PARATHION

Parathion use was initially restricted in 1991. Subsequent review of continued worker exposure and its environmental risk resulted in a voluntary agreement between parathion manufacturers and the US EPA in 2001 to halt parathion production and sale and to phase out existing end-use parathion products. Since October 2003, production, importation, or application of parathion in the United States is illegal. Prior to these restrictions and product-use registration cancellations, parathion was used broadly as an insecticide and acaricide (HSDB, 2004; 66 FR 36356, 2001).
Past uses:

Parathion is used primarily as an acaracide and insecticide (Hathaway, 1996).

It is used to control many types of insects including: aphids, mites, beetles, Lepidoptera, leaf hoppers, leafminers, wireworms, rootworms, symphilids, and nematodes (HSDB , 1999).
Application sites include: vegetable crops, orchard crops, field crops, ornamentals, aquatic crops, and non-crop sites (EPA, 1988).

Parathion was synthesized for agricultural use in 1944 and is more poisonous on a mg/kg basis than many other organophosphates developed since (Geiger, 1993).
Its use is severely restricted or banned in many countries; it is considered a "Restricted Use Pesticide" in the US (ACGIH, 1991; HSDB , 1999).
HSDB (1999) lists only two US manufacturers of parathion.

FORMS

Parathion is available commercially as a dilute spray prepared from emulsifiable concentrates of 50% or less, or from 15% or 25% wettable powders. The compound is also available as dust containing concentrations of 5% or less (Hayes & Law, 1991).
Parathion is also available as granules (10% concentration) and in aerosol formulations (10% concentration) (ACGIH, 1991; Hartley & Kidd, 1987; IPCS, 1992).
The technical grade, which is approximately 98% pure, is a yellow to brown liquid (Hayes & Law, 1991).
Types of parathion formulations include: emulsifiable concentrates, granules, concentrates, baits, dusts, wettable powders, and impregnated materials (EPA, 1988).

SOURCES

Parathion can be derived from sodium ethylate, thiophosphoryl chloride, and sodium p-nitrophenate (Lewis, 1997).
Parathion can be produced by combining p-nitrophenol with O,O-diethyl phosphorochlorothioate and using dehydrochlorination (Ashford, 1994).
Parathion is not known to occur naturally (Howard, 1991).

-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 parathion, but could potentially occur in individual cases.

USES: Parathion is an organophosphate acaracide and insecticide. The use of parathion is severely restricted or banned in many countries. Since October 2003, production, importation, or application of parathion in the US is illegal.

TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop.

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

WITH POISONING/EXPOSURE

MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to parathion. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete.
CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

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

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

ACUTE CLINICAL EFFECTS

SUMMARY

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 parathion, but could potentially occur in individual cases.
USES: Parathion is an organophosphate acaracide and insecticide. The use of parathion is severely restricted or banned in many countries. Since October 2003, production, importation, or application of parathion in the US is illegal.
TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop.
EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.

EXPOSURE

MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to parathion. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete.
CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

ACID BASE

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

CARDIOVASCULAR

BRADYCARDIA: Bradycardia and hypotension occur following moderate to severe poisoning (Ganendran, 1974) with one study reporting hypotension (systolic blood pressure less than 90 mmHg) in 20% of patients (Bardin et al, 1987).
HYPERTENSION: Hypertension occurred in 83% of the cases of parathion poisoning (Tsachalinas et al, 1971). However, this study did not have comparisons from a control population.
TACHYCARDIA: Tachycardia is a common effect following exposure (Zwiener & Ginsburg, 1988; Hantson et al, 1995), and in one study, a heart rate of greater than 100 beats/minute was reported in 49% of patients (Bardin et al, 1987).
CARDIAC DYSRHYTHMIAS: Cardiac dysrhythmias and conduction defects have been reported in patients with severe organophosphate poisoning (Wren et al, 1981; Kiss & Fazekas, 1982). ECG abnormalities may include: sinus bradycardia, A-V dissociation, idioventricular rhythms, multiform premature ventricular extrasystoles, polymorphic ventricular tachycardia, prolongation of the PR, QRS, and QT intervals, and "torsade de pointes" polymorphous ventricular dysrhythmias (Brill et al, 1984; Ludomirsky et al, 1982).
MYOCARDITIS: Protracted toxic myocarditis has been suspected (Wren et al, 1981; Kiss & Fazekas, 1982).

DERMATOLOGIC

DIAPHORESIS: Profuse sweating may occur as one of the muscarinic signs of organophosphate poisoning (Ganendran, 1974).
PALLOR: Pallor is sometimes noted following exposure (Done, 1979).
DERMATITIS: Dermal sensitization has occurred with some organophosphates following skin exposure (Milby et al, 1964). In general, organophosphates can react with proteins and are potential haptens for allergic reactions.

ENDOCRINE

HYPERGLYCEMIA: Hyperglycemia can occur following severe poisoning (Namba, 1972). In one case, hyperglycemia occurