATION

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

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

LARGE SPILL DECONTAMINATION

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

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

FURTHER CONTACT INFORMATION

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

ANTIDOTES

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

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

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

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

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

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

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

PREHOSPITAL DECONTAMINATION

INGESTION: Prehospital gastrointestinal decontamination is NOT recommended because of the potential for early coma or seizures and aspiration.
DERMAL: Remove contaminated clothing. Wash skin thoroughly with soap and water. Systemic toxicity can result from dermal exposure.
OCULAR: Copious eye irrigation.

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 depends on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975).

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

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

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

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

SMALL SPILL DECONTAMINATION

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

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

LARGE SPILL DECONTAMINATION

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

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

FURTHER CONTACT INFORMATION

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

ANTIDOTES

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

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

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

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

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

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

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

SUMMARY

ORAL: The probable lethal oral dose of dichlorvos in humans is between 50 and 500 mg/kg. This is equal to 1 teaspoon to 1 ounce for a 150 pound person (Sittig, 1991).
INHALATION: The lowest lethal inhalation dose of dichlorvos for humans is 1 mg/m(3) (OHM/TADS , 2002).
Children tend to be more sensitive to organophosphates than adults (Zweiner & Ginsburg, 1988).

CASE REPORTS

ADULT: A dose of 400 mg/kg was lethal to an adult despite aggressive treatment (Hayes & Laws, 1991).
CHILD: The lethal dose for a child who ate dichlorvos-contaminated bait was estimated to be less than 20 mg/kg (Hayes & Laws, 1991).

PESTICIDE CLASSIFICATION

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

MAXIMUM TOLERATED EXPOSURE

CONCENTRATION LEVEL

Human volunteers receiving oral doses of 2 mg/day dichlorvos for 28 days had plasma cholinesterase levels decreased to 71% of the levels in control subjects; erythrocyte enzymes were not affected. Other volunteers exposed to 0.5 mg/m(3) for 5 hours/night, 4 nights/week for 2 weeks also had a gradual reduction of plasma cholinesterase activity, but no physiological changes, clinical effects, or neurological impairment (Hayes & Laws, 1991).
In general, the likelihood of poisoning varies with the inherent toxicity of the insecticide, though there are reports of serious poisonings and deaths following environmental exposure to compounds presumed to have relatively low toxic potential (Baker et al, 1978; Dunphy et al, 1980).

OCCUPATIONAL

Reductions in plasma cholinesterase levels have been observed from occupational exposure to pesticide applicators containing dichlorvos (Hayes & Laws, 1991). Thirteen workers who were exposed to an average concentration of 0.7 mg/m(3) for 12 months had erythrocyte cholinesterase levels reduced by 35%, and their serum enzymes reduced by 60%. There were no adverse clinical effects reported (Proctor et al, 1988).

RISK FACTORS

The maximum tolerated exposure in humans would depend on several factors. Among these are prior exposure to cholinesterase inhibitors, genetic and nutritional factors, and presence of various disease states. Persons with serious liver disease developed reduction of cholinesterase at exposure levels where healthy persons were unaffected (Hayes & Laws, 1991).

ROUTE OF EXPOSURE

INHALATION

The threshold for inhibition of plasma cholinesterase has been estimated to be approximately 0.1 mg/m(3) for 24 hours/day, or 0.4 mg/m(3) for 5 hours/day (Hayes & Laws, 1991).
The RfC (inhalation Reference Concentration) has been estimated at 5 x 10(-4) mg/m(3) ((EPA, 1997)).

INGESTION

The RfD (oral Reference Dose) has been estimated at 5 x 10(-4) mg/kg/day ((EPA, 1997)).

INTRAVENOUS

A 19-year-old man who injected 1 ml (concentration 550 g/L) of dichlorvos into a cubital vein 2 hours prior to presentation developed nausea and abdominal pain approximately 1 hour after injection. The patient became unconscious, hypotensive, and tachycardic 2 hours after admission. He experienced 3 tonic-clonic seizures during the first 5 hours of admission. The patient developed decreased, unstable pseudocholinesterase levels and was treated with pralidoxime 500 mg/h until his pseudocholinesterase levels were 5279 IU (normal range 3714 to 11,513 IU), and the medication was discontinued. The patient was released after 2 days of stable plasma pseudocholinesterase levels, and upon follow-up, no abnormalities were reported (Buyukcam et al, 2011).

ANIMAL DATA

DOG - Dichlorvos given at a dose of 0.13 to 0.37 mg/kg/day had no apparent effect in dogs, whereas 0.65 mg/kg/day reduced brain cholinesterase levels to 88% of normal, and 1.30 mg/kg/day decreased brain cholinesterase levels to 33% of normal (Hayes & Laws, 1991).

Domestic animals tolerate equivalent doses better in slow-release formulations (Hayes & Laws, 1991).

MONKEY - Monkeys receiving 1.4 to 2 mg/m(3) by continuous inhalation exposure for one week had markedly decreased blood cholinesterase levels, whereas rats were only mildly affected at these doses. Lower concentrations of 0.8 to 1.8 mg/m(3) had no apparent effect on cholinesterase inhibition after 22 days, but after a 50 day exposure period at these concentrations, animals had a decrease in erythrocyte cholinesterase levels (Hayes & Laws, 1991).

Continuous exposure to 0.27 mg/m(3) or less over 4 days had no effect on cholinesterase levels in monkeys and rats (Hayes & Laws, 1991).

RAT - A dietary level of 1,000 ppm for at least 90 days produced no clinical signs in rats, although doses as low as 5 ppm reduced blood cholinesterase (Hayes & Laws, 1991).

Carcinogenicity Ratings for CAS62-73-7 :

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

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): B2 ; Listed as: Dichlorvos

B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.

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): 2B ; Listed as: Dichlorvos

2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Dichlorvos
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 CAS62-73-7 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor: 2.9x10(-1) per mg/kg-day
RfD: 5x10(-4) mg/kg-day

Inhalation:

Unit Risk:
RfC: 5x10(-4) mg/m3

Drinking Water:

Unit Risk: 8.3x10(-3) per mg/L

TOXICITY VALUES

References: Bingham et al, 2001 HSDB, 2002 Lewis, 2000 ) OHM/TADS, 2002 RTECS, 2002
- LC50- (INHALATION)MOUSE:
- LC50- (INHALATION)RAT:
- LD50- (ORAL)CHICKEN:
- LD50- (ORAL)DOG:
- LD50- (INTRAPERITONEAL)HAMSTER:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (INTRAVENOUS)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)MOUSE:
- LD50- (SUBCUTANEOUS)MOUSE:
- LD50- (ORAL)PIG:
- LD50- (ORAL)RABBIT:
- LD50- (SKIN)RABBIT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LD50- (SUBCUTANEOUS)RAT:
- LDLo- (INTRAVENOUS)DOG:
- LDLo- (INTRAPERITONEAL)MOUSE:
- LDLo- (ORAL)RAT:
- TCLo- (INHALATION)RABBIT:
- TDLo- (ORAL)CHICKEN:
- TDLo- (ORAL)DOG:
- TDLo- (INTRAPERITONEAL)MOUSE:
- TDLo- (ORAL)MOUSE:
- TDLo- (SUBCUTANEOUS)MOUSE:
- TDLo- (ORAL)PIG:
- TDLo- (SKIN)PRIMATE:
- TDLo- (ORAL)RABBIT:
- TDLo- (INHALATION)RAT:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (ORAL)RAT:
- TDLo- (SKIN)RAT:
- TDLo- (SUBCUTANEOUS)RAT:

CALCULATIONS

AMBIENT CONVERSIONS

CONVERSION FACTORS:

1 ppm = 9.04 mg/m(3) (at 68 degrees F and 760 mmHg) (NIOSH , 2002)

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS62-73-7 (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

Dichlorvos (DDVP)

TLV:

TLV-TWA: 0.1 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: 220.98

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 CAS62-73-7 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS62-73-7 (National Institute for Occupational Safety and Health, 2007):

Listed as: Dichlorvos
REL:

TWA: 1 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: [skin]

Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.

