LEPTOPHOS
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
LEPTOPHOS ABAR (VELSICOL) O-(4-BROMO-2,5-DICHLOROPHENYL) O-METHYL PHENYLPHOSPHONOTHIOATE O-(2,5-DICHLORO-4-BROMOPHENYL) O-METHYL PHENYLTHIOPHOSPHONATE FOSVEL K62-105 LEPTON MBCP O-METHYL-O-(4-BROMO-2,5-DICHLOROPHENYL)PHENYL THIOPHOSPHONATE O-METHYL O-2,5-DICHLORO-4-BROMOPHENYL PHENYLTHIOPHOSPHONATE NK 711 OLEOPHOSVEL OMS 1438 PHENYLPHOSPHONOTHIOIC ACID O-(4-BROMO-2,5- DICHLOROPHENYL) O-METHYL ESTER PHOSPHONOTHIOIC ACID, PHENYL-, O-(4-BROMO-2,5- DICHLOROPHENYL) O-METHYL ESTER PHOSVEL PSL V.C.S. VCS 5-D VCS-506 VELSICOL 506 VELSICOL VCS 506 VVS-506
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
- (EPA, 1985; HSDB , 1990; RTECS , 1990)
USES/FORMS/SOURCES
Leptophos is used internationally on cotton, certain vegetables, and tobacco, but has been denied registration as a pesticide in the USA (EPA, 1985; Lewis, 1996; Budavari, 1996; HSDB , 2000; Whitacre et al, 1976).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- The following are symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for leptophos, but could potentially occur in individual cases.
- USES: Leptophos is an organophosphate insecticide used internationally on cotton, certain vegetables, and tobacco, but has been denied registration as a pesticide in the USA.
- 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 develop.
- EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. This particular organophosphate is considered obsolete by the WHO; exposure is rare.
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 several patients following exposure to leptophos. 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 (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
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 develop. EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. This particular organophosphate is considered obsolete by the WHO; exposure is rare. The following are symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for leptophos, but could potentially occur in individual cases. 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 several patients following exposure to leptophos. 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 (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.
METABOLIC ACIDOSIS: Metabolic acidosis has occurred in several cases of severe poisoning (Hui, 1983; Meller et al, 1981; Moore & James, 1981).
Bradycardia and hypotension occur following moderate to severe poisoning (Ganendran, 1974). A heart rate of less than 60 beats/min occurred in 21% of patients and hypotension (systolic blood pressure less than 9 mmHg) occurred in 20% of patients in one study (Bardin et al, 1987). Hypertension can occur as a nicotinic effect of organophosphate poisoning (Lund & Monteagudo, 1986). TACHYCARDIA: Tachycardia is also common (Zwiener & Ginsburg, 1988a). A heart rate of greater than 100 beats/min was reported in 49% of patients in one study (Bardin et al, 1987). DYSRHYTHMIAS: Cardiac dysrhythmias and conduction defects have been reported in patients with severe organophosphate poisoning (Wren et al, 1981; Kiss & Fazekas, 1982; Chhabra & Sepaha, 1970). ECG abnormalities may include sinus bradycardia, A-V dissociation, idioventricular rhythms, multiform premature ventricular extrasystoles, polymorphic ventricular tachycardia, prolongation of the PR, QRS, and QT intervals, and Torsades de pointes polymorphous ventricular dysrhythmias (Brill et al, 1984; Ludomirsky et al, 1982). MYOCARDITIS: Occurrence of a protracted toxic myocarditis has been suspected (Wren et al, 1981; Kiss & Fazekas, 1982; Chhabra & Sepaha, 1970).
SWEATING: Sweating is a consistent but not universal sign, and profuse sweating may occur as one of the muscarinic signs of organophosphate poisoning (Ganendran, 1974). Sweating was present in 23% of patients in one study (Bardin et al, 1987). DERMATITIS: Dermal sensitization may occur (Milby et al, 1964), and leptophos has caused allergic contact dermatitis (Matshushita et al, 1985).
