MALATHION
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
Lice Care Lice Rid Malathion Lotion USP CAS 121-75-5 1,2-Di(ethoxycarbonyl)ethyl O,O-dimethyl phosphorodithioate American Cyanamid 4,049 Carbethoxy malathion Carbetovur Carbetox Carbofos Carbophos Chemathion Cimexan Compound 4049 Cythion Detmol MA Detmol MA 96% Dicarboethoxyethyl O,O-dimethyl phosphorodithioate Diethyl (dimethoxyphosphionthioylthio) butanedioate Diethyl (dimethoxyphosphinothioylthio) succinate Diethyl mercaptosuccinate S-ester with O,O dimethylphosphorodithioate Diethyl mercaptosuccinate, O,O-dimethyl phosphorodithioate Diethyl mercaptosuccinic acid O,O-dimethyl phosphorodithioate EL 4049 Emmatos Emmatos Extra ENT 17,034 Ethiolacar Etiol Experimental insecticide 4049 Extermathion Forthion Fosfothion Fosfotion Fosfotion 550 Fyfanon Hilthion Hilthion 25 WDP Karbofos Kop-thion Kypfos Latka 4049 (Czech) Malacide Malafor Malagran Malakill Malamar Malamar 50 Malaphele Malaphos Malasol Malaspray Malatol Malatox Maldison Malmed Malphos Mercaptosuccinic acid diethyl ester Mercaptothion Moscarda O,O-dimethyl S-(1,2-bis(ethoxycaronyl)ethyl)dithiophoshate O,O-dimethyl S-(1,2-dicarbethoxyethyl) dithiophosphate O,O-dimethyl S-(1,2-dicarbethoxyethyl) thiothionophosphate O,O-dimethyl S-(1,2-dicarbethoxyethyl) phosphorodithioate Oleophosphothion Ortho malathion Phosphothion Prentox malathion 95% spray Prioderm Sadofos Sadophos SF 60 Siptox I Sumitox TAK TM-4049 Vegfru Malatox Vetiol Zithiol (RTECS, 2006)
Lice Care Lice Rid Malathion Lotion USP CAS 121-75-5
1,2-Di(ethoxycarbonyl)ethyl O,O-dimethyl phosphorodithioate American Cyanamid 4,049 Carbethoxy malathion Carbetovur Carbetox Carbofos Carbophos Chemathion Cimexan Compound 4049 Cythion Detmol MA Detmol MA 96% Dicarboethoxyethyl O,O-dimethyl phosphorodithioate Diethyl (dimethoxyphosphionthioylthio) butanedioate Diethyl (dimethoxyphosphinothioylthio) succinate Diethyl mercaptosuccinate S-ester with O,O dimethylphosphorodithioate Diethyl mercaptosuccinate, O,O-dimethyl phosphorodithioate Diethyl mercaptosuccinic acid O,O-dimethyl phosphorodithioate EL 4049 Emmatos Emmatos Extra ENT 17,034 Ethiolacar Etiol Experimental insecticide 4049 Extermathion Forthion Fosfothion Fosfotion Fosfotion 550 Fyfanon Hilthion Hilthion 25 WDP Karbofos Kop-thion Kypfos Latka 4049 (Czech) Malacide Malafor Malagran Malakill Malamar Malamar 50 Malaphele Malaphos Malasol Malaspray Malatol Malatox Maldison Malmed Malphos Mercaptosuccinic acid diethyl ester Mercaptothion Moscarda O,O-dimethyl S-(1,2-bis(ethoxycaronyl)ethyl)dithiophoshate O,O-dimethyl S-(1,2-dicarbethoxyethyl) dithiophosphate O,O-dimethyl S-(1,2-dicarbethoxyethyl) thiothionophosphate O,O-dimethyl S-(1,2-dicarbethoxyethyl) phosphorodithioate Oleophosphothion Ortho malathion Phosphothion Prentox malathion 95% spray Prioderm Sadofos Sadophos SF 60 Siptox I Sumitox TAK TM-4049 Vegfru Malatox Vetiol Zithiol (RTECS, 2006)
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.
BEILSTEIN HANDBOOK REFERENCE:4-03-00-01136 BEILSTEIN REFERENCE NUMBER:1804525 EPA PESTICIDE CHEMICAL CODE:057701 STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:51631
USES/FORMS/SOURCES
Malathion is a nonsystemic acaracide and insecticide and is considered the least toxic of the organophosphates. It is used for the control of mosquitoes, flies, and spiders on fruits, vegetables, and ornamental plants, as well as for animal ectoparasites (Baselt, 2000a; Bingham et al, 2001a; Lewis, 1997a; Sittig, 1991a; Hartley & Kidd, 1990a). Malathion is also used in the treatment of pediculus humanus capitis (head lice and their ova) infections of the scalp hair. It is able to kill nits at all stages of parasitic development and molting (Prod Info OVIDE(R) topical lotion, 2005; Meinking et al, 2004).
THERAPEUTIC USE - The lotion is supplied in bottles of 2 ounces and contains 0.5% malathion. Each bottle contains 0.005 g of malathion per mL in a vehicle of isopropyl alcohol (78%), terpineol, dipentene, and pine needle oil (Prod Info OVIDE(R) topical lotion, 2005). INSECTICIDE - It is sold as a 99.6% technical grade liquid. Other available formulations include emulsifiable concentrates, wettable powders, dusts, aerosols, and ultralow-volume concentrates (ACGIH, 1991a; Sittig, 1991a).
Malathion is produced by adding O,O-dimethyl dithiophosphoric acid to diethyl maleate (Ashford, 1994a; Lewis, 1997a). It is not known to occur as a natural product (Howard, 1991a).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
The following are signs and symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for malathion, but could potentially occur in individual cases. USES: Malathion is a nonsystemic acaracide and insecticide and is considered the least toxic of the organophosphates. Malathion is also used in the treatment of pediculus humanus capitis (head lice and their ova) infections of the scalp hair. 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.
- 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 can develop. EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. The following are signs and symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for malathion, but could potentially occur in individual cases.
Following malathion exposure, nicotinic effects can include: tachycardia and hypertension, while muscarinic effects can produce bradycardia (HSDB, 2006). BRADYCARDIA: Bradycardia can occur following moderate to severe organophosphate poisoning (Karki et al, 2004; Kamijo et al, 1999; Ganendran, 1974). Total peripheral vascular resistance may be low and cardiac output increased in patients with pre-existing vascular disease (Buckley et al, 1994) HYPOTENSION: Hypotension can occur following moderate to severe organophosphate poisoning (Karki et al, 2004; Kamijo et al, 1999; Ganendran, 1974). CARDIAC DYSRHYTHMIAS: Cardiac dysrhythmias and conduction defects have been reported in severely poisoned patients (Wren et al, 1981; Kiss & Fazekas, 1982; Chhabra & Sepaha, 1970; Agarwal, 1993). The dysrhythmias cover a range of ECG abnormalities including: sinus bradycardia or tachycardia, atrioventricular and/or intraventricular conduction delays, idioventricular rhythm, multiform premature ventricular extrasystoles, ventricular tachycardia or fibrillations, torsades de pointes, prolongation of the PR, QRS, and/or QT intervals, ST-T wave changes, and atrial fibrillation (Karki et al, 2004; Kamijo et al, 1999).
DIAPHORESIS: Profuse sweating may occur as one of the muscarinic signs of malathion poisoning (HSDB, 2006). SENSITIZATION: Dermal sensitization to malathion has been reported following skin exposure, (Milby et al, 1964) with one study reporting an incidence of 23% (Bardin et al, 1987). HYPERSENSITIVITY: Urticaria, angioedema, and nonspecific skin rash have been reported following exposure to malathion (Schanker et al, 1992). SYSTEMIC ABSORPTION: Based on previous experience with organophosphates including malathion, significant skin absorption may occur following topical application (Guloglu et al, 2004; Bjornsdottir & Smith, 1999; Elgart, 1999). SCALP IRRITATION: Irritation of the scalp and skin may develop with therapeutic use of 0.5% malathion lotion (Prod Info OVIDE(R) topical lotion, 2005).
MUSCARINIC EFFECTS: Muscarinic effects can produce nausea, vomiting, salivation, and diarrhea following malathion exposure (HSDB, 2006). ACUTE PANCREATITIS: Acute pancreatitis has been reported following oral ingestion of organophosphates, including malathion parathion, difonate, coumaphos, diazinon, mevinphos and dermal exposure to dimethoate (Hsiao et al, 1996). FECAL INCONTINENCE: Fecal incontinence may occur in severe organophosphate poisoning (Koga et al, 1999; Kecik et al, 1993), and has been reported following oral malathion exposure (Sudakin et al, 2000a).
INVOLUNTARY URINATION: Involuntary urination occurs in severe cases of organophosphate poisoning (Wu et al, 2001; Koga et al, 1999), and has been reported following malathion exposure (Lee & Tai, 2001; Sudakin et al, 2000a).
CONJUNCTIVITIS: Conjunctivitis may occur following inadvertent exposure of 0.5% malathion lotion (Prod Info OVIDE(R) topical lotion, 2005). MIOSIS: Miosis can result from malathion exposure, a muscarinic effect of the organophosphate. However, the nicotinic effects following severe poisoning can possibly lead to mydriasis (HSDB, 2006). Although miosis is typical and useful diagnostically, it may not always be present following organophosphate poisoning (Guven et al, 2004a; Nair et al, 2001).