Note(s):

IDLH:

IDLH: 100 mg/m3
Note(s): Not Listed

OSHA PEL Values for CAS62-73-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Dichlorvos (DDVP)
Table Z-1 for Dichlorvos (DDVP):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 1

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: Yes
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS62-73-7 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS62-73-7 (U.S. Environmental Protection Agency, 2010):

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

10 (4.54)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS62-73-7 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS62-73-7 (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 CAS62-73-7 (U.S. Environmental Protection Agency, 2010):

Listed as: Dichlorvos
Reportable Quantity, in pounds: 10

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

Threshold Planning Quantity, in pounds:

1000
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 CAS62-73-7 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Dichlorvos [Phosphoric acid, 2,2-dichloroethenyl dimethyl ester]
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS62-73-7 (49 CFR 172.101 - App. B, 2005):

Listed as Dichlorvos
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS62-73-7 (EPA, 2005):

Listed as: Phosphoric acid, 2,2-dichloroethenyl 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 CAS62-73-7 (NFPA, 2002):

Listed as: Dichlorvos
Hazard Ratings:

Health Rating (Blue): 3

(3) Seriously toxic material. Short term exposure could cause serious temporary or residual injury even though prompt medical treatment is given. Includes known or suspect small animal carcinogens, mutagens, or teratogens.

Flammability Rating (Red): 1

(1) Slightly combustible. Materials that require considerable preheating before ignition can occur. This rating includes most ordinary combustible materials.

Instability Rating (Yellow): [blank cell]

([blank cell]) Sufficient information was not available for a severity rating to be assigned.

Oxidizer/Water-Reactive Designation: Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

Persons poisoned by dermal exposure to organophosphate compounds should be treated by a medical team wearing rubber gloves and aprons. It may be necessary for medical personnel to wear respirators if the affected individual has been poisoned by exposure to high airborne concentrations. No leather items not fully covered by rubber or impervious plastic should be worn by the treatment team.
The affected person's clothing should be placed in a sealed plastic bag to prevent further contamination. Local authorities should be consulted regarding appropriate toxic waste disposal. Leather clothing items are extremely difficult to decontaminate, and often must be disposed of by incineration.

HANDLING

NORMAL HANDLING PROCEDURES: Wear safety glasses, gloves, gas mask, top boots, and overalls with long sleeves and a closed collar (CHRIS , 2002; ITI, 1995). Rubber gloves, face shield or goggles, and respirator should be worn (Hartley & Kidd, 1990).

STORAGE

CONTAINER

Dichlorvos should be stored in tightly sealed containers (OHM/TADS , 2002; Sittig, 1991).
Wash containers that have held organophosphorus pesticides with bleaching powder suspended in water or with another alkaline solution. After soaking them for 24 hours, rinse the containers with hot water (HSDB , 2002).
Dichlorvos will not corrode nickel, aluminum, hastelloy b., or stainless steel type 316 (OHM/TADS , 2002)

ROOM/CABINET RECOMMENDATIONS

Dichlorvos should be stored in cool areas with adequate ventilation (Sittig, 1991).
To ensure proper shelf-life, dichlorvos should be stored at temperatures below 80 degrees F (HSDB , 2002).
Keep dichlorvos far from heat and water (OHM/TADS , 2002).

INCOMPATIBILITIES

Iron and mild steel may be corroded by dichlorvos (HSDB , 2002).
Dichlorvos is incompatible with strong acids and strong alkalis (NIOSH , 2002).
Some plastics, rubber, and coatings are attacked by dichlorvos (Pohanish & Greene, 1997).

-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.

To prevent prolonged skin contact with dichlorvos, appropriate clothing, which includes safety glasses, a gas mask, gloves, top boots, and overalls with long sleeves and a closed collar, should be worn. If clothing becomes wet or contaminated, it should be promptly removed and replaced (ITI, 1995; NIOSH , 2002; Sittig, 1991).

Personal protective equipment, comprised of overalls made of polyvinyl chloride or a tight fabric, gloves, a face shield (8-inch minimum), and rubber boots, must be provided to workers that handle and apply organophosphorus pesticides. A respirator with an activated-carbon gas filter cartridge capable of protecting for the amount of hours worked is also necessary when working with these pesticides (HSDB , 2002).

Protective clothing should be washed at least once per week and every time contamination knowingly occurs. Soak the clothing in a solution of calcium carbonate for several hours prior to washing (HSDB , 2002).

Bodily contact with dichlorvos should be avoided; if, however, bodily contact does occur, immediately wash away the material with plenty of water or soap and water (AAR, 2000; NIOSH , 2002).