Nausea, vomiting, diarrhea, abdominal cramps and hypersalivation are common muscarinic signs of organophosphate poisoning. Vomiting and diarrhea occurred in 38% and 21% of patients, respectively, in one study (Bardin et al, 1987). FECAL INCONTINENCE: Fecal incontinence occurs in severe poisoning (Hayes, 1965). PANCREATITIS: Acute pancreatitis has been reported following the ingestion of parathion, malathion, difonate, coumafos, diazanon, and mevinphos and also following dermal exposure to dimethoate. This is postulated to be due to excessive cholinergic stimulation of the pancreas and the occurrence of ductal hypertension (Hsiao et al, 1996). SALIVATION: Salivation commonly occurs. More than 50% of patients in one study had excessive salivation (Bardin et al, 1987).
URINARY INCONTINENCE: Involuntary urination occurs in the more severe poisonings (Done, 1979). Immune-complex nephropathy with proteinuria may have occurred in one case of malathion poisoning. Amorphous crystalluria with decreased urine output were associated with one case of diazinon poisoning; no serum creatinine or BUN abnormalities were seen (Albright et al, 1983; Wedin et al, 1984).
Miosis, lacrimation, and blurred vision are common, and mydriasis may occur in severe poisonings (Bardin et al, 1987; Milby, 1971; Whorton & Obrinsky, 1983; Dixon, 1957). Severely poisoned individuals may exhibit mydriasis (Dixon, 1957).
CHOLINESTERASE DEFICIENCY: The hallmark of organophosphate poisoning is the inhibition of plasma pseudocholinesterase or erythrocyte acetylcholinesterase, or both (Namba, 1972). HEMORRHAGE: Tendency to bleeding, probably related to platelet dysfunction, may occur (Ziemen, 1984).
ALLERGIC CONTACT DERMATITIS: Chronic skin exposure to some organophosphates may lead to dermal sensitization (Milby et al, 1964; Coye, 1984). Leptophos has caused allergic contact dermatitis (Matshushita et al, 1985).
MUSCLE WEAKNESS: Muscle weakness, fatigability and fasciculations occur commonly. Fasciculations were present in 33/61 patients (54%) in one study (Bardin et al, 1987). PARALYSIS: Muscle paralysis occasionally supervenes (Done, 1979). A case of paralysis of the diaphragm has occurred in a person who ingested malathion; full recovery required 9 months (Rivett & Potgieter, 1987).
Headache, dizziness, muscle spasms and profound weakness are common. The earliest manifestations of poisoning are often: giddiness, uneasiness, restlessness, anxiety and tremulousness (Grob & Garlick, 1950). Alterations of level of consciousness, anxiety, paralysis, seizures and coma may occur. Seizures may be an early symptoms after a significant exposure. Seizures may be more common in children (Joy, 1982; Zwiener & Ginsburg, 1988a). ATAXIA: Initial central nervous system effects are commonly followed by headache, ataxia, drowsiness, difficulty concentrating, mental confusion, and slurred speech (Grob & Garlick, 1950). COMA: In severe poisoning, coma supervenes, rarely followed by generalized convulsions (Grob & Garlick, 1950). PARALYSIS: Paralytic symptoms can occur in patients with organophosphate poisoning (Wadia et al, 1987; Rivett & Potgieter, 1987). Severe cases progress to complete paralysis, impaired respiration and death. The nerve damage of organophosphate-induced delayed neuropathy is frequently permanent. Mechanism appears to involve phosphorylation of esterases in peripheral nervous tissue (Johnson, 1975). PERIPHERAL NEUROPATHY: Leptophos is known to cause peripheral neuropathy in humans (HSDB , 2000) and is positive in the hen assay system (Abdelsalam, 1999). Peripheral neuropathy of the mixed sensory-motor type may be delayed by 6 to 21 days following exposure to some organophosphates. Recovery may be slow and takes weeks to months and may be incomplete (Done, 1979). Dyskinesias may develop. Choreoathetosis (involuntary movements) have been observed (Joubert et al, 1984) along with choreiform dyskinesias (Joubert & Joubert, 1988) and opisthotonos (a type of spasm) (Smith, 1977).
PSYCHOSIS: Psychosis may be noted following acute poisoning (Gershon & Shaw, 1961; Conyers & Goldsmith, 1971; Joubert & Joubert, 1988). Organophosphates may exacerbate psychotic symptoms in persons with pre-existing schizophrenic tendencies; it is not clear if these symptoms can be induced by organophosphates in the absence of pre-existing abnormality (Levin & Rodnitzky, 1976). CONFUSION: Acute or chronic exposure to organophosphates may impair concentration, induce confusion, lead to slurred speech and drowsiness. Use may lead to slowness of thoughts (Levin & Rodnitzky, 1976). AMNESIA: Impaired memory is a major CNS effect of organophosphate exposure and may occur in the absence of other overt clinical signs; it has been found in workers chronically exposed to organophosphates (Levin & Rodnitzky, 1976). DEPRESSION: Depression, correlated with the severity of cholinesterase inhibition, has occurred in cases of acute organophosphate poisoning; this finding is consistent with the theory of affective disorders being the result of cholinergic predominance in the central nervous system (Levin & Rodnitzky, 1976).
Dyspnea, rales, bronchorrhea, bronchospasm, or tachypnea may be noted in moderately severe organophosphate poisonings (Lund & Monteagudo, 1986; Bardin et al, 1987; Hayes, 1965). Acute lung injury may occur in severe cases (Chhabra & Sepaha, 1970). Bronchospasm may be an effect of the muscarinic activity of organophosphates (Lund & Monteagudo, 1986). HYPERVENTILATION: A respiratory rate greater than 30 breaths/min was reported in 39% of patients in one study (Bardin et al, 1987). RESPIRATORY FAILURE: Acute respiratory insufficiency, due to any combination of depression of the respiratory center, respiratory paralysis, bronchospasm or increased bronchial secretions, is the main cause of death in many acute organophosphate poisonings (Lerman & Gutman, 1988; Anon, 1984). PNEUMONITIS: Aspiration of commercial organophosphate preparations which contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986). Leptophos releases toxic and irritating fumes of bromide, chloride, oxides of phosphorus, and oxides of sulfur when heated to decomposition (Lewis, 1996). Inhalation exposure to such fumes may lead to respiratory tract irritation with possible chemical pneumonitis or acute lung injury.
CHRONIC CLINICAL EFFECTS
- Peripheral polyneuropathy has been described in chronically exposed leptophos manufacturing workers (HSDB , 2000). Leptophos has caused allergic contact dermatitis (Matshushita et al, 1985).
- In general, chronic exposure to organophosphates can lead to cumulative depression of cholinesterase levels until a critical lack of activity causes symptoms of organophosphate poisoning to appear, in a pattern similar to that of acute poisoning (Coye et al, 1986). The level of chronic exposure which can be tolerated depends on the rate of uptake and degradation of the organophosphate in the body in relation to its potency in inhibiting acetylcholinesterase, and the rate of the individual's replenishment of acetylcholinesterase activity.
- Chronic and subchronic leptophos exposure has resulted in delayed peripheral neuropathy in chickens (Abou-Donia & Preissig, 1976; Abou-Donia & Graham, 1979).
- No adverse immunologic effects were seen in mice fed doses of leptophos up to 170 mg/kg daily for 12 weeks (Koller et al, 1976).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
Universal precautions should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids. Vomiting containing organophosphates should be placed in a closed impervious container for proper disposal.
- DECONTAMINATION OF SPILLS/SUMMARY
A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a). NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).
Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 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, 1978a). Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 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, 1978a). Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination. NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.
FURTHER CONTACT INFORMATION For further information contact the National Pesticide Telecommunications Network at 1-800-858-7378 or contact on the web at http://nptn.orst.edu. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378. The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675. CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.
-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.
ORAL EXPOSURE DERMAL EXPOSURE EYE EXPOSURE INHALATION EXPOSURE PERSONNEL PROTECTION Universal precautions should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids. Vomiting containing organophosphates should be placed in a closed impervious container for proper disposal.
DECONTAMINATION OF SPILLS/SUMMARY A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a). NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).
Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 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, 1978a). Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 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, 1978a). Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination. NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.
FURTHER CONTACT INFORMATION For further information contact the National Pesticide Telecommunications Network at 1-800-858-7378 or contact on the web at http://nptn.orst.edu. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378. The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675. CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.
ANTIDOTES
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
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. Leptophos has a partition coefficient on the order of 2 million when partitioned between octanoland water. Prolonged toxic effects of this chemical would be expected on the basis of deposition in fat (Davies et al, 1975).
MAXIMUM TOLERATED EXPOSURE
- Leptophos is not included in the World Health Organization (WHO) classification and believed to be obsolete as pesticide (World Health Organization, 2006).
Note that CHILDREN MAY EXHIBIT DIFFERENT PREDOMINANT SIGNS of organophosphate poisoning from adults. In a study on 25 children poisoned by organophosphate or carbamate compounds, the major symptoms in most of them were CNS depression, stupor, flaccidity, dyspnea, and coma. Other classical signs of organophosphate poisoning, such as miosis, fasciculations, bradycardia, excessive salivation and lacrimation, and gastrointestinal symptoms, were infrequent (Sofer et al, 1989). Children tend to be more sensitive to organophosphates than adults (Zwiener & Ginsburg, 1988).
Delayed neuropathy produced by Leptophos, an organophosphate pesticide, investigations by the Environmental Protection Agency (EPA), and foreign poisonings attributed to its action are reviewed. Delayed neurotoxicity is discussed. Delayed neurotoxins are not only capable of producing immediate and reversible cholinergic distress like other organophosphate pesticides, but also of producing permanent paralysis which does not appear until 2 to 3 weeks after exposure (Shea, 1977).
- Carcinogenicity Ratings for CAS21609-90-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): Not Listed IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS21609-90-5 (U.S. Environmental Protection Agency, 2011):
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS21609-90-5 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS21609-90-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS21609-90-5 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS21609-90-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS21609-90-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS21609-90-5 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS21609-90-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS21609-90-5 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS21609-90-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Leptophos Reportable Quantity, in pounds: 500 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS21609-90-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS21609-90-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS21609-90-5 (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 CAS21609-90-5 (NFPA, 2002):
-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
- Wear a self-contained positive pressure breathing apparatus when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 21609-90-5.
-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.
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS21609-90-5 (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 CAS21609-90-5 (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, leptophos releases toxic fumes of oxides of sulfur, phosphorus, and gaseous ions of chloride and bromide (Sax & Lewis, 1989).
DUST/VAPOR HAZARD
- When heated to decomposition, leptophos releases toxic fumes of oxides of sulfur, phosphorus, and gaseous ions of chloride and bromide (Sax & Lewis, 1989).
REACTIVITY HAZARD
- When heated to decomposition, leptophos releases toxic fumes of oxides of sulfur, phosphorus, and gaseous ions of chloride and bromide (Lewis, 1996).
- Most organophosphate pesticides degrade relatively rapidly in the environment; a notable exception is LEPTOPHOS, which is lipophilic (Abou-Donia, 1983).
Leptophos degrades in the presence of light to form desbromoleptophos and leptophos oxon, which are each two- to three times MORE NEUROTOXIC than the parent compound (Sanborn et al, 1977; Abou-Donia, 1979; Abou-Donia et al, 1980).
- All organophosphate esters undergo hydrolysis in water; generally the water-soluble products of hydrolysis are less toxic than the parent compound (Minton & Murray, 1988).
EVACUATION PROCEDURES
- 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 CAS21609-90-5 (AIHA, 2006):
- DOE TEEL Values for CAS21609-90-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Leptophos; (Fosvel) 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 CAS21609-90-5 (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 CAS21609-90-5 (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, 1975a; (EPA, 1978). 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, 1975). 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 disposible containers (EPA, 1975; Ford, 1989). Scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R), or similar material. Re-absorb scrubbing liquid and dispose as above (Ford, 1989). Several washes may be required for decontamination (EPA, 1978).
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 disposible containers (EPA, 1975; Ford, 1989). Containers should be sealed to prevent further decontamination. After the bulk of the material has been removed, further decontaminate spoiled surfaces with alkaline treatment as described above, or with concentrated alkaline detergent. Absorb and dispose of waste water as described above. Water spray may be used to reduce or knock down vapors (AAR,1987). Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. Consult the local Emergency Response Committee for guidance.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- During its' use as an insecticide, leptophos has been released to the environment (HSDB, 2003).
ENVIRONMENTAL FATE AND KINETICS
ENVIRONMENTAL TOXICITY
- References: (HSDB , 1990)
LC50 - CUTTROAT TROUT: 5.3 mcg/L for 96H -- 10 deg C LC50 - RAINBOW TROUT: 20 mcg/L for 96H -- 20 deg C LC50 - PROCAMBARUS: > 7000 mcg/L for 96H -- 12 deg C LC50 - LAKE TROUT: 30 mcg/L for 96H -- 12 deg C LC50 - FATHEAD MINNOW: > 30,000 mcg/L for 96H -- 5 deg C LC50 - BLUEGILL: 22 mcg/L for 96H -- 5 deg C LC50 - RAINBOW TROUT: 35 mcg/L for 96H -- 12 deg C LC50 - (ORAL) JAPANESE QUAIL: 1500 ppm LC50 - (ORAL) RING-NECKED PHEASANT: 1075 ppm LC50 - (ORAL) MALLARD DUCKS: 1635 ppm
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Leptophos is a whitish, crystalline powder or colorless, amorphous solid material; the technical grade product is a light tan, waxy powder solid (EPA, 1985; Budavari, 1996; HSDB , 2000).
DENSITY
- NORMAL TEMPERATURE AND PRESSURE
FREEZING/MELTING POINT
70.2-70.6 degrees C; 258-159 degrees F (Worthing, 1979) Technical product: 55-67 degrees C (Budavari, 1989)
SOLUBILITY
Soluble in xylene (Spencer, 1982) 470 g/L in acetone (Worthing, 1979) 1.3 kg/L benzene (Worthing, 1979) 142 g/L in cyclohexane (Worthing, 1979) 59 g/L in heptane (Worthing, 1979) 24 g/L in 2-propanol (Worthing, 1979)
-REFERENCES
GENERAL BIBLIOGRAPHY- 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
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- 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
- 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
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- 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
- 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
- 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
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- Product Information: DUODOTE(TM) IM injection, atropine, pralidoxime chloride IM injection. Meridian Medical Technologies,Inc, Columbia, MD, 2006.
- Product Information: DUONEB(R) inhalation solution, ipratropium bromide albuterol sulfate inhalation solution. Dey, Napa, CA, 2005.
- Product Information: DuoDote(R) intramuscular injection solution, atropine and pralidoxime chloride intramuscular injection solution. Meridian Medical Technologies(TM), Inc. (per Manufacturer), Columbia, MD, 2011.
- Product Information: Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, isoproterenol HCl intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection. Hospira, Inc. (per FDA), Lake Forest, IL, 2013.
- Product Information: PRALIDOXIME CHLORIDE intramuscular injection, pralidoxime chloride intramuscular injection. Meridian Medical Technologies, Inc. (per DailyMed), Columbia, MD, 2003.
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