DIMETHOATE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
DIMETHOATE AC-12880 AC-12682 AC-18682 ACETIC ACID, O,O-DIMETHYLDITHIOPHOSPHORYL-, N-MONOMETHYLAMIDE SALT AMERICAN CYANAMID 12880 BI-58 BI 58 EC 8014 BIS HC CEKUTHOATE CL 12880 CYGON CYGON 2-E CYGON 4E CYGON INSECTICIDE DAPHENE DE-FEND DEMOS-L40 DEVIGON DIMATE 267 DIMET DIMETATE DIMETHOAAT (Dutch) DIMETHOAT (German) DIMETHOATE-267 DIMETHOAT TECHNISCH 95% DIMETHOGEN O,O-DIMETHYLDITHIOPHOSPHORYLACETIC ACID, N-MONOMETHYLAMIDE SALT O,O-DIMETHYL-DITHIOPHOSPHORYLESSIGSAEURE MONOMETHYLAMID (German) O,O-DIMETHYL S-(2-(METHYLAMINO)-2-OXOETHYL) PHOSPHORODITHIOATE O,O-DIMETHYL-S-(N-METHYL-CARBAMOYL)-METHYL- DITHIOFOSFAAT (Dutch) (O,O-DIMETHYL-S-(N-METHYL-CARBAMOYL-METHYL)- DITHIOPHOSPHAT) (German) O,O-DIMETHYL METHYLCARBAMOYLMETHYL PHOSPHORODITHIOATE O,O-DIMETHYL S-METHYLCARBAMOYLMETHYL PHOSPHORODITHIOATE O,O-DIMETHYL S-(N-METHYLCARBAMOYLMETHYL) DITHIOPHOSPHATE O,O-DIMETHYL S-(N-METHYLCARBAMOYLMETHYL) PHOSPHORODITHIOATE O,O-DIMETHYL S-(N-METHYLCARBAMYLMETHYL) PHOSPHORODITHIOATE O,O-DIMETHYL S-(N-METHYLCARBAMYLMETHYL) THIOTHIONOPHOSPHATE O,O-DIMETHYL-S-(N-MONOMETHYL)-CARBAMYL METHYL DITHIOPHOSPHATE O,O-DIMETHYL-S-(2-OXO-3-AZA-BUTYL)-DITHIOPHOSPHAT (German) O,O-DIMETIL-S-(N-METIL-CARBAMOIL-METIL)-DITIOFOSFATO (Italian) DIMETON DIMEVUR DITHIOPHOSPHATE DE O,O-DIMETHYLE ET DES(-N-METHYLCARBAMOYL-METHYLE) (French) EI-12880 EXPERIMENTAL INSECTICIDE 12,880 FERKETHION FIP FORTION NM FOSFAMID FOSFOTOX FOSFOTOX R FOSFOTOX R 35 FOSTION MM L-395 LURGO S-METHYLCARBAMOYLMETHYL O,O-DIMETHYL PHOSPHORODITHIOATE N-MONOMETHYLAMIDE of O,O- DIMETHYLDITHIOPHOSPHORYLACETIC ACID NC-262 OMS 94 OMS 111 PEI 75 PERFECTHION PERFEKTHION PERFEKTION PHOSPHAMID PHOSPHAMIDE PHOSPHORODITHIOIC ACID, O,O-DIMETHYL ESTER, ESTER with 2-MERCAPTO-N-METHYLACETAMIDE PHOSPHORODITHIOIC ACID, O,O-DIMETHYL ESTER, S-ESTER with 2-MERCAPTO-N-METHYLACETAMIDE PHOSPHORODITHIOIC ACID, O,O-DIMETHYL-S- (2-(METHYLAMINO)-2-OXOETHYL) ESTER RACUSAN REBELATE ROGODIAL ROGOR ROGOR 40 ROGOR L ROGOR 20L ROGOR P ROXION ROXION U.A. SINORATOX SYSTOATE TRIMETION
IDENTIFIERS
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.
SYNONYM REFERENCE
- (RTECS , 1991; Budavari, 1989)Clayton & Clayton, 1981;(EPA, 1985; Sax & Lewis, 1989)
USES/FORMS/SOURCES
A more recent source states that the use of dimethoate has been restricted; dry formulations are no longer permitted (Sax & Lewis, 1987). It is used as a systemic and contact insecticide and acaricide (Hayes, 1982). Because of its relatively low toxicity to mammals, dimethoate has been used in veterinary medicine to control bots in livestock (Hayes, 1982).
Dimethoate is available as emulsifiable concentrates of 20, 40, and 50% technical grade, as a 30% concentrate for ultralow volume applications, and in 20% wettable powder and 5% granules (Hayes, 1982). GERMANY: Organophosphates are often mixed with oil for ease of application. This enhances their absorption and toxicity.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- The following are general effects due to organophosphates, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for dimethoate, but could potentially occur in individual cases.
- USES: Dimethoate, an organophosphate compound, is used as a systemic and contact insecticide. It is registered for use in the US and other countries; however it is not available for residential use in the US.
- TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop.
- EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.
MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps. SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop. DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to dimethoate. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete. CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults. INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
- Dimethoate can be absorbed by the ingestion, inhalation or dermal exposure routes (ILO, 1983). With an estimated oral LD50 of 15 to 30 mg/kg in humans, dimethoate is a highly toxic substance (Hayes & Laws, 1991). The actual lethal dose for humans depends on the route and rate of exposure, as well as on the medical treatment received (Hayes & Laws, 1991).
- Based on its acute oral LD50 of 28 to 600 mg/kg in rats, dimethoate would be considered in the moderately toxic group of organophosphates (Morgan, 1989). A wide range of acute LD50 values have been reported in different species, possibly due to increased toxicity upon storage in older studies. Some of this increased toxicity was attributed to a solvent effect when glycol ether solvents were used. Formulations in glycol ether solvents have been discontinued (Hayes & Laws, 1991).
- Dimethoate itself was not irritating to the eyes. However, severe irritation from occupational exposure has apparently been traced to bis(dimethoxythiophosphoryl) disulfide, which can be formed during neutralization of the acid intermediate (Hayes & Laws, 1991).
- Dimethoate produces a spectrum of acute effects typical of organophosphate compounds, but with a slow onset (ILO, 1983). The hallmark of organophosphate poisoning is inhibition of plasma pseudocholinesterase and erythrocyte acetylcholinesterase (Namba, 1972).
- Symptoms of organophosphate poisoning include nausea, vomiting, abdominal cramps, diarrhea, headache, giddiness, vertigo, weakness, sensation of tightness in the chest (after inhalation exposures), excessive tearing, loss of accommodation, ocular pain, blurring or dimness of vision, miosis, loss of muscle coordination, slurring of speech, fasciculations and twitching of muscles (particularly of tongue and eyelids) (Minton & Murray, 1988).
- Other acute effects include generalized profound weakness, mental confusion, disorientation, drowsiness, difficulty in breathing, excessive salivation and respiratory mucus, oronasal frothing, cyanosis, pulmonary rales and rhonchi, hypertension, hypotension, cardiac arrhythmias, random jerky movements, incontinence, convulsions, and coma (Minton & Murray, 1988).
- Death from organophosphate poisoning occurs primarily from respiratory arrest arising from failure of the respiratory center, paralysis of respiratory muscles, intense bronchoconstriction, or all three (HSDB , 1996). In severe cases when the patient has been unconscious for some time, brain damage can occur from lack of oxygen (ILO, 1983). Some symptoms of acute organophosphate poisoning, based upon experience with parathion, can persist for days to months. These include fatigue, ocular symptoms, EEG abnormalities, gastrointestinal complaints, excessive dreams, and intolerance to exposure to organophosphates (ILO, 1983).
- Delayed effects may be most pronounced with highly lipid-soluble phosphorothioates, such as dimethoate. After an initial period of apparent recovery, clinical effects may recur for up to several weeks after an acute exposure (Minton & Murray, 1988).
- In a case of dimethoate poisoning by subcutaneous injection, initial symptoms included dizziness, blurred vision, muscle fibrillations, abdominal cramps, and vomiting. Muscle fasciculations developed 16 hours later, together with pain and edema in the affected arm. Both serum and red blood cell cholinesterase levels were decreased and normalized very slowly. Other complications included metabolic acidosis, hyperthermia, leukocytosis, hypokalemia, sinus tachycardia, and elevated liver enzymes (Jovanovic et al, 1990). Adult respiratory distress syndrome (ARDS) and acute tubular necrosis developed in one case of fatal dimethoate overdose (Betrosian et al, 1995).
- Delayed toxicity can occur after exposure to dimethoate. Sudden collapse and death occurred 17 hours after apparent recovery in one case of dimethoate poisoning (Hayes & Laws, 1991). The mechanism for delayed onset or relapse may be a combination of its high lipid solubility and the requirement for metabolic activation.
- An "intermediate syndrome" has been described in patients who developed profound proximal muscle and cranial nerve weakness 1 to 4 days after dimethoate exposure and who had apparently recovered (Senanayake & Karalliedde, 1987; De Bleecker et al, 1992; De Bleecker et al, 1993).
- Some organophosphates can induce delayed neurological effects of a combined sensory-motor peripheral polyneuropathy. Sensation of numbness or tingling in the extremities may appear several weeks after acute exposure. It is not clear if all organophosphates have this activity (Cherniack, 1986; Wadia et al, 1987).
- Delayed neurotoxicity has been reported following acute human exposure to the closely related compound, omethoate (Curtes et al, 1981). Dimethoate was inactive in the standard atropinized hen assay for detecting delayed neurotoxicity, at a dose of 130 ppm in the diet for 4 weeks (Clayton & Clayton, 1994). Patients who developed an intermediate neurotoxicity syndrome from dimethoate overdose did not develop the classical delayed peripheral neuropathy (De Bleecker et al, 1993).
- Dimethoate poisoning has been associated with acute glaucoma (Francois & Verbraeken, 1977). This is unusual in that certain organophosphates are used in clinical practice to treat glaucoma (PDR, 1996).
- One case of acute pancreatitis has been reported following dermal exposure to dimethoate (Marsh et al, 1988). This may be related to the muscarinic effects of dimethoate, which are exerted through the parasympathetic nervous system on the exocrine glands. The possible contribution of excessive alcohol consumption was not taken into account in this case, however.
- Pulmonary aspiration of commercial organophosphate preparations which contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986).
- Di-methyl derivatives, such as dimethoate, produce a dimethylphosphorylated enzyme, which undergoes rapid spontaneous deactivation and/or "aging" by de-acylation; diethylphosphorylated enzyme is much slower to de-acylate (Johnson, 1989).
- The liver was the main site of distribution of (32P)-dimethoate and its derivatives after 24 hours in rats, but after 72 and 168 hours, the highest concentrations were in the skin and bones because of conversion to inorganic phosphate (Hayes & Laws, 1991).
- Pretreatment of rats with phenobarbital increased susceptibility to dimethoate (Hayes & Laws, 1991). This implies that dimethoate is activated by a cytochrome P450-dependent oxidative pathway.
- Phosphorothioates, such as dimethoate, must be metabolically activated by oxidation of the P=S bond to the phosphate form before producing toxicity; they therefore generally have a slower onset of toxic effects than do direct-acting organophosphate esters (Minton & Murray, 1988). The P=O derivatives of dimethoate may be up to 1,000 times more active than the parent compound for inhibition of human plasma cholinesterases (Hayes & Laws, 1991).
- Dimethoate is metabolized very rapidly in the liver to form at least four active metabolites (Sanderson & Edson, 1964; Hayes & Laws, 1991). One of the active species is thought to be dimethoxon, which is 75 to 100 times more potent than dimethoate in inhibiting rat brain cholinesterase (Hayes & Laws, 1991).
- Metabolites identified in rats after administration of (32)P-dimethoate included the monomethylphosphate, dimethylphosphate, thiophosphoric acid, dimethoate carboxylic acid, dimethylphosphorothioic acid, dimethoate carboxylic acid, and dimethylphosphorodithioic acid (Hassan, 1969).
- Urinary metabolites of dimethoate in mice included MeO(HS)P(O)SMe, MeO(HO)P(O)SMe, (MeO)(2)P(S)SMe, and (MeO)(2)P(O)SMe; these were shown to arise by S-methylation of the intermediate O,O-dialkyl phosphorodithoic acids in vivo, rather than from impurities (Mahajna et al, 1996).
CHRONIC CLINICAL EFFECTS
- In general, chronic exposure to organophosphate compounds can lead to cumulative depression of cholinesterase levels until a critical lack of activity causes symptoms of organophosphate poisoning to appear, in a pattern similar to that of acute poisoning (Coye et al, 1986). The level of chronic exposure which can be tolerated depends on the rate of uptake and degradation of the organophosphate in the body in relation to its potency in inhibiting acetylcholinesterase, and the rate of the individual's replenishment of acetylcholinesterase activity.