EYE/FACE PROTECTION

Individuals working with dichlorvos should not wear contact lenses (HSDB , 2002).

Wear splash-proof safety goggles to prevent the possibility of liquid dichlorvos coming in contact with the eyes (HSDB , 2002).

RESPIRATORY PROTECTION

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

Wear a self-contained positive pressure breathing apparatus when working in the vicinity of spills or leaks or when fighting fires (AAR, 2000).

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 62-73-7.

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.
Dichlorvos releases toxic fumes of chlorides and oxides of phosphorus when heated to decomposition (Lewis, 2000).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS62-73-7 (NFPA, 2002):

Listed as: Dichlorvos
Flammability Rating: 1

(1) Slightly combustible. Materials that require considerable preheating before ignition can occur. This rating includes most ordinary combustible materials.

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 CAS62-73-7 (NFPA, 2002):

Listed as: Dichlorvos
Extinguishing Method(s): 5, 2

5: Flammable liquid fires can be extinguished using carbon dioxide, dry chemical, foam, and vaporizing liquid extinguishers, as long as the fires are small to moderate in size and the flammable liquid reservoir is shallow. Use of foam to form a blanket over a flammable liquid is not effective when the liquid is water-soluble. Certain alcohol resistant foams are effective extinguishing agents for polar, non-polar, and water-soluble liquid fires. These foams are preferred for fighting flammable liquid fires except those that involve water reactive flammable liquids.
2: "Water or foam may cause frothing" refers to a situation where materials with a flash point above 212 degrees F (100 degrees C) are burning. Potentially violent frothing can be dangerous to fire fighters near the burning liquid. However, when highly viscous liquids are burning, fire fighters can intentionally cause frothing on the liquid surface to prevent further introduction of oxygen.

Extinguish small fires involving dichlorvos with dry chemical, carbon dioxide, water spray, or foam. Use water spray, fog or foam to extinguish large fires involving dichlorvos. Fight fire from maximum distance while wearing protective clothing along with a self-contained breathing apparatus with full face piece operating on pressure-demand mode. Dike runoff from fire control water for later disposal, as it may release poisonous gases or cause water pollution (AAR, 2000; HSDB , 2002; Sittig, 1991).

From as far a distance as possible, apply water to affected containers to keep them cool (AAR, 2000).

COMBUSTION TOXICITY

The release of toxic gases and vapors, including hydrogen chloride gas, phosphoric acid mist, and carbon monoxide, is possible in fires involving dichlorvos (ACGIH, 1991; HSDB , 2002).
CHRIS (2002) reports that this compound is "stable to heat."

DUST/VAPOR HAZARD

Dichlorvos releases toxic fumes of chlorides and oxides of phosphorus when heated to decomposition (Lewis, 2000).

The vapor pressure of dichlorvos is much higher than that of most other chemicals (Zenz, 1994). Because of its high vapor pressure relative to the other organophosphates, it represents a greater inhalation hazard. Insecticidal concentrations (thus, concentrations exceeding the TLV) can be produced in interstices of relatively large spaces, through evaporation of small amounts of dichlorvos (Hayes & Laws, 1991).

REACTIVITY HAZARD

Dichlorvos will undergo hydrolysis in the presence of water and will be decomposed readily by strong acids and bases (EPA, 1990; HSDB , 2002). In saturated aqueous solutions at room temperature, dichlorvos hydrolyzes at a rate of 3 percent per day; it is completely hydrolyzed in 1 hour at high pH or in boiling water (ACGIH, 1991).

Dichlorvos is "slowly hydrolyzed in water and in acidic media, and rapidly hydrolyzed by alkalis, to dimethyl hydrogen phosphate and dichloroacetaldehyde" (Hartley & Kidd, 1990).

Some plastics, rubber and coatings are attacked by dichlorvos (Pohanish & Greene, 1997; Sittig, 1991).

Dichlorvos may emit toxic fumes of chloride, phosgene gas, and oxides of phosphorus when heated to decomposition (AAR, 2000; Lewis, 2000).

Dichlorvos may corrode iron and mild steel (Hartley & Kidd, 1990).