DERMAL SENSITIZATION: Dermal sensitization to malathion has been reported following skin exposure (Milby et al, 1964). HYPERSENSITIVITY: Urticaria, angioedema, and nonspecific skin rash have been reported following exposure to malathion (Schanker et al, 1992).
Malathion can elicit a nicotinic effect at the neuromuscular level, producing generalized muscle fasciculations, muscle cramps, and eventually weakness following exposure (HSDB, 2006). MUSCLE WEAKNESS: Organophosphate compounds cause skeletal muscle weakness and is proposed to occur through 3 different mechanism: cholinergic phase of poisoning, intermediate syndrome, and delayed peripheral neuropathy (Karalliedde & Henry, 1993).
Malathion poisoning has produced typical neurologic effects of organophosphate poisoning. Giddiness, anxiety, headache, and restlessness followed by ataxia, drowsiness, and confusion are common with moderate to severe exposures. In more severe toxicity, tremors, confusion, drowsiness, slurred speech, coma, loss of reflexes and seizures may develop (HSDB, 2006). INTERMEDIATE SYNDROME: A Type II neurological effects involve paralysis appearing from 12 hours to 7 days after organophosphate exposure including several reports following malathion toxicity; this paralysis is unresponsive to atropine and may be due to a persistent excess of acetylcholine at nicotinic receptors (Aygun, 2004 ; Karki et al, 2004; Villamangca et al, 2000; Sudakin et al, 2000). Several investigators have proposed that intermediate syndrome (IMS) may develop as a result of several factors: inadequate oxime therapy, the dose and route of exposure, the chemical structure of the organophosphates, the time to initiation of therapy, and possibly efforts to decrease absorption or enhance elimination of the organophosphates (Sudakin et al, 2000; Villamangca et al, 2000). PATHOPHYSIOLOGY: IMS can occur due to an organophosphate-induced alteration in postjunctional acetylcholine receptors. Based on this alteration, it has been suggested by some that a delay in oxime therapy may contribute to the development of IMS. Clinical presentation is described as the delayed development of proximal and diaphragmatic muscle paralysis after the resolution of initial organophosphate (OP) poisoning. Unlike delayed polyneuropathy that may occur after OP poisoning, symptoms of IMS usually occur within 24 to 96 hours. Unlike delayed polyneuropathy, IMS does not begin distally and progress and it often involves cranial nerves or proximal weakness. This syndrome can increase the risk of death due to respiratory depression. Agents that may produce this syndrome include: malathion, fenthion, dimethoate, monocrotophos, and methamidophos (Lee & Tai, 2001; Sudakin et al, 2000a). ONSET: Intermediate syndrome develops after the resolution of cholinergic signs and before the onset of delayed neuropathy (Sudakin et al, 2000a; Nisse et al, 1998; De Bleecker, 1995). CLINICAL SIGNS: Paralytic signs include inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis, and death (Villamangca et al, 2000; Nisse et al, 1998; Good et al, 1993).
DELAYED POLYNEUROPATHY: Delayed polyneuropathy has been observed in patients following organophosphate exposure, with the motor component more pronounced than the sensory component (Moretto & Lotti, 1998). Although appearing to be a rare complication (Aygun et al, 2003; Wadia et al, 1987), it has occurred in reports and typically appears 4 to 21 days after acute exposure resulting in progressive distal weakness and ataxia in the lower limbs (Nisse et al, 1998; Cherniack, 1988).
Organophosphate poisoning has been associated with a variety of psychiatric syndromes with reports of adverse effects including: memory deficits, irritability, combative behavior, delirium, hallucinations, depression, and psychosis (Agarwal, 1993; Devinsky et al, 1992). NEUROBEHAVIORAL TESTS: Worse performance on neurobehavioral tests has been found in patients previously acutely poisoned with organophosphates as compared to controls (Ruckart et al, 2004; Steenland et al, 1994) ANXIETY: Anxiety and/or restlessness have been associated with malathion toxicity (HSDB, 2006), and are commonly reported with organophosphate poisoning (Levin & Rodnitzky, 1976; Rosenthal & Cameron, 1991).
BRONCHOSPASM: Bronchospasm has occurred following organophosphate poisonings, including malathion exposure (HSDB, 2006; Dive et al, 1994). BRONCHORRHEA: Bronchorrhea (excessive bronchial mucosa secretion) may occur as a muscarinic effect following malathion exposure (HSDB, 2006), and these excessive secretions necessitated mechanical ventilation by 74% of patients who suffered organophosphate poisoning (n=23) (Lee & Tai, 2001). DYSPNEA: Dyspnea, increased bronchial secretions, bronchospasm, chest tightness, and heartburn have occurred in severe and moderately severe organophosphate poisonings including malathion (Hayes, 1965; Dive et al, 1994). HYPERVENTILATION: Hyperventilation has been reported following the cutaneous absorption of organophosphates (Bjornsdottir & Smith, 1999). RESPIRATORY FAILURE: Acute respiratory insufficiency, due to any combination of CNS depression, respiratory paralysis, bronchospasm, acute lung injury, or increased bronchial secretions, is the main cause of death in acute organophosphate poisonings (Lin et al, 2004; Nair et al, 2001). PNEUMONIA: Aspiration of preparations containing hydrocarbon solvents may cause potentially fatal lipoid pneumonitis (Lund & Monteagudo, 1986).
FEVER: In a retrospective review of 23 adults with organophosphate poisoning due to malathion ingestion, fever (38 degrees C or higher) was reported in 18 (78%) patients within 24 hours of admission (Lee & Tai, 2001).
CHRONIC CLINICAL EFFECTS
In a controlled human study, a 24 mg malathion dose was required for more than 14 days to produce significant decreases in blood cholinesterase activity. There was moderate irritation of the nose and eyes, but no signs of cholinesterase inhibition in 4 men exposed to an airborne concentration of 84.8 mg/m(3) for 42 days. Almost half of a group of human volunteers had contact sensitization reactions to malathion; once a person is sensitized, even very weak dilutions (1:1,000,000) can evoke an allergic response (Millby & Epstein, 1964). Malathion can cause lung and liver damage (NIOSH/OSHA). Other signs and symptoms of chronic exposure include fatigue, visual disturbances, headache, nausea, and muscle twitching (Sare, 1972). Malathion was one of the insecticides implicated in an outbreak of eye disease (Saku disease) in Japan (Ishikawa, 1971). One man chronically exposed to malathion developed eye disease, abdominal pain, headaches, and numbness in the lower extremities (Ishikawa, 1972). In an unusual incident of occupational poisoning involving several thousand sprayers, mixers, and supervisors, the severe effects were attributed to impurities rather than to malathion itself (Hayes & Laws, 1991).
Experimental animal studies have shown that malathion can induce increased levels of serotonin (a sign of stress) in rats (Barteau & Deen, 1978). In rats, chronic malathion poisoning (13 weeks) produced pulmonary edema and damage to the heart, kidneys, and liver (Sosnierz, 1977). Ingestion of malathion at a dose of 1 ppm in the drinking water for 6 months produced pathological changes in the liver and blood in rats (Lox & Davis, 1983). Nervous system function was impaired in rats, mice, and rabbits given malathion orally or by inhalation (Lox & Davis, 1983). In mice, chronic (14 day) oral exposure to malathion at a dose as low as 0.1 mg/kg/day produced mast cell degranulation (Rodgers & Xiong, 1997).
-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, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975). NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).
Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975a). Chlorine-active compounds such as sodium hypochlorite (household bleach) or calcium hypochlorite (bleaching powder, chlorinated lime) may also be used to detoxify organophosphate spills (EPA, 1975a). While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED.
- SMALL SPILL DECONTAMINATION
Three cups of Arm & Hammer washing soda (sodium carbonate) or Arm & Hammer baking soda (sodium bicarbonate) may be combined with one-half cup of household bleach and added to a plastic bucket of water. The washing soda is more alkaline and may be more efficacious, if available. Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978). Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 1975a). NOTE: Do NOT use a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent. Call the National Pesticide Telecommunications Network for further assistance at 1-800-858-7378 or on the web at http://nptn.orst.edu.
- LARGE SPILL DECONTAMINATION
Sprinkle or spray the area with a mixture of one gallon of sodium hypochlorite (bleach) mixed with one gallon of water. Then spread calcium hydroxide (hydrated or slaked lime) liberally over the area and allow to stand for at least one hour (Pesticide User's Guide, 1976). Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978). Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination. NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.
FURTHER CONTACT INFORMATION For further information contact the National Pesticide Telecommunications Network at 1-800-858-7378 or contact on the web at http://nptn.orst.edu. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378. The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675. CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.
-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, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; EPA, 1975). NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).
Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975a). Chlorine-active compounds such as sodium hypochlorite (household bleach) or calcium hypochlorite (bleaching powder, chlorinated lime) may also be used to detoxify organophosphate spills (EPA, 1975a). While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED.
SMALL SPILL DECONTAMINATION Three cups of Arm & Hammer washing soda (sodium carbonate) or Arm & Hammer baking soda (sodium bicarbonate) may be combined with one-half cup of household bleach and added to a plastic bucket of water. The washing soda is more alkaline and may be more efficacious, if available. Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978). Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 1975a). NOTE: Do NOT use a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent. Call the National Pesticide Telecommunications Network for further assistance at 1-800-858-7378 or on the web at http://nptn.orst.edu.