- An oral dose of 18 milligrams/day (approximately 0.26 milligram/kilogram/day) for 21 days did not inhibit cholinesterase in a human volunteer; an oral dose of 2.5 milligrams/day for 4 weeks had no effect in 20 human volunteers (Sanderson & Edson, 1964). The no-effect dose for cholinesterase inhibition in human volunteers was 15 mg/day for approximately 27 days (HSDB , 1996).
- Inhibition of cholinesterase was apparent with oral doses of 10 to 30 mg/day for 20 to 39 days; doses as high as 60 mg/day produced no apparent clinical effects (Hayes & Laws, 1991). Doses of 0.434 mg/kg/day or greater produced cholinesterase inhibition in humans after 20 days of oral exposure (HSDB , 1996; Edson et al, 1967). The no-effect dose was 0.2 mg/kg/day (Edson et al, 1967).
- Spraying applicators exposed for 12 days over a 2-week period did not have depressed cholinesterase levels following an estimated dermal dose of 176 to 8,100 mcg/cm(2)/day (Copplestone et al, 1976). An average reduction in plasma cholinesterase of 37.1% was seen in a group of greenhouse workers with mean dermal exposure to 914 mg/day and exposure by the respiratory route to 17 mg/day (Aljaghbir et al, 1992).
- Dermal sensitization has been reported with occupational exposure to dimethoate (Pambor & Bloch, 1985; Schena & Barba, 1992).
- No inhibition of cholinesterase was seen at a dose of 0.6 mg/kg/day in rats and 4 mg/kg/day in guinea pigs. The no-effect dietary dose in rats has been reported to be 1 to 32 ppm (Hayes & Laws, 1991). Cholinesterase inhibition was the only effect seen in rats given 5 milligrams/kilogram/day in the diet (Sanderson & Edson, 1964).
-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.
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). 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; reabsorb 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; reabsorb 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
-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.
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). 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; reabsorb 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; reabsorb 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
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
One man died after drinking approximately 200 milliliters of an unknown formulation of dimethoate, but a woman survived an entire 250-milliliter bottle of 20% concentration after aggressive emergency treatment (Hayes, 1982). The actual lethal dose of an organophosphate can vary widely and depends strongly on the route and rate of exposure and on the aggressiveness of the treatment used, as well as on pre-existing conditions in the individual.
MAXIMUM TOLERATED EXPOSURE
The lowest published toxic dose in man has been reported to range from 286 to 300 milligrams/kilogram by the oral route. Sensory effects, fasciculations, bradycardia, hypotension, and coma occurred (RTECS , 1988). Children may be more sensitive to organophosphates than adults (Zwiener & Ginsburg, 1988). An oral dose of 18 milligrams/day (approximately 0.26 milligram/kilogram/day) for 21 days did not inhibit cholinesterase in a human volunteer. An oral dose of 2.5 milligrams/day for 4 weeks had no effect in 20 human volunteers (Sanderson & Edson, 1964). Inhibition of cholinesterase was apparent from oral doses of 10 to 30 milligrams/day for 20 to 39 days, and doses as high as 60 milligrams/day produced no apparent clinical effects (Hayes, 1982). In general, the likelihood of poisoning varies with the inherent toxicity of the insecticide, but serious poisonings and deaths have occurred following environmental exposures to compounds presumed to have relatively low toxic potential (Baker et al, 1978; Dunphy et al, 1980).
The World Health Organization (WHO) has classified dimethoate, technical grade, as moderately hazardous (class II) as a pesticide (World Health Organization, 2006).
In a team of 12 men spraying and mixing dimethoate for 12 days over a 2-week period in the Sudan, whole blood cholinesterase was not depressed relative to pre-exposure levels. They had not been spraying for 2 weeks prior to the first cholinesterase determination. Greatest exposure occurred on the lower leg (approximately 1 microgram/square centimeter). Total calculated dermal exposure per day ranged from 176 to 8,100 micrograms/square centimeter, and respiratory exposure was 5 to 29 micrograms/day. Exposures were estimated by gas chromatography of benzene extracts from cellulose pads worn at various places on the clothing and body. Under these conditions of exposure, the applicators did not exhibit signs of organophosphate poisoning (Copplestone et al, 1976). While results of field studies are necessarily subject to some variability, this study did use concurrent controls of unexposed persons (the two field supervisors) and also corrected for recovery of the dimethoate from the sampling pads. The latter is especially important because of the relative lability of dimethoate.
Six workers were monitored for dermal and respiratory exposure to dimethoate during spraying of tomatoes in a green house. The mean dermal exposure was 914 mg/day and the mean respiratory exposure was 17 mg/day. These exposures resulted in a 37.1 percent reduction in plasma cholinesterase in the workmen, a value which exceeds the limits set by WHO (Aljaghbir et al, 1992).
No cholinesterase inhibition occurred in rats given a cumulative dose of 0.6 milligram/kilogram/day of dimethoate; the no-effect dose for guinea pigs was 4 milligrams/kilogram/day. No inhibition was seen in rats given 0.5 milligram/kilogram/day in the diet. Cholinesterase inhibition was the only effect seen in rats given 5 milligrams/kilogram/day in the diet (Sanderson & Edson, 1964). The no-effect dietary dose in rats has been reported to be 1 to 32 ppm (Hayes, 1982). The no-effect dietary dose for inhibition of erythrocyte and plasma cholinesterase in dogs was 10 and 50 ppm respectively (Hayes, 1982).
- Carcinogenicity Ratings for CAS60-51-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Dimethoate IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS60-51-5 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 2x10(-4) mg/kg-day
Inhalation: Drinking Water:
References: RTECS, 1991 Budavari & O'Neil, 1989; Hayes, 1982 HSDB, 1991 LD50- (ORAL)CAT: LD50- (ORAL)CHICKEN: LD50- (ORAL)DOG: LD50- (INTRAPERITONEAL)GUINEA_PIG: LD50- (ORAL)GUINEA_PIG: LD50- (INTRAPERITONEAL)HAMSTER: LD50- (ORAL)HAMSTER: LD50- (SUBCUTANEOUS)HAMSTER: LD50- (ORAL)HUMAN: LD50- (INTRAPERITONEAL)MOUSE: LD50- (ORAL)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: LD50- (ORAL)RABBIT: LD50- (SKIN)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (INTRAVENOUS)RAT: LD50- (ORAL)RAT: LD50- (SKIN)RAT: LD50- (SUBCUTANEOUS)RAT:
CALCULATIONS
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS60-51-5 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS60-51-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS60-51-5 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS60-51-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS60-51-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS60-51-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Phosphorodithioic acid, O,O-dimethyl S-[2(methylamino)-2-oxoethyl] ester Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Dimethoate Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS60-51-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS60-51-5 (U.S. Environmental Protection Agency, 2010b):
Listed as: Dimethoate P or U series number: P044 Footnote: Listed as: Phosphorodithioic acid, O,O-dimethyl S-[2-(methylamino)-2-oxoethyl] ester P or U series number: P044 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS60-51-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Dimethoate Reportable Quantity, in pounds: 10 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS60-51-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS60-51-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS60-51-5 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS60-51-5 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Patients 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 patient 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 patient's clothing should be placed in a sealed plastic bag to prevent further contamination and disposed of as hazardous waste. 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. If medical personnel are accidentally exposed, decontamination procedures as outlined in the DERMAL EXPOSURE section, should be followed.
STORAGE
Store in sealed original containers, in well-aired, fresh and dry storehouses or in shaded and possibly well-aired places (HSDB , 1991).
- ROOM/CABINET RECOMMENDATIONS
Chemical formulations must be stored above 45 degrees F, and temperature should not exceed 25 to 30 degrees C (HSDB , 1991). Storage areas must be located at suitable distance from inhabited buildings, animal shelters, and food stores; moreover, they must be inaccessible to unauthorized persons, children and domestic animals (HSDB , 1991).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Wear full protective clothing when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
- First responders, emergency medical, and emergency department personnel should take proper precautions (wear rubber gowns, rubber aprons, rubber gloves, etc) when treating patients with organophosphate poisoning to avoid contamination. Emesis containing organophosphates should be placed in closed impervious containers for proper disposal.
- DECONTAMINATION: Remove contaminated clothing. Wash the skin, including the hair, beneath the nails, groin, and umbilical area, three times.