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 CAS62-73-7 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS62-73-7 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Dichlorovos (Dichlorvos)
TEEL-0 (units = mg/mg3): 0.1
TEEL-1 (units = mg/mg3): 0.3
TEEL-2 (units = mg/mg3): 20
TEEL-3 (units = mg/mg3): 100
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 CAS62-73-7 (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 CAS62-73-7 (National Institute for Occupational Safety and Health, 2007):

IDLH: 100 mg/m3
Note(s): 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.
Sand or other noncombustible absorbent materials, such as vermiculite, dry sand, or earth, can be used to absorb small spills, and the mixture can then be disposed of in canisters (HSDB , 2002; Sittig, 1991).
Deposit land spills in an excavated pit, pond, lagoon, or other holding area. Adsorb the bulk material with fly ash or cement powder, and dike the surface flow with sand bags or soil. To prevent solids from dissolving in rain or fire-fighting water, cover the spilled material with a plastic sheet (AAR, 2000).
For water spills, natural deep water pockets, excavated lagoons, or sand bag barriers can be used to trap spilled material at the bottom. If spills have been dissolved in concentrations of 10 ppm or greater, they should first be treated with activated carbon at ten times the amount spilled, then removed with mechanical dredges of lifts (AAR, 2000).
DECONTAMINATION OF SPILLS
- A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975).

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, 1975a).
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 effective 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 decontamination (EPA, 1975).
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, 1975a).

WASTE TREATMENT OPTIONS

PHYSICAL TREATMENT

A furnace equipped with an afterburner and alkali scrubber is recommended for the incineration of dichlorvos. Alkaline hydrolysis, which yields no toxic residues, followed by burial in soil is also a recommended disposal method for this compound (Sittig, 1991).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Dichlorvos is released to air, water, and soil through its use as an insecticide and during its production and disposal. It is not known to occur naturally (Howard, 1991).

ENVIRONMENTAL FATE AND KINETICS

Dichlorvos will exist almost entirely in the vapor phase when released into the atmosphere. In ambient air, vapor-phase dichlorvos will react with photochemically generated hydroxyl radicals with a half-life of two days and a rate constant of 9.24x10(-12) cm(3)/molecule-sec at 25 degrees C. Vapor-phase dichlorvos also reacts with ozone; this reaction has a half-life of 320 days and a rate constant of 3.58x10(-20) cm(3)/molecule-sec at 25 degrees C (Howard, 1991).
HSDB (2002) lists the half-life for the reaction of vapor-phase dichlorvos with hydroxyl radicals as 13.6 hours.
Direct photolysis of dichlorvos in the atmosphere will not occur (Howard, 1991).

WATER

SURFACE WATER
- As it does not adsorb appreciably to sediment, dichlorvos remains in the aqueous phase when released into water. In polluted waters where acclimated microorganisms may exist or in more acidic waters, biodegradation may be an important process, but degradation of dichlorvos occurs primarily by hydrolysis in most bodies of water (Howard, 1991).
- Volatilization of dichlorvos from environmental waters will occur slowly, as indicated by the Henry's Law constant of 9.58x10(-7) atm-m(3)/mol (at 25 degrees C) (Howard, 1991).
- The half-life of dichlorvos in water is pH dependent. It is estimated at 5 hours at pH 8, 8 hours at pH 7, 35 hours at pH 6, and 77 hours at pH 5.4. Dichlorvos hydrolyzes in water to form dimethyl phosphoric acid and dichloroacetic acid (Verschueren, 2000).

SOIL

TERRESTRIAL
- The EPA (1990) reports that "dichlorvos degrades fairly rapidly with half-lives of 2 to 8 hours in soils ranging in texture from sand to silt. The mobility of dichlorvos is inversely correlated with soil organic matter content. Preliminary data also suggest that dichlorvos is intermediately to very mobile in a variety of soils ranging in texture from sandy loam to clay."
- The half-life of dichlorvos was reduced from 0.9 to 0.75 days in clay and from 0.85 to 0.70 days in calcareous soil when in the presence of active microorganisms (Howard, 1991).
- "If released on land, dichlorvos will leach into the ground water where it will hydrolyze and also degrade through chemical and biological processes with reported half-lives ranging from 1.5 to 17 days" (Howard, 1991).

ABIOTIC DEGRADATION

As it does not absorb UV light above 240 nm, dichlorvos is not a candidate for photolysis. The rate of hydrolysis of dichlorvos in water increases with increasing pH value, temperature, and concentration (Howard, 1991).