LARGE SPILL DECONTAMINATION Sprinkle or spray the area with a mixture of one gallon of sodium hypochlorite (bleach) mixed with one gallon of water. Then spread calcium hydroxide (hydrated or slaked lime) liberally over the area and allow to stand for at least one hour (Pesticide User's Guide, 1976). Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978). Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination. NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure - Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.
FURTHER CONTACT INFORMATION For further information contact the National Pesticide Telecommunications Network at 1-800-858-7378 or contact on the web at http://nptn.orst.edu. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378. The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675. CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.
ANTIDOTES
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
- The acute oral lethal dose is estimated to be below 1 g/kg; almost all reported fatalities from malathion have involved ingestion (Hathaway et al, 1996).
- It has been estimated that it would take more than 60 grams of orally administered malathion to be lethal in a 70 kilogram man (Baselt, 2000; Becker & Sullivan, 1986).
- OHM/TADS (2002) reports that 860 mg/kg is the estimated lethal dose in man.
- Between 1983 and 1987, there were 45,598 cases of organophosphate exposure reported to the American Association of Poison Control Centers National Data Collection System, representing 1.1% of all reported poisonings. Of these cases, there were 24 fatalities from exposure to organophosphates (either alone or mixed with other pesticides) (Hall & Rumack, 1992).
- Of the 19 fatalities where the identity of the offending organophosphate was known, 12 (63%) were due to either malathion or diazinon (Hall & Rumack, 1992).
- With administration of atropine and supportive treatment, several children and adults have survived ingestions of up to 50 grams of malathion (Baselt, 2000).
MAXIMUM TOLERATED EXPOSURE
- The World Health Organization (WHO) has classified malathion as pesticide class III (Slightly hazardous) (World Health Organization, 2006).
There is a body of clinical experience that suggests that humans are more susceptible to the toxic effects of malathion than are rats; however, there have been repeated demonstrations of the relative safety of malathion to humans (ACGIH, 1991; Hathaway et al, 1996): All organophosphate esters undergo hydrolysis in water; generally the water-soluble products of hydrolysis are less toxic than the parent compound (Minton & Murray, 1988). No effect on blood cholinesterase was found when malathion was fed to human volunteers for 47 days at the rate of 16 mg/man/day (ACGIH, 1991). Volunteers dosed dermally with malathion had no change of blood cholinesterase or other injury while excreting an average of 47 mg/man/day and a maximum of 220 mg/man/day (ACGIH, 1991).
Delayed respiratory failure developed in a 53-year-old man 30 hours after ingesting about 300 mL of 50% malathion. Following supportive care, including atropine and pralidoxime treatment, his condition gradually improved and he was extubated on day 13 and transferred to the psychiatric service 5 days later (Berman et al, 2015). An adult developed severe toxicity but survived after ingesting 60 mL of a 50% malathion solution (Bentur et al, 2003). An adult developed severe toxicity but recovered after ingesting 100 ml of 15% malathion (Dive et al, 1994). In a group of workers with an average exposure of 3.3 mg/m(3) for 5 hours (maximum of 56 mg/m(3)), the cholinesterase levels in the blood were not significantly decreased, and none exhibited signs of cholinesterase inhibition (Hathaway et al, 1996). In a human experiment in which four men were exposed 1 hour daily for 42 days to an airborne concentration of 84.8 mg/m(3), there was moderate irritation of the nose and conjunctiva, but there were no cholinergic signs or symptoms (Hathaway et al, 1996). Non-lethal intoxication has occurred in agricultural workers, but has usually been the result of gross exposures with concomitant skin absorption (Hathaway et al, 1996).
- Carcinogenicity Ratings for CAS121-75-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Malathion EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Malathion 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): 2A ; Listed as: Malathion 2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Malathion 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 CAS121-75-5 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 2x10(-2) mg/kg-day
Inhalation: Drinking Water:
Bingham et al, 2001 Budavari, 2000 Hartley & Kidd, 1990 Hayes & Laws, 1991 HSDB, 2002 ITI, 1995 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002 LC50- (INHALATION)RAT: LCLo- (INHALATION)CAT: LD50- (ORAL)CHICKEN: LD50- (SUBCUTANEOUS)CHICKEN: LD50- (INTRAPERITONEAL)DOG: LD50- (ORAL)GOAT: LD50- (INTRAPERITONEAL)GUINEA_PIG: LD50- (ORAL)GUINEA_PIG: LD50- (SKIN)GUINEA_PIG: LD50- (SUBCUTANEOUS)GUINEA_PIG: LD50- (INTRAPERITONEAL)HAMSTER: LD50- (INTRAPERITONEAL)MOUSE: 193 mg/kg 420 mg/kg (Bingham et al, 2001) 420-474 mg/kg (HSDB, 2002) 985 mg/kg (Hayes & Laws, 1991)
LD50- (INTRAVENOUS)MOUSE: LD50- (ORAL)MOUSE: 190 mg/kg 400-500 mg/kg (Hayes & Laws, 1991) 1025 mg/kg (Bingham et al, 2001) 4000 mg/kg (OHM/TADS, 2002) 4059 mg/kg (Hayes & Laws, 1991; HSDB, 2002)
LD50- (SKIN)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: LD50- (ORAL)RABBIT: LD50- (SKIN)RABBIT: LD50- (SUBCUTANEOUS)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (INTRAVENOUS)RAT: LD50- (ORAL)RAT: 290 mg/kg 599 mg/kg (ITI, 1995) male, 1375 mg/kg (Bingham et al, 2001; Budavari, 2000; Hayes & Laws, 1991; OHM/TADS, 2002) female, 1000 mg/kg (Bingham et al, 2001; Hayes & Laws, 1991) 1156 mg/kg (OHM/TADS, 2002) 1400 mg/kg (Hayes & Laws, 1991; ITI, 1995) 1401 mg/kg (Hayes & Laws, 1991) 2800 mg/kg (Hartley & Kidd, 1990) male, 2830 (Hayes & Laws, 1991; OHM/TADS, 2002) male, 5843 mg/kg (Hayes & Laws, 1991; HSDB, 2002) 8000 mg/kg (Hayes & Laws, 1991) 10,700 mg/kg (Hayes & Laws, 1991) 12,500 mg/kg (Hayes & Laws, 1991)
LD50- (SKIN)RAT: 4100 mg/kg (Hartley & Kidd, 1990) male, 4444 mg/kg (Hayes & Laws, 1991) female, 4444 mg/kg (Hayes & Laws, 1991) >4444 mg/kg
LD50- (SUBCUTANEOUS)RAT: 400 mg/kg -- lacrimation; muscle contraction/spasticity; true cholinesterase 1000 mg/kg (HSDB, 2002; Lewis, 2000)
LD50- (ORAL)SHEEP: LDLo- (INTRAARTERIAL)CAT: LDLo- (ORAL)HUMAN: 246 mg/kg -- dermatitis; chronic pulmonary edema; decrease in blood pressure 8 mL/kg -- acute pulmonary edema; gastrointestinal changes 471 mg/kg -- coma; dyspnea; decrease in blood pressure
LDLo- (ORAL)RABBIT: TCLo- (INHALATION)RAT: TDLo- (ORAL)DOG: TDLo- (ORAL)GOAT: TDLo- (SUBCUTANEOUS)GUINEA_PIG: TDLo- (INTRAVENOUS)HUMAN: TDLo- (ORAL)HUMAN: TDLo- (ORAL)MOUSE: TDLo- (ORAL)RABBIT: 368 mg/kg for 21W-intermittent -- decrease in cellular and humoral immune responses female, 540 mg/kg at 28-30D of pregnancy -- effects to embryo
TDLo- (SUBCUTANEOUS)RABBIT: TDLo- (INTRAPERITONEAL)RAT: TDLo- (ORAL)RAT: 462 mg/kg for 22W-continuous -- spleen weight changes; decrease in cellular and humoral immune responses 900 mg/kg for 90D-intermittent -- weight loss or decreased weight gain 1050 mg/kg for 21D-intermittent -- changes to liver; biochemical changes 2250 mg/kg for 45D-intermittent -- gastrointestinal and biochemical changes 3358 mg/kg for 14D-continuous -- changes in fluid intake and in clotting factors female, 191 mg/kg at 9D of pregnancy -- post-implantation mortality female, 283 mg/kg at 9D of pregnancy -- developmental abnormalities of the urogenital system female, 5550 mg/kg at 91D prior to mating and 1-20D of pregnancy -- developmental abnormalities of the body wall female, 43,920 mg/kg at multigenerations -- weaning or lactation index effects; effects on growth statistics and other postnatal effects
TDLo- (SUBCUTANEOUS)RAT:
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS121-75-5 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS121-75-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS121-75-5 (National Institute for Occupational Safety and Health, 2007):
Listed as: Malathion REL: IDLH: IDLH: 250 mg/m3 Note(s): Not Listed
- OSHA PEL Values for CAS121-75-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS121-75-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS121-75-5 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS121-75-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS121-75-5 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS121-75-5 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS121-75-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS121-75-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS121-75-5 (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 CAS121-75-5 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Malathion is a human poison by ingestion and skin absorption (it can penetrate intact skin) and is a cholinesterase inhibitor. Wear appropriate protective clothing when handling or using malathion. Maintain a regular inspection schedule of containers for any leakage (Lewis, 1997; Lewis, 2000; Sittig, 1991).