A single washing with soap and water can remove up to 80 to 92 percent of an organophosphate on the skin if done immediately (Fredriksson, 1961). If delayed, the same procedure may remove only 50 to 70 percent. Following a soap and water wash, a second wash with 95 percent ethanol will leave only about a 5 to 10 percent organophosphate residue (Fredriksson, 1961). The best results of skin decontamination are achieved with a thorough soap and water wash, followed by a 95 percent ethanol wash, followed by a second soap and water wash (Fredriksson, 1961). Tincture of green soap contains 30 percent ethanol, and has been recommended for dermal decontamination of organophosphate exposures.
- LEATHER: Leather absorbs organophosphates and is extremely difficult to decontaminate. Rescuers should not wear leather items that are not completely covered by rubber or impervious plastic. Contaminated leather items may need to be disposed of by incineration.
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 60-51-5.
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004) Combustible material: may burn but does not ignite readily. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form.
When heated to decomposition, dimethoate releases highly toxic fumes of oxides of carbon, nitrogen, phosphorus, and sulfur (Sax & Lewis, 1989).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS60-51-5 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- 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 CAS60-51-5 (NFPA, 2002):
- Choose an extinguishing agent suitable for fires in surrounding material (AAR, 1987).
- Water may be used in flooding quantities as fog (AAR, 1987).
When heated to decomposition, dimethoate releases highly toxic fumes of oxides of carbon, nitrogen, phosphorus, and sulfur (Sax & Lewis, 1989).
DUST/VAPOR HAZARD
- When heated to decomposition, dimethoate releases highly toxic fumes of oxides of carbon, nitrogen, phosphorus, and sulfur (Sax & Lewis, 1989).
REACTIVITY HAZARD
- When heated to decomposition, dimethoate releases highly toxic fumes of oxides of carbon, nitrogen, phosphorus, and sulfur (Sax & Lewis, 1989).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 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: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas.
- 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 CAS60-51-5 (AIHA, 2006):
- DOE TEEL Values for CAS60-51-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Dimethoate TEEL-0 (units = mg/m3): 6 TEEL-1 (units = mg/m3): 15 TEEL-2 (units = mg/m3): 30 TEEL-3 (units = mg/m3): 30 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 CAS60-51-5 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS60-51-5 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
DECONTAMINATION OF SPILLS A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975a). 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, 1975b). Alternatively, the material can be inactivated with strong detergent (Ford, 1989). 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. Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding decontamination of spills.
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies, and reporting may be required. Water spray may be used to reduce or knock down vapors (AAR, 1987).
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, 1975b). Scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R), or similar material. Re-absorb scrubbing liquid and dispose as above (Ford, 1989). Several washes may be required for decontamination (EPA, 1978).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and approved personal protection equipment. Get fire-fighting equipment ready (Ford, 1989). Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime, lime or lime water when in dilute solutions), and calcium carbonate (crushed limestone) may be used for detoxification (EPA, 1975a). 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, 1975b). After the bulk of the material has been removed, further decontaminate spoiled surfaces with alkaline treatment as described above, or with concentrated alkaline detergent. Absorb and dispose of waste water as described above. Water spray may be used to reduce or knock down vapors (AAR, 1987). Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies, and reporting may be required. Consult the local Emergency Response Committee for guidance.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Release of dimethoate to the environment will result from its production and use as a contact and systemic insecticide. The USEPA has cancelled the registration of dust formulations of dimethoate and prohibits its application without the use of personal protective equipment (HSDB, 2003).
ENVIRONMENTAL FATE AND KINETICS
OTHER Terrestrial Fate: If dimethoate is released to the soil, it will not adsorb to the soil and will be subject to considerable leaching (HSDB , 1991). Terrestrial Fate: It should not be susceptible to hydrolysis in soils (HSDB , 1991). Terrestrial Fate: Biodegradation may be an important fate process with 77 percent degradation reported in clay loam soil in 2 weeks compared to 18 and 20 percent degradation in the same soil that had been autoclaved or irradiated (HSDB , 1991). Terrestrial Fate: Soil half-lives ranging from 2.5 to 16 days have been reported (HSDB , 1991). Aquatic Fate: If released to water, dimethoate will not be expected to sorb to sediment, to hydrolyze, or to bioconcentrate in aquatic organisms (HSDB , 1991). Aquatic Fate: Direct photolysis and evaporation from water are not expected to be important processes (HSDB , 1991). It may be subject to biodegradation based on a half-life of 8 weeks in raw river water (Eichelberger & Litchtenberg, 1971). Atmospheric Fate: If dimethoate is released to the atmosphere, it may be subject to oxidation (HSDB , 1991). Atmospheric Fate: The estimated vapor phase half-life in the atmosphere is 2.83 days as a result of H atom abstraction by photochemically produced hydroxyl radicals (HSDB , 1991).