BIODEGRADATION

Although it was resistant to degradation in an 8-day laboratory test using a sewage inoculum, dichlorvos is listed as being amenable to biological treatment after acclimation. It has been shown that dichlorvos degrades more rapidly in polluted than in unpolluted waters (Howard, 1991).

Products of biodegradation are dichloroethanol, dichloroacetic acid, and ethyl dichloroacetate (Howard, 1991).

BIOACCUMULATION

BIOCONCENTRATION FACTOR

Log Bioconcentration Factor (BCF) in fish: 0.28 (Howard, 1991)

ENVIRONMENTAL TOXICITY

Published Values (CHRIS , 2002; HSDB , 2002; OHM/TADS , 2002; Verschueren, 2000)

LC50 - AMERICAN EEL: 1.8 ppm for 96H - saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - ANGUILLA ROSTRATA: 1800 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - ANODONTA ANATINA: 0.6-2.2 ml/L for 2D (Verschueren, 2000)
LC50 - ANODONTA ANATINA: 0.34-0.44 ml/L for 4D (Verschueren, 2000)
LC50 - ANODONTA CYGNEA: 0.66-1.2 ml/L for 2D (Verschueren, 2000)
LC50 - ANODONTA CYGNEA: 0.33-0.39 ml/L for 4D (Verschueren, 2000)
LC50 - ATLANTIC SILVERSIDE: 1.25 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - BARILIUS BENDELISIS: 0.5 mg/L (Verschueren, 2000)
LC50 - BLUEGILL: 0.7 ppm for 48H (CHRIS, 2002)
LC50 - BLUEGILL: 1000 mcg/L for 24H (Verschueren, 2000)
LC50 - BLUEGILL SUNFISH: 0.48 ppm for 96H -- freshwater (OHM/TADS, 2002)
LC50 - BLUEGILL SUNFISH: 1.0 ppm for 24H -- freshwater (OHM/TADS, 2002)
LC50 - BLUEGILL SUNFISH: 0.869 ppm for 96H -- freshwater (OHM/TADS, 2002)
LC50 - BLUEHEAD: 1.44 ppm for 96H - saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - CRANGON SEPTEMSPINOSA: 4 mcg/L for 96H (Verschueren, 2000)
LC50 - CUTTROAT TROUT, 2.5 g: 170 mcg/L for 96H -- 12 degrees C; static bioassay; 100% technical material (HSDB, 2002)
LC50 - DAPNIA PULEX: 0.07 mcg/L for 48H (Verschueren, 2000)
LC50 - FATHEAD MINNOW, 0.7 g: 11,600 mcg/L for 96H -- 17 degrees C; static bioassay (HSDB, 2002)
LC50 - FUNDULUS HETEROCLITUS: 2680 mcg/L (Verschueren, 2000)
LC50 - FUNDULUS HETEROCLITUS: 3700 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - FUNDULUS MAJALIS: 2300 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - GAMMARUS FASCIATUS: 0.40 mcg/L for 96H (Verschueren, 2000)
LC50 - GAMMARUS LACUSTRIS, mature: 0.50 mcg/L for 96H -- 21 degrees C; 100% technical material (HSDB, 2002)
LC50 - GAMMARUS LACUSTRIS: 0.50 mcg/L for 96H (Verschueren, 2000)
LC50 - GRASS SHRIMP: 0.015 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - HERMIT CRAB: 0.045 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - LEPOMIS MACROCHIRUS: 869 mcg/L for 96H (Verschueren, 2000)
LC50 - MENIDIA MENIDIA: 1250 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - MOSQUITOFISH, 0.2 g: 5270 mcg/L for 96H -- 17 degrees C; static bioassay; 100% technical material (HSDB, 2002)
LC50 - MUGIL CEPHALUS: 200 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - MUMMICHOG: 3.7 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - MUMMICHOG: 2.68 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - NORTHERN PUFFER: 2.25 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - PAGURUS LONGICARPUS: 45 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - PALAEMONETES VULGARIS: 15 mcg/L for 96H -- saltwater (Verschueren, 2000)
LC50 - PTERONARCYS: 0.10 mcg/L for 96H -- 15 degrees C; second year class in a static bioassay; 100% technical material (HSDB, 2002)
LC50 - PTERONARCYS CALIFORNICA: 0.10 mcg/L for 96H (Verschueren, 2000)
LC50 - SAND SHRIMP: 0.004 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - SIMOCEPHALUS SERRULATUS: 0.26 mcg/L for 48H (Verschueren, 2000)
LC50 - SPHAEROIDES MACULATUS: 2250 mcg/L for 96H (Verschueren, 2000)
LC50 - STRIPED KILLIFISH: 2.3 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - STRIPED MULLET: 0.2 ppm for 96H -- saltwater; static lab bioassay (OHM/TADS, 2002)
LC50 - THALASSOMA BIFASCIATUM: 1400 mcg/L for 96H (Verschueren, 2000)
LC50 - UNIO PICTORUM: 2.8-7.1 ml/L (Verschueren, 2000)
LC50 - UNIO PICTORUM: 0.5-0.69 ml/L for 4D (Verschueren, 2000)
LD50 - (UNREPORTED) MALLARD, young: 7.8 mg/kg (CHRIS, 2002)
TL50 - SCUD: 0.0018 ppm for 24H -- freshwater (OHM/TADS, 2002)
TL50 - SCUD: 0.0004 ppm for 96H -- freshwater (OHM/TADS, 2002)
TLm - FRESH WATER CRUSTACEA: 0.025-3.2 ppm for 48H (CHRIS, 2002)