HANDLING
- Wear appropriate protective clothing when handling or using malathion (ITI, 1995; Sittig, 1991).
STORAGE
Containers should be protected against physical damage; maintain a regular inspection schedule of containers for any leakage. Keep containers of malathion dry and tightly closed. Do not store or transport near food, and report spills immediately (HSDB , 2002; ITI, 1995; Sittig, 1991). Prolonged contact with iron or iron-containing materials reportedly breaks down malathion and causes it to completely lose its insecticidal activity (Sittig, 1991). Stack containers so that air can circulate freely at the bottom and inside of the piles (HSDB , 2002). "Pesticide containers must be provided with labels indicating the degree of toxicity of the product they contain. The labels must not only give a short desription of how to use the preparation, but also state basic precautions to be taken when applying it" (HSDB , 2002).
- ROOM/CABINET RECOMMENDATIONS
Store containers of malathion where possible leakage cannot endanger people or the environment. Outdoor or detached storage is preferred, but if this is not possible, store in a standard combustible liquid storage room (ITI, 1995; Sittig, 1991). "Rooms used for storage only should be soundly constructed and fitted with secure locks. Floors should be kept clear and pesticides clearly identified. If repacking is carried out in storage rooms, adequate light should be available; floors should be impervious and sound" (HSDB , 2002). The recommended storage temperature for malathion is 20-25 degrees C (HSDB , 2002). CHRIS (2002) recommends storing this compound below 120 degrees F; decomposition may occur at higher temperatures.
Malathion is incompatible with magnesium, strong oxidizers, and alkaline pesticides. Metals, some plastics, rubber, and coatings are attacked by malathion (NIOSH , 2002; Pohanish & Greene, 1997; Sittig, 1991). Malathion may corrode copper, iron, lead, steel, and tin plate (ACGIH, 1991; Bingham et al, 2001). Malathion is decomposed by alkalis and acids (Hartley & Kidd, 1990).
-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.
- Metabolites of malathion were detected in urine samples of workers exposed dermally in high-volume air-blasting applications; fluorescent tracer showed that 75% of total dermal exposure was in areas of the skin covered with protective clothing or gloves (Fenske, 1988).
- Any employee whose work involves likely skin exposure to malathion or malathion formulations (e.g., mixing, formulating, or applying malathion) shall wear full-body coveralls, impervious gloves and footwear, and safety goggles. Remove and replace work clothing that becomes wet or contaminated, and change into clean clothing before leaving the workplace (NIOSH , 2002; Sittig, 1991).
- The following information is for personnel protection for ORGANOPHOSPHATES in general.
Closed spaces should be ventilated before entry. 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% of an organophosphate on the skin if done immediately. If delayed, the same procedure may remove only 50-70% (Fredriksson, 1961). Following a soap and water wash, a second wash with 95% ethanol will leave only about a 5-10% organophosphate residue (Fredriksson, 1961). The best results of skin decontamination are achieved with a thorough soap and water wash, followed by a 95% ethanol wash, followed by a second soap and water wash (Fredriksson, 1961). Tincture of green soap contains 30% 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. Contaminated clothing and footwear should be removed and isolated at the incident site. Any contaminated clothing should be discarded as hazardous waste. Repeated laundering may not remove organophosphate from clothing (Clifford & Nies, 1989).
- "Overalls polluted with malathion should be shaken and soaked in a soap-and-soda solution for 6-8 hours. Then the overalls must be washed 2-3 times in a hot soap-and-solution and rinsed carefully. Containers are decontaminated with 5% caustic or washing soda (300-500 grams per 10 liters of water). The containers are filled with this solution, kept 5-12 hours, then washed with ample water. If soda is not on hand, wood ash may be used instead" (HSDB , 2002).
EYE/FACE PROTECTION
- Direct contact with malathion can lead to discomfort and irritation; wear safety goggles to prevent any reasonable probability of eye contact (Sittig, 1991).
- Do not wear contact lenses while working with malathion (NIOSH , 2002).
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 121-75-5.
-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.
Malathion is a ClassIIIB combustible liquid; however, it ignites with difficulty (NIOSH , 2002; Sittig, 1991). When malathion is involved in a fire, poisonous gases will be produced. It is also possible for containers to explode (CHRIS , 2002).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS121-75-5 (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 CAS121-75-5 (NFPA, 2002):
- A fire involving malathion should be extinguished with agents suitable to the surrounding combustibles (HSDB , 2002; Sittig, 1991).
- Extinguish fires involving malathion with dry chemical, alcohol foam, or carbon dioxide. Use water in flooding quantities as fog. Fire should not be extinguished if the flow cannot be stopped or safely confined (dike the area surrounding the fire to prevent water runoff). Flooding quantities of water, applied from a maximal distance, can be used to cool affected containers (CHRIS , 2002; HSDB , 2002)
Oxides of phosphorus and sulfur are released when malathion is heated to decomposition (Lewis, 2000) Sulfur dioxide and phosphoric acid are generated when malathion is involved in a fire (CHRIS , 2002). Malathion decomposes explosively above 100 degrees C (HSDB , 2002).
DUST/VAPOR HAZARD
- Toxic fumes of oxides of sulfur and phosphorus are emitted when malathion is heated to decomposition (Lewis, 2000).
REACTIVITY HAZARD
- Malathion is incompatible with magnesium, strong oxidizers, and alkaline pesticides. Metals, some plastics, rubber and coatings are attacked by this compound (NIOSH , 2002; Pohanish & Greene, 1997; Sittig, 1991).
- In the manufacturing of malathion, the phosphorus sulfide dissolved in toluene is treated first with methanol, then with diethyl maleate. Use of insufficient toluene has led to a runaway exothermic reaction and explosion (Urben, 2000).
- Toxic fumes of oxides of sulfur and phosphorus are emitted when malathion is heated to decomposition (Lewis, 2000).
- 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.
- AIHA ERPG Values for CAS121-75-5 (AIHA, 2006):
- DOE TEEL Values for CAS121-75-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Malathion TEEL-0 (units = mg/m3): 1 TEEL-1 (units = mg/m3): 15 TEEL-2 (units = mg/m3): 120 TEEL-3 (units = mg/m3): 390 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 CAS121-75-5 (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):
Listed as: Malathion Proposed Value: AEGL-1 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Malathion Proposed Value: AEGL-2 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-2 is the airborne concentration 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.
Listed as: Malathion Proposed Value: AEGL-3 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS121-75-5 (National Institute for Occupational Safety and Health, 2007):
IDLH: 250 mg/m3 Note(s): Not Listed
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.
The spill area should be ventilated; the spill can then be absorbed in dry sand, earth, vermiculite, or similar absorbent material. Ensure that disposal conforms with local, state, and federal regulations (HSDB , 2002). Evacuate all workers from the spill area. Personnel wearing appropriate protective clothing and equipment may spread vermiculite or another absorbent on the spill, then scoop it up and place it into a suitable container for proper disposal. The spill area should be scrubbed with industrial detergent and water (Sittig, 1991). ITI (1995) recommends dissolving spilled malathion into a combustible solvent such as an alcohol, then burning in an open furnace (ignite from a safe distance) or sprinkling into the fire chamber of a furnace equipped with afterburner and scrubber (ITI, 1995). Alternatively, it can be poured into sodium bisulfate in a large evaporating dish, then sprinkled with water and neutralized. Spilled malathion can be mixed with equal parts crushed limestone and sand. After spraying with a flammable solvent, place into an open incinerator and light with an excelsior train. Or, after mixing with the limestone and sand, place in paper box and ignite in an incinerator equipped with an afterburner and alkaline scrubber (OHM/TADS , 2002). "Spills of malathion on floors shall be absorbed with absorbing clay. Sweeping compound may be utilized to facilitate the removal of all visible traces of malathion-contaminated clay. Equipment and fixtures contaminated with malathion shall be decontaminated with an alkaline solution (5% sodium hydroxide)" (HSDB , 2002). As some poison will be present in the smoke from an open fire used to destroy pesticides, attempt burning from an isolated place only (HSDB , 2002). LAND SPILL: Create a holding area to contain the liquid or solid material (seal with an impermeable flexible membrane liner if time permits). Use soil, sand bags, foamed polyurethane, or foamed concrete to dike surface flow. Use fly ash or cement powder to absorb the bulk liquid (HSDB , 2002). WATER SPILL: Apply activated carbon at ten times the amount spilled in regions where malathion is dissolved at concentrations of 10 ppm or greater. Use suction hoses to remove trapped material. Immobilized masses of pollutants and precipitates can be removed with mechanical dredges or lifts (HSDB , 2002). "Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices (HSDB , 2002). DECONTAMINATION OF ORGANOPHOSPHATE 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. The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used. 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). 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 decontamination of large areas may be regulated by various governmental agencies and reporting may be required.