ENVIRONMENTAL TOXICITY
- Published Values (HSDB , 1991)
1. LC50 GAMMARUS LACUSTRIS: 0.20 mg/l/96h 2. LC50 PTERONARCYS: 0.043 mg/l/96h 3. LC50 RAINBOW TROUT: 6.2 mg/l/96h 4. LC50 BLUEGILL: 6.0 mg/l/96h 5. LC50 JAPANESE QUAIL: 346 mg/l 5-day diet 6. LC50 RING-NECKED PHEASANT: 332 mg/l 5-day diet 7. LC50 MALLARD DUCK: 1011 mg/l in 5-day diet 8. LD50 (ORAL) REDWINGED BLACKBIRD: 6.60-17.8 mg/kg 9. LD50 (ORAL) STARLING: 31.6 mg/kg 10. LD50 (ORAL) PHEASANT: 15 mg/kg 11. LD50 (ORAL) SPARROW: 22 mg/kg 12. LD50 (ORAL) BLACKBIRD: 26 mg/kg 13. LC50 MOSQUITO FISH: 40-60 mg/l 14. LD50 HONEY BEE: 0.9 mcg/bee 15. LC50 RAINBOW TROUT: 58.0 mg/l/24h 16. LC50 CARP: 22.39 mg/l/168h 17. LD50 (ORAL) MALLARD DUCK (MALE): 41.7 mg/kg 18. LD50 (ORAL) MALLARD DUCK (FEMALE): 63.5 mg/kg
- The effect of dimethoate, sprayed on farmlands, was studied for several weeks on three species of endogenous birds. The birds studied were Savannah Sparrow, Song Sparrow, and America Finch. Sampled birds were treated with 0.24 grams of dimethoate per square meter of seeds given on the morning of the 16 days of the study. The results show the birds to be temporarily intoxicated, losing some of their motor skills. This is a dangerous condition, since it inhibits the ability of the birds to find food and render them more vulnerable to predators (Brunet & Cyr, 1992).
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Dimethoate occurs as colorless crystals with a camphor-like odor (Hayes, 1982).
VAPOR PRESSURE
- 8.5x10(-6) mmHg (at 25 degrees C) (Worthing & Walker, 1983)
- 1.1 mPa (at 25 degrees C) (Hartley & Kidd, 1987)
- Because of its low vapor pressure, the vapor hazard of dimethoate is minimal (Sanderson & Edson, 1964).
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
SOLID: 1.277 g/cm(3) (at 65 degrees C) (Budavari, 1989) SOLID: 1.281 g/cm(3) (at 50 degrees C) (Hayes, 1982)
FREEZING/MELTING POINT
51-52.5 degrees C; 125 degrees F (Budavari, 1989; EPA, 1985) 45-47 degrees C; 113-117 degrees F (technical product) (EPA, 1985)
BOILING POINT
- 117 degrees C (at 0.1 mmHg) (Hartley & Kidd, 1987)
FLASH POINT
- 130-132 degrees C (Clayton & Clayton, 1982)
SOLUBILITY
very slightly soluble in water (Budavari, 1989) > 5000 mg/L (HSDB , 1991) 25,000 ppm (Kenaga, 1980) 2-3% (Spencer, 1982)
soluble in most organic solvents, except saturated hydrocarbons (Budavari, 1989) ACETONE: very soluble (Sunshine, 1969) AROMATIC HYDROCARBONS: slightly soluble (Sunshine, 1969) CHLOROFORM: very soluble (Sunshine, 1969) CYCLOHEXANONE: soluble (Spencer, 1982) DIETHYL ETHER: slightly soluble (Sunshine, 1969) ETHANOL: very soluble (Sunshine, 1969) HEXANE: slightly soluble (Spencer, 1982) METHANOL: soluble (Spencer, 1982) PETROLEUM ETHER: insoluble (Sunshine, 1969) XYLENE: slightly soluble (Spencer, 1982)
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 0.05 (HSDB , 1991)
HENRY'S CONSTANT
- 1.0x10(-10) atm-m(3)/mol (Ehrenfeld et al, 1986)
SPECTRAL CONSTANTS
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