Dichlorvos is non-phytotoxic and non-persistent (Worthing & Walker, 1983).

PROTOZOAN TOXICITY: Dichlorvos, at a concentration of 15.0 mg/L, caused an 80% decrease in the activity of the acetycholine esterase enzyme in the protozoan, Tetrahymena pyriformis. Significant decreases in the ALT and LDH enzyme activities were also noted (Mojzis et al, 1993).

BIOLOGICAL OXYGEN DEMAND: Persists 62 days in water at 20 degrees C (CHRIS , 2002)

FOOD CHAIN CONCENTRATION: "Prolonged exposure to organophosphorus pesticides at concentrations as low as 0.01 parts per billion are toxic to marine animals due to bioconcentration" (CHRIS , 2002).

Scottish fish farmers reported a suspected reduction in the sensitivity of salmon lice to the organophosphate dichlorvos. A study was conducted using pre-adult and adult lice from marine salmon sites showing a variation in 'sensitivities' to dichlorvos and exposed to a range of dose levels of dichlorvos for up to 48 hours. The results showed that lice from different geographic areas do exhibit differences in sensitivity to dichlorvos (Jones et al, 1992).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

220.98

DESCRIPTION/PHYSICAL STATE

Dichlorvos is a colorless to amber oily liquid with an odor characteristic of the aromatic compounds (HSDB, 2005; AAR, 2000; ACGIH, 1991; OHM/TADS , 2002).

VAPOR PRESSURE

6x10(-3) mbar (at 10 degrees C) (Verschueren, 2000)

0.012 mmHg (at 20 degrees C) (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Hayes & Laws, 1991)

2.15x10(-3) mmHg (at 20 degrees C) (Verschueren, 2000)

5.27x10(-2) mmHg (at 25 degrees C) (Howard, 1991)

0.0158 mmHg (at 25 degrees C) (HSDB, 2005)

0.01 mmHg (at 30 degrees C) (Clayton & Clayton, 1993)

0.01 mmHg (NIOSH, 2005)

0.032 mmHg (at 32 degrees C) (EPA, 1990)

0.032 mmHg (at 32.2 degrees C) (OHM/TADS, 2005)

1.6 Pa (at 20 degrees C) (Hartley & Kidd, 1990)

3.9 Pa (at 30 degrees C) (Hartley & Kidd, 1990)

SPECIFIC GRAVITY

NORMAL TEMPERATURE AND PRESSURE

(25 degrees C; 77 degrees F and 760 mmHg)
1.415 (at 25/4 degrees C) (CHRIS, 2005; ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; ITI, 1995)
1.42 (at 77 degrees F) (NIOSH, 2005)

DENSITY

NORMAL TEMPERATURE AND PRESSURE

(25 degrees C; 77 degrees F and 760 mmHg)
1.415 g/mL (Clayton & Clayton, 1993)

TEMPERATURE AND/OR PRESSURE NOT LISTED

1.65-1.67 g/mL (EPA, 1990)
1.44 g/mL (Verschueren, 2000)

FREEZING/MELTING POINT

MELTING POINT

84 degrees C (OHM/TADS, 2005)
-60 degrees C (Bingham et al, 2001)
<-60 degrees C (Verschueren, 2000)

BOILING POINT

221 degrees C (at 760 mmHg) ((ATSDR, 1997); Bingham et al, 2001)

140 degrees C; 284 degrees F; 413.2 K (at 1 atm) (CHRIS, 2005)

140 degrees C (at 20 mmHg) (OHM/TADS, 2005; ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Howard, 1991)

120 degrees C (at 14 mmHg) (OHM/TADS, 2005; Lewis, 2001; Lewis, 2000; Sittig, 1991)

120 degrees C (at 19 mbar) (Verschueren, 2000)

117 degrees C (at 10 mmHg) (EPA, 1990; Hartley & Kidd, 1990)

88 degrees C (at 3 mmHg) (Lewis, 2000)

84 degrees C (at 1 mmHg) (Budavari, 2000; Clayton & Clayton, 1993)

74 degrees C (at 1 mmHg) (Hartley & Kidd, 1990)

72 degrees C (at 0.5 mmHg) (Budavari, 2000; ITI, 1995)

35 degrees C (at 0.05 mmHg) ((ATSDR, 1997); Hartley & Kidd, 1990)

30 degrees C (at 0.01 mmHg) (Budavari, 2000)

Decomposes (NIOSH, 2005)

FLASH POINT

>175 degrees F (open cup) (HSDB, 2005; NIOSH, 2005; AAR, 2000)

79.4 degrees C (OHM/TADS, 2005)

SOLUBILITY

IN WATER

1 g/100 mL (at 20 degrees C) (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; HSDB , 2002)
0.5 g/100 mL (NIOSH, 2005; Budavari, 2000)
16000 mg/L (at 25 degrees C) ((ATSDR, 1997); Howard, 1991)
Slightly soluble in water (EPA, 1990; Lewis, 2001; Lewis, 2000)
Dichlorvos "hydrolyzes at a rate of 3% per day in saturated aqueous solution at room temperature; at high pH or in boiling water, it completely hydrolyzes in 1 hour" (Bingham et al, 2001).

IN ORGANIC SOLVENTS

Solubility in glycerine: 0.5 g/100 mL (at 20 degrees C) (ACGIH, 1991; Budavari, 2000; Clayton & Clayton, 1993)
Solubility in kerosene: 2 to 3 g/kg (HSDB, 2005)
Soluble in chloroform and acetone (HSDB, 2005)
Slightly soluble in glycerol (Lewis, 2001; Lewis, 2000)
Dichlorvos is miscible with aromatic and chlorinated hydrocarbon solvents, alcohols, most nonpolar and organic solvents, and aerosol propellants. It is miscible in toluene, 2-propanol, and dichloromethane (HSDB, 2005; ACGIH, 1991; Lewis, 2001; Lewis, 2000; Budavari, 2000; Bingham et al, 2001; EPA, 1990).
Dichlorvos is moderately soluble in mineral oils, isoparaffinic hydrocarbons, diesel oil, and kerosene (Hartley & Kidd, 1990).

OCTANOL/WATER PARTITION COEFFICIENT

Log Kow = 1.16 ((ATSDR, 1997))

Log Kow = 1.43 (HSDB, 2005)

Log Kow = 1.47 ((ATSDR, 1997))

Log Kow = 1.5 (Verschueren, 2000)

HENRY'S CONSTANT

7.01x10(-8) atm-m(3)/mol (at 25 degrees C) ((ATSDR, 1997))

4.6x10(-7) atm-m(3)/mol (estimated from vapor pressure and water solubility) (HSDB, 2005)

6.61x10(-7) atm-m(3)/mol (at 25 degrees C) ((ATSDR, 1997))

8.58x10(-7) atm-m(3)/mol ((ATSDR, 1997))

9.58x10(-7) atm-m(3)/mol (at 25 degrees C) (Howard, 1991)

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Information to evaluate chemical incidents

Information to evaluate chemical incidents