Malathion can be hydrolyzed under controlled conditions. Hydrolyzation is almost instantaneous at pH 12, and 50% hydrolysis at pH 9 takes 12 hours (Sittig, 1991). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
Malathion is readily biodegrades; the main destruction mechanism is believed to be enzyme-catalyzed hydrolysis. Biodegradation half-lives in soil have been reported to range from a few hours to 1 week. Malathion also biodegrades in seawater, with measured half-lives of 2 to 3.3 days (ATSDR, 2003 ). Eleven of 15 isolated salt-marsh organism cultures were able to degrade malathion as a sole carbon source. The remaining four of 15 cultures were able to degrade malathion when 0.2% peptone was added as an additional carbon source (ATSDR, 2003 ). Degradation products include malathionmonocarboxylic acid, malathiondicarboxylic acid and various phosphothionates, resulting from carboxyesterase cleavage. Phosphatase activity produces desmethylmalathion, phosphomonothionates and phosphodithionates, 4-carbon dicarboxylic acids and corresponding ethylethers (Verschueren, 2001).
Malathion was found to biodegrade more quickly in unsterile seawater than in sterile systems (ATSDR, 2003 ).
Dissolve malathion in a flammable solvent (e.g., alcohols) and burn in a furnace equipped with an afterburner and scrubber (ITI, 1995; Sittig, 1991).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- INTRODUCTION INTO THE ENVIRONMENT
Malathion in the environment is the result of its manufacture and direct application as a broad spectrum insecticide and acaricide. It may also be released in waste during production, formulation or processing, or through spills. It is not known to occur as a natural product (HSDB, 2004; ATSDR, 2003 ; Howard, 1991).
Agricultural and landscape workers may be exposed to malathion through crop and animal treatment, insecticide storage, or other operations in which the material is handled or used (HSDB, 2004). Dermal contact appears to be the primary route of exposure to malathion. Ingestion may also be an important exposure route. Inhalation exposure has not been shown to be of significant concern (ATSDR, 2003 ).
- GENERAL POPULATION EXPOSURE
Malathion is used to control head and body lice; people may be exposed to when it is used in this capacity. Similarly, owners of pets treated with malathion for flea control may come into contact with the chemical when handling the animal(s) (HSDB, 2004). Malathion is a component of certain household landscape and gardening insecticide products. Home gardeners and their families may be exposed to malathion through its use in home gardens or through ingestion of "backyard" fruits or vegetables treated with the chemical, especially if the foods are not washed prior to consumption (HSDB, 2004; ATSDR, 2003 ). People in the vicinity of malathion application sites may be exposed to the compound in ambient air or through contact with treated plants or soil (HSDB, 2004). Malathion residue has been detected at various levels in drinking and ground water, food samples, and ambient air from numerous sites across the globe (HSDB, 2004). A study was done to determine the effect of food processing on the fate of 30 different organophosphate pesticides. Malathion was one of the most persistent and remained at detectable levels in foods even after baking, boiling and frying (Hori et al, 1992).
ENVIRONMENTAL FATE AND KINETICS
In the atmosphere, malathion exists primarily in vapor form, though it may also exist adsorbed to particulate matter. It is degraded through reaction with photochemically-produced hydroxyl radicals and through indirect photolysis. It may be removed from air through wet deposition (HSDB, 2004; ATSDR, 2003 ). The photooxidation half-life ranges from 1 hour to 9.8 hours based on an estimated rate constant for vapor phase reaction with hydroxyl radicals in air (Howard et al, 1991). Oxidation through indirect photolysis transforms malathion to malaoxon, its oxygen analog (ATSDR, 2003 ). Malathion was transformed to malaoxon by oxidation, to DEF (Butifos) via hydrolysis, and loss through selective volatilization of breakdown products (Brown et al, 1993). The half-life of the reaction between malathion and photochemically-produced hydroxyl radicals is estimated to be 5 hours. The rate constant for this reaction has been estimated at 77 x 10(-12) mc(3)/molecule-sec at 25 degrees C (HSDB, 2004). The estimated vapor phase half-life for malathion in air as a result of hydrogen abstraction by photochemically-produced hydroxyl radicals is 1.5 days (HSDB , 2002; Howard, 1991) .
Malathion absorbs light at wavelengths >290 nm and is therefore susceptible to photolysis (HSDB, 2004). Direct photolysis does not appear to be a significant factor in malathion degradation. Malathion exposed to natural sunlight and UV irradiation (max. wavelength 360 nm) as thin films on glass was relatively stable to sunlight and showed 16% degradation under UV after 25 hours (ATSDR, 2003 ). The atmospheric photolysis half-life ranges from 41.3 days (990 hours) to 833 days (20,000 hours) based on aqueous photolysis data (Howard et al, 1991). A study showed that malathion adsorbed to particulate matter photodegrades when exposed to irradiation at wavelengths >290 nm, but did not photodegrade when adsorbed to kaolin. Malathion adsorbed to fly ash was 70% degraded after 40 minutes irradiation, though authors attributed this rapid reaction to the presence of metals and metal oxides in the fly ash (ATSDR, 2003 ).
SURFACE WATER Malathion in water degrades predominantly through hydrolysis, which occurs more rapidly at basic pHs. At the environmentally relevant pH range of 5 - 9, malathion hydrolysis should be significant. It is stable to hydrolysis at acidic pHs (ATSDR, 2003 ). Reported aquatic hydrolysis reactions include (Verschueren, 2001): - no hydrolysis found after 12 days between pH 5 and pH 7
- 36 hour hydrolysis half-life at pH 8
- 12 day hydrolysis half-life at pH 9
- instantaneous hydrolysis at pH 12
A review of malathion's hydrolysis at various pHs yielded the following (ATSDR, 2003 ): Hydrolysis half-life is reported to range from 0.2 weeks at pH 8.0 to 21 weeks at pH 6.0 (Howard, 1991). The first-order hydrolysis half-life is 8.8 years (7.7x10(-4) hours) based on the reported rate constant 2.5x10(-2) M(-1)s(-1) at pH 7 and 0 degrees C (Howard et al, 1991). Temperature has a demonstrated affect on malathion hydrolysis. The rate reportedly increases by a factor of 4 for each 10 degrees C temperature increase (ATSDR, 2003 ). Hydrolysis degradation products include malaoxon, malathion alpha and beta monoacid, O,O-dimethylphosphorodithioic acid, diethyl fumarate, diethyl thiomalate, and O,O-dimethylphosphorothionic acid (HSDB, 2004).
Malathion is susceptible to indirect photolysis, especially in the presence of photosensitizers such as humic acids. Based on limited data, direct photolysis of malathion in water is not a significant fate process (ATSDR, 2003 ). The aqueous photolysis half-life ranges from 41.3 days (990 hours) to 833 days (20,000 hours) based on aqueous photolysis rate constant at pH 6 for wave lengths >290 nm (low half-life) and for summer sunlight at 30 degrees C (high half-life) (Howard et al, 1991).
If malathion is released into water it may moderately sorb to sediment. It is subject to biodegradation and may be subject to photooxidation at surface levels. However, volatilization will not be an important fate process (Howard, 1991). Based on malathion's organic carbon partition coefficient (Koc) of 31, it is not expected to sorb significantly to suspended solids or sediment in water (HSDB, 2004). The half-life of malathion in surface water ranges from 4.2 days (100 hours) to 51.5 days (1236 hours) based on unacclimated aerobic die-away test data (low half-life) and estuarine water grab sample data (Howard et al, 1991).
Malathion's Henry's Law constant of 4.9 x 10(-9) atm-m(3)/mole indicates it will not volatilize from water surfaces (HSDB, 2004). Volatilization half-lives of 2 x 10(5) hours and 2 x 10(6) hours have been estimated for malathion in a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec) and a model lake (1 m deep, flowing 0.01 m/sec, wind velocity of 0.5 m/sec), respectively (HSDB, 2004).
GROUND WATER
TERRESTRIAL Malathion is moderately to very highly mobile in soils, though leaching to groundwater is generally insignificant due to its rapid degradation rate; most malathion is degraded in higher layers of soil before it is able to move to greater soil depths. It is degraded primarily through biodegradation via enzyme-catalyzed hydrolysis and hydrolysis, especially in soils of higher moisture content and alkaline pH. Degradation half-lives ranging from a few hours to approximately 1 week have been reported (HSDB, 2004; ATSDR, 2003 ). It is subject to significant hydrolysis and biodegradation (especially in soils with a pH <7, where the rate of hydrolysis will be slower). The 24-hour degradation rate has been reported at 50-90% in both sterile and nonsterile soils (Howard, 1991). Hydrolysis did not occur in soils with pH 2, occurred slowly in soils with pH 9 (<50% degraded in 2 days), and was rapid at pH 11 (>99% degraded in 1 day). At pH 9, malathion degradation products included thiomalic acid, dimethyl thiophosphate, and diethyl thiomalate (HSDB, 2004). The half-life of malathion in soil ranges from 3 days (72 hours) to 7 days (168 hours) based on unacclimated aerobic soil grab sample data (Howard et al, 1991).
Photodegradation on soil surfaces is not an important fate process; reported photodegradation half-life on sandy loam soil at pH 6.5 was 173 days (ATSDR, 2003 ). Volatilization from both moist and dry soil surfaces is not expected to occur (HSDB, 2004; ATSDR, 2003 ).
ABIOTIC DEGRADATION
- In the atmosphere, malathion exists primarily in vapor form, though it may also exist adsorbed to particulate matter. It is degraded through reaction with photochemically-produced hydroxyl radicals and through indirect photolysis. It may be removed from air through wet deposition (HSDB, 2004; ATSDR, 2003 ).
- Malathion in water degrades predominantly through hydrolysis, which occurs more rapidly at basic pHs. At the environmentally relevant pH range of 5 - 9, malathion hydrolysis should be significant. It is stable to hydrolysis at acidic pHs. It may moderately sorb to sediment. It is subject to biodegradation and may be subject to photooxidation at surface levels. However, volatilization will not be an important fate process (ATSDR, 2003 ; Howard, 1991).
- Malathion is moderately to very highly mobile in soils, though leaching to groundwater is generally insignificant due to its rapid degradation rate; most malathion is degraded in higher layers of soil before it is able to move to greater soil depths. It is degraded primarily through biodegradation via enzyme-catalyzed hydrolysis and hydrolysis. Volatilization from soil surfaces is not expected, nor will photodegradation on soil surfaces be an important fate process(HSDB, 2004; ATSDR, 2003 ).
BIODEGRADATION
- Biodegradation is the primary degradation process for malathion in soils and sediment and occurs mainly through enzyme-catalyzed hydrolysis. Biodegradation is rapid, the rate increasing in the presence of high organic matter content. Degradation rates in water are relative to pH, salinity, and temperature, as well as to other biological processes (raw river water as opposed to distilled water) (HSDB, 2004; ATSDR, 2003 ; Howard, 1991).
BIOACCUMULATION
Reported bioconcentration factor (BCF) values do not clearly indicate whether malathion bioconcentrates in aquatic organisms at a significant level. It is believed malathion is partially metabolized in fish and other organisms, making it unlikely to biomagnify in the food chain (ATSDR, 2003 ). Malathion has an estimated BCF of 37 calculated from water solubility. It is not expected to extensively bioconcentrate in aquatic organisms; however, it may bioconcentrate moderately in some species based on the reported BCF for shrimp (Howard, 1991): Paneaeous setiferous (white shrimp), 15 values ranging from 150-1917 with an average BCF of 869 Paneaeous azkecus (brown shrimp), 14 values ranging from 200-1667 with an average BCF of 959 Coho salmon, BCF 29.3 Triaenodes tardus (caddisfly) egg masses, BCF 10 Lake trout, BCF 7.36 Pseudorasbora parva (motsugo), no bioconcentration
A Japanese study reported a mean BCF for malathion in freshwater willow shiner (Gnathopogon caerulescens) of 34.4 (ATSDR, 2003 ). BCFs ranging from 23 - 135 have been reported for malathion in bluegill sunfish, with BCFs of 4.2 - 18 reported for edible tissues of the fish (ATSDR, 2003 ). An BCF of 13.1 was calculated for malathion using a octanol water partition coefficient (log Kow) of 2.36. This value suggests bioconcentration in aquatic organisms will be low (HSDB, 2004). No bioconcentration was seen in the freshwater fish Pseudorasbora parva (HSDB, 2004).
ENVIRONMENTAL TOXICITY
LC50 - AMERICAN EEL: 0.50 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - AMERICAN EEL (Anguilla rostrata): 82 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - ATLANTIC SILVERSIDE (Menidia menidia): 125 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - BANDED KILLIFISH: 0.24 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - BASS: 0.29 mg/L for 96H (Verschueren, 2001) LC50 - BLACK BULLHEAD: 12.9 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - BLUEGILL: 0.089-0.131 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - BLUEGILL: 0.120 ppm for 24H (OHM/TADS, 2002) LC50 - BLUEGILL: 0.103 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - BLUEGILL: 120 mcg/L for 24H (Verschueren, 2001) LC50 - BLUEGILL (Lepomis macrochirus): 110 mcg/L for 96H -- flow-through bioassay (HSDB, 2004) LC50 - BLUEHEAD (Thalassoma bifasciatum): 27 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - BROOK TROUT, 2.13 g: 0.12 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - BROOK TROUT, 1.15 g: 0.13 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - BROWN TROUT: 0.2 ppm for 96H - static (OHM/TADS, 2002) LC50 - BROWN TROUT (Salmo trutta), 1.1g: 101 mcg/L for 96H -- at 12 degrees C; 95% confidence limit 84 - 115 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - BULLHEAD (Ictalurus melas), 1.2 g: 12,900 mcg/L for 96H -- at 18 degrees C; 95% confidence limit 10700 - 15600 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - CARP: 1.9 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - CARP: 6.59 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - CARP (Cyprinus carpio), 0.6g: 6590 mcg/L for 96H - at 18 degrees C; 95% confidence limit 4920 - 8820 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - CARP (Cyprinus carpio): 9.8-10 mg/L for 48H (Verschueren, 2001) LC50 - CHANNEL CATFISH: 8.97 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - CHANNEL CATFISH (Ictalurus punctatus), 1.5 g: 8970 mcg/L for 96H -- at 18 degrees C; 95% confidence limit 6780 - 12,000 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - CHINOOK SALMON (Oncorhynchus tschawytscha): 23 mcg/L for 96H -- static bioassay (HSDB, 2004) LC50 - COHO SALMON (Oncorhynchus kisutch): 101 mcg/L for 96H (Verschueren, 2001) LC50 - COHO SALMON (Oncorhynchus kisutch), 0.9g: 170 mcg/L for 96H -- at 12 degrees C; 95% confidence limit 160 - 180 mcg/L static bioassay; technical purity 95% (HSDB, 2004) LC50 - COHO SALMON, 1.7 g: 0.265 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - CROAKER: 1 ppm for 24H (approximate) -- saltwater (OHM/TADS, 2002) LC50 - CUTTHROAT TROUT, 0.33 g: 0.15 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - CUTTHROAT TROUT (Salmo clarki), 1.0g: 280 mcg/L for 96H - at 12 degrees C; 95% confidence limit 270 - 310 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - CUTTHROAT TROUT, 1.25 g: 0.2 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - EASTERN MUD MINNOW: 0.14 mg/L for 14D -- freshwater (Verschueren, 2001) LC50 - EASTERN MUD MINNOW: 0.24 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - FATHEAD MINNOW: 8.65 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - FATHEAD MINNOW: 11 ppm for 336H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - FATHEAD MINNOW: 16 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - FATHEAD MINNOW (Pimephales promelas): 14 mg/L for 96H (Verschueren, 2001) LC50 - FATHEAD MINNOW (Pimephales promelas): 9000 mcg/L for 96H (Verschueren, 2001) LC50 - FLAGFISH: 349 mcg/L for 96H -- freshwater (Verschueren, 2001) LC50 - GOLDFISH (Carassius auratus), 0.9g: 10,700 mcg/L for 96H -- at 18 degrees C; 95% confidence limit 8340 - 13,800 mcg/L; static bioassay; technical purity 95% (HSDB, 2004; OHM/TADS, 2002) LC50 - GREEN SNAKEHEAD (Channa punctatus): 3.22 mg/L for 96H (Verschueren, 2001) LC50 - GREEN SUNFISH (Lepomis cyanellus): 120 mcg/L for 96H (Verschueren, 2001) LC50 - GREEN SUNFISH (Lepomis cyanellus), 1.1g: 175 mcg/L for 96H -- at 18 degrees C; 95% confidence limit 134 - 228 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - GUPPY: 1.2 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - GUPPY (Lebistes reticulatus): 0.819 mg/L for 1W (Verschueren, 2001) LC50 - HARLEQUIN FISH: 8 ppm for 48H -- static and flow-through; freshwater (OHM/TADS, 2002) LC50 - INDIAN MAJOR CARP (Cirrhinus mrigala): 5.4 mg/L for 48H (Verschueren, 2001) LC50 - KILLIFISH: 0.15 ppm for 48H -- saltwater (OHM/TADS, 2002) LC50 - LARGEMOUTH BASS (Micropterus salmoides): 50 mcg/L for 96H - static bioassay (HSDB, 2004) LC50 - LARGEMOUTH BASS: 0.17 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - LARGEMOUTH BASS (Micropterus salmoides), 0.9 g: 285 mcg/L for 96H -- at 18 degrees C; 95% confidence limit 254 - 320 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - MARINE FISH: 0.008-3.2 ppm for 96H (OHM/TADS, 2002) LC50 - MINNOW: 8.7 mg/L for 96H (Verschueren, 2001) LC50 - MUMMICHOG (Fundulus heteroclitus): 70 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - MUMMICHOG (Fundulus heteroclitus): 80 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - MUMMICHOG (Fundulus heteroclitus): 240 mcg/L for 96H - static bioassay (HSDB, 2004) LC50 - NORTHERN PUFFER (Sphaeroides maculatus): 3250 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - PERCH: 0.26 mg/L for 96H (Verschueren, 2001) LC50 - PINFISH: 1 ppm for 24H (approximate) -- saltwater (OHM/TADS, 2002) LC50 - PUMPKINSEED SUNFISH: 0.48 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - RAINBOW TROUT (Salmo gairdneri): 68 mcg/L for 96H -- static bioassay (HSDB, 2004) LC50 - RAINBOW TROUT (Salmo gairdneri): 170 mcg/L for 96H (Verschueren, 2001) LC50 - RAINBOW TROUT (Salmo gairdneri), 1.4g: 200 mcg/L for 96H - at 12 degrees C; 95% confidence limit 160 - 240 mcg/L; static bioassay; technical, 95% (HSDB, 2004) LC50 - RAINBOW TROUT: 0.100 ppm for 24H -- freshwater (OHM/TADS, 2002) LC50 - RAINBOW TROUT: 0.11 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - RAINBOW TROUT, 0.41 g: 0.12 ppm for 96H -- flow-through; freshwater (OHM/TADS, 2002) LC50 - REDEAR SUNFISH (Lepomis microlophus), 3.2g: 62 mcg/L for 96H -- at 24 degrees C; 95% confidence limit 58 - 67 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - REDEAR SUNFISH (Lepomis microlophus): 170 mcg/L for 96H (Verschueren, 2001) LC50 - SALVELINUS NAMAYCUSH (LAKE TROUT), 0.3g: 76 mcg/L for 96H -- at 12 degrees C; 95% confidence limit 47 - 123 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - SHEEPSHEAD MINNOW: 0.2 ppm for 24H (approximate) -- saltwater (OHM/TADS, 2002) LC50 - SHEEPSHEAD MINNOW (Cyprinodon variegatus): 51 mcg/L for 96H -- freshwater (Verschueren, 2001) LC50 - SMALLMOUTH BASS: 0.285 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - SPOT: 1.25 ppm for 24H (approximate) -- saltwater (OHM/TADS, 2002) LC50 - SPOTTED BARB (Puntius ticto): 0.0074 ppm for 96H -- freshwater (OHM/TADS, 2002) LC50 - STRIPED BASS: 0.039 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - STRIPED BASS, fingerling: 0.24 ppm for 96H -- static; freshwater (OHM/TADS, 2002) LC50 - STRIPED BASS (Morone saxatilis): 14 mcg/L for 96H - flow-through bioassay (HSDB, 2004) LC50 - STRIPED MULLET (Mugil cephalus): 550 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - STRIPED MUMMICHOG (Fundulus majalis): 250 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - SUNFISH: 0.17 mg/L for 96H (Verschueren, 2001) LC50 - THREE-SPINE STICKLEBACK (Gasterosteus aculeatus): 76.9 mcg/L for 24H -- static bioassay (HSDB, 2004) LC50 - THREE-SPINE STICKLEBACK (Gasterosteus aculeatus): 77 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - TROUT: 0.10 ppm for 24H -- freshwater (OHM/TADS, 2002) LC50 - VIRGINALIS YELLOWFIN (Chingata): 7.0 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - WALLEYE (Stizostedion vitreum), 1.3g: 64 mcg/L for 96H - at 18 degrees C; 95% confidence limit 59 - 70 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - WESTERN MOSQUITOFISH (Gambusia affinis): 0.2 mg/L for 96H (Verschueren, 2001) LC50 - WHITE PERCH: 1.1 mg/L for 96H -- saltwater (Verschueren, 2001) LC50 - YELLOW PERCH (Perca flavescens), 1.4 g: 263 mcg/L for 96H -- at 18 degrees C; 95% confidence limit 205 - 338 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC100 - TROUT: 5.0 ppm -- freshwater (OHM/TADS, 2002) LC100 - YELLOW PERCH: 5.0 ppm -- freshwater (OHM/TADS, 2002) TLm - ATLANTIC SALMON: 0.033 ppm for 24H -- freshwater (OHM/TADS, 2002) TLm - ATLANTIC SALMON: 0.12 ppm for 96H -- freshwater (OHM/TADS, 2002) TLm - BLUEGILL: 0.090 ppm for 96H -- freshwater (CHRIS, 2002; (OHM/TADS, 2002) TLm - FATHEAD: 12.5 ppm for 96H -- soft water & hard water (OHM/TADS, 2002)
LC50 - AMERICAN OYSTER (Crassostrea virginica), egg: 9070 ppb for 48H -- saltwater (Verschueren, 2001) LC50 - AMERICAN OYSTER (Crassostrea virginica), larvae: 2660 ppb for 14D -- saltwater (Verschueren, 2001) LC50 - COCKLE: 3.3-10 ppm for 48H - static; aerated; saltwater (OHM/TADS, 2002) LC50 - OYSTER, eggs: 9.07 ppm for 48H -- lab conditions; saltwater (OHM/TADS, 2002) LC50 - OYSTER, larvae: 2.66 ppm for 336H -- lab conditions; saltwater (OHM/TADS, 2002)
LC50 - CADDISFLY (Limnephilus sp.), juvenile: 1.3 mcg/L for 96H - at 15 degrees C; 95% confidence limit 0.8 - 2.0 mcg/L; static bioassy; technical purity 95% (HSDB, 2004) LC50 - CADDISFLY (Hydropsyche sp.), juvenile: 5.0 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 2.9 - 8.6 mcg/L; static bioassay, technical purity 95% (HSDB, 2004) LC50 - CADDISFLY (Hydropsyche betteni): 0.34 mcg/L for 30D (Verschueren, 2001) LC50 - DAMSELFLY (Lestes congener), juvenile: 10 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 0.8 - 2.0 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - FAWN DARNER DRAGONFLY (Boyeria vinosa): 2.3 mcg/L for 30D (Verschueren, 2001) LC50 - MIDGE (Chironomus riparius), 4th instar larvae: 1.9 mcg/L for 24H (Verschueren, 2001) LC50 - MOSQUITO (Aedes caspius): 28 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Aedes excrucians): 68 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Aedes punctor): 51 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Aedes quasirusticus): 34 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Aedes rusticus): 86 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Aedes vexans): 55 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Anopheles atroparvus): 83-151 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Anopheles quadrimaculatus): 69 mcg/L for 24H (Verschueren, 2001) LC50 - MOSQUITO (Culex pipiens): 84 mcg/L (Verschueren, 2001) LC50 - MOSQUITO (Culex theileri): 48-154 mcg/L (Verschueren, 2001) LC50 - RUSTY SNAKETAIL DRAGONFLY (Ophiogomphus rupinsulensis): 0.52 mcg/L for 30D (Verschueren, 2001) LC50 - SHORTWING STONE FLY (Claassenia sabulosa), second year class: 2.8 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 1.4 - 4.3 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - SNIPE FLY (Atherix variegata), juvenile: 385 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 246 - 602 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - SOWBUG (Asellus brevicaudus), mature: 3000 mcg/L for 96H -- at 21 degrees C; 95% confidence limit 1500 - 8500 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - STONEFLY (Isoperla sp.), second year class: 0.69 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 0.20 - 0.24 mcg/L; static bioassy; technical purity 95% (HSDB, 2004) LC50 - STONEFLY (Acroneuria lycorias): 1.0 mcg/L for 96H (Verschueren, 2001) LC50 - STONEFLY (Acroneuria lycorias): 0.3 mcg/L for 30D (Verschueren, 2001) LC50 - STONEFLY (Pteronarcella badia): 1.1 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 0.8 - 1.5 mcg/L; naiad; static bioassay; technical purity 95% (HSDB, 2004) LC50 - STONEFLY (Pteronarcys californica), second year class: 10 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 7.0 - 13 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - STONEFLY (Pteronarcys dorsata): 11 mcg/L for 30D (Verschueren, 2001) NOEC - CADDISFLY (Hydropsyche betteni): 0.24 mcg/L for 30D (Verschueren, 2001) NOEC - FAWN DARNER DRAGONFLY (Boyeria vinosa): 1.65 mcg/L for 30D (Verschueren, 2001) NOEC - RUSTY SNAKETAIL DRAGONFLY (Ophiogomphus rupinsulensis): 0.28 mcg/L for 30D (Verschueren, 2001) NOEC - STONEFLY (Acroneuria lycorias): 0.17 mcg/L for 30D (Verschueren, 2001) NOEC - STONEFLY (Pteronarcys dorsata): 9.4 mcg/L for 30D (Verschueren, 2001) TLm - CADDISFLY (Arctopsyche groundis): 0.032 ppm for 96H -- xylene; freshwater (OHM/TADS, 2002) TLm - STONEFLY (Claassenia sabulosa): 0.056 ppm for 96H -- xylene; freshwater (OHM/TADS, 2002) TLm - STONEFLY (Pteronarcys californica): 0.100 ppm for 96H -- xylene; freshwater (OHM/TADS, 2002) Malathion is toxic to bees (Hartley & Kidd, 1990).
LC50 - AMERICAN LOBSTER (Homarus americanus): 3.7 mcg/L for 48H -- larval and juvenile stages (Zulkosky et al, 2005) LC50 - BROWN SHRIMP: 0.33-1 ppm for 48H - static; aerated; saltwater (OHM/TADS, 2002) LC50 - CRAYFISH (Orconectes nais), early instar: 180 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 140 - 230 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - FAIRY SHRIMP (Streptocephalus proboscideus): 6.4 mg/L for 24H -- Streptoxkit F test (Verschueren, 2001) LC50 - FRESHWATER SHRIMP (Gammarus fasciatus): 0.5 mcg/L for 5D (Verschueren, 2001) LC50 - FRESHWATER SHRIMP (Gammarus fasciatus): 0.76 mcg/L for 96H (Verschueren, 2001) LC50 - GRASS SHRIMP (Palaemonetes vulgaris): 82 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - GRASS SHRIMP: 0.032 ppm for 24H -- saltwater (OHM/TADS, 2002) LC50 - LONG-ARMED HERMIT CRAB (Pagurus longicarpus): 83 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - MARINE CRUSTACEA: 0.033-0.083 ppm for 96H (CHRIS, 2002; (OHM/TADS, 2002) LC50 - MISSISSIPPI GRASS SHRIMP (Palaemonetes kadiakensis): 9.0 mcg/L for 5D (Verschueren, 2001) LC50 - MISSISSIPPI GRASS SHRIMP (Palaemonetes kadiakensis): 12 mcg/L for 96H (Verschueren, 2001) LC50 - MISSISSIPPI GRASS SHRIMP (Palaemonetes kadiakensis): 90 mcg/L for 96H -- 21 degrees C; mature; static bioassay; technical purity 95% (HSDB, 2004) LC50 - ORIENTAL SHRIMP (Palaemon macrodactylus): 22 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - ORIENTAL SHRIMP (Palaemon macrodactylus): 34 mcg/L for 96H -- freshwater (Verschueren, 2001) LC50 - PINK SHRIMP: 1 ppm for 48H (approximate) -- saltwater (OHM/TADS, 2002) LC50 - RED SWAMP CRAYFISH (Procambarus clarki): 49 mg/L for 96H (Verschueren, 2001) LC50 - SCUD (Gammarus lacustris), mature : 0.76 mcg/L for 96H -- at 15 degrees C; 95% confidence limits 0.63 - 0.92 mcg/L; static bioassay; technical purity 95% (HSDB, 2004) LC50 - SCUD (Gammarus lacustris): 1.0 mcg/L for 96H (Verschueren, 2001) LC50 - SCUD (Gammarus pseudolimnaeus): 0.023 mcg/L for 30D (Verschueren, 2001) LC50 - SEVENSPINE BAY SHRIMP (Crangon septemspinosa): 33 mcg/L for 96H -- saltwater (Verschueren, 2001) LC50 - WATER FLEA (Daphnia sp.): 0.9 mcg/L for 50H (HSDB, 2004) LC50 - WATER FLEA (Daphnia magna): 2.6 x 10(-15) mg/L for 24H (Verschueren, 2001) LC50 - WATER FLEA (Daphnia magna): 0.9 mcg/L for 24H (Verschueren, 2001) LC50 - WATER FLEA (Daphnia magna): 1.8 mcg/L for 48H (Verschueren, 2001) LC50 - WATER FLEA (Daphnia magna): 3.0 mcg/L for 1W (Verschueren, 2001) LC50 - WATER FLEA (Daphnia pulex): 1.8 mcg/L for 48H (Verschueren, 2001) LC50 - WATER FLEA (Simocephalus serrulatus): 3.5 mcg/L for 48H (Verschueren, 2001) NOEC - SCUD (Gammarus pseudolimnaeus): 0.008 mcg/L for 30D (Verschueren, 2001) NOEC - WATER FLEA (Daphnia magna): 0.6 mcg/L for 21D (Verschueren, 2001) TLm - WATER FLEA (Daphnia magna): 0.0009 ppm for 48H -- 59% active in xylene; freshwater (OHM/TADS, 2002)
LC50 - (ORAL) BOBWHITE: 3300-3700 ppm for 5D (OHM/TADS, 2002) LC50 - (ORAL) BOBWHITE QUAIL: 3500 mg/kg for 8D (Hartley & Kidd, 1990) LC50 - (ORAL) BOBWHITE (Colinus virginianus), 14 days old: 3497 ppm in 5D diet -- 95% confidence limit 2959-4117 ppm; technical purity 95% (HSDB, 2004) LC50 - (ORAL) DOTURNIX: 2000-2300 ppm for 5D (OHM/TADS, 2002) LC50 - (ORAL) JAPANESE QUAIL (Coturnix japonica), 2 week olds: 2128 ppm in 5D diet -- 95% confidence limit 1780 - 2546 ppm; technical purity 95% (HSDB, 2004) LD50 - (ORAL) MALLARD (Anas platyhynchos), 3-4 months, female: 1485 mg/kg -- 95% confidence limit 1020-2150 mg/kg; sample purity 95% (HSDB, 2004) LC50 - (ORAL) MALLARD: >5000 ppm for 5D (OHM/TADS, 2002) LC50 - (ORAL) PHEASANT: 2500-4500 ppm for 5D (OHM/TADS, 2002) LC50 - (ORAL) RING-NECKED PHEASANT (Phasianus colchisus), 10 days old: 2639 ppm in 5D diet -- 95% confidence limit 2220-3098 ppm; technical purity 95% (HSDB, 2004)
EC9 - CILIATE (Tetrahymena pyriformis): 10 mg/L for 96H (Verschueren, 2001) LC50 - ROTIFER (Brachionus calyciflorus): 1090 mg/L for 24H -- Rotoxkit F test (Verschueren, 2001)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Malathion is variously described as a colorless or yellow to deep brown, noncombustible liquid with a characteristic, mercaptan, garlic-like or skunk-like odor. It is a soild at temperatures below 37 degrees F (ACGIH, 1991; Ashford, 1994; Budavari, 2000; CHRIS , 2002; Harbison, 1998; HSDB , 2002; Lewis, 2000; NIOSH , 2002; Sittig, 1991).
PH
VAPOR PRESSURE
- 1.78x10(-4) mmHg (at 25 degrees C) (HSDB , 2002)
- 4x10(-5) mmHg (at 30 degrees C) (ACGIH, 1991; Budavari, 2000; Hayes & Laws, 1991; OHM/TADS , 2002)
- approximately 4x10(-5) mmHg (at 20 degrees C) (Lewis, 1997)
- 7.9x10(-6) mmHg (at 20 degrees C) (Howard, 1991)
- 5.3 mPa (at 30 degrees C) (Hartley & Kidd, 1990)
- 4X10(-5) mmHg (Harbison, 1998; NIOSH , 2002)
SPECIFIC GRAVITY
- NORMAL TEMPERATURE AND PRESSURE
(25 degrees C; 77 degrees F and 760 mmHg) 1.23 (at 25/4 degrees C) (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; ITI, 1995; Lewis, 2000)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
1.21 (NIOSH , 2002) 1.23 (OHM/TADS , 2002)
FREEZING/MELTING POINT
2.85 degrees C (ACGIH, 1991; Hartley & Kidd, 1990; Hayes & Laws, 1991; Verschueren, 2001) 2.9 degrees C (Budavari, 2000; Howard, 1991; ITI, 1995; Lewis, 2000; OHM/TADS , 2002) 3 degrees C (Lewis, 1997; Sittig, 1991) 2.85-3.7 degrees C (Bingham et al, 2001)
BOILING POINT
- 156-157 degrees C (at 0.7 mmHg) (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Howard, 1991; ITI, 1995; Hartley & Kidd, 1990; Hayes & Laws, 1991; Sittig, 1991; Verschueren, 2001)
- 156 degrees C (at 0.7 mmHg) (Lewis, 2000)
- 140 degrees F (decomposes) (NIOSH , 2002)
- 157 degrees C (OHM/TADS, 2001)
- 156-157 degrees C (under 0.7 mmHg) (with slight decompostion) (Lewis, 1997)
FLASH POINT
- >163 degrees C (Sittig, 1991)
- 163 degrees C (Pensky-Martens closed cup) (HSDB , 2002)
- >325 degrees F (CHRIS , 2002)
- >325 degrees F (open cup) (NIOSH , 2002)
- >325 degrees F (tag open cup) (HSDB , 2002)
EXPLOSIVE LIMITS
SOLUBILITY
Malathion is slightly soluble in water (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Howard, 1991; Lewis, 2000). 145 mg/L (at 25 degrees C) (Hartley & Kidd, 1990; OHM/TADS , 2002) 143 ppm (at 20 degrees C) (Howard, 1991) 145 mg/L (at 20 degrees C) (Verschueren, 2001) 0.02% (Harbison, 1998; NIOSH , 2002) 145 ppm (at 20 degrees C) (HSDB , 2002) 145 ppm (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Hayes & Laws, 1991) Malathion is sparingly soluble (ITI, 1995).
It is miscible with many organic solvents including (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; ITI, 1995; Lewis, 2000): It has limited solubility in certain paraffin hydrocarbons (Budavari, 2000). >10% in ethanol, ether, and benzene (HSDB , 2002) Malathion has limited solubility in petroleum ether, petroleum oils, and some types of mineral oil (ACGIH, 1991; Bingham et al, 2001; Hartley & Kidd, 1990). "Petroleum ether is soluble to about 35% in malathion" (Budavari, 2000).
Malathion is stable in aqueous solutions buffered at pH 5.26, but at a pH above 7.0 or below 5.0, it is rapidly hydrolyzed (Budavari, 2000; Hayes & Laws, 1991).
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 2.36 (Howard, 1991)
- 4.9X10(-9) atm-m(3)/mole (at 25 degrees C) (HSDB , 2002)
HENRY'S CONSTANT
- 2x10(-8) atm-m(3)/mol (approximate - calculated from water solubility and vapor pressure) (Howard, 1991; HSDB , 2002)
SPECTRAL CONSTANTS
239 (Aldermaston, Eight Peak Index of Mass Spectra, UK) (HSDB , 2002) Intense Mass Spectral peaks: 125 m/z (100%), 173 m/z (98%), 93 m/z (96%), 158 m/z (54%) (HSDB , 2002) Intense Mass spectral peaks: 127 m/z, 285 m/z, 330 m/z (HSDB , 2002)
OTHER/PHYSICAL
- LIQUID WATER INTERFACIAL TENSION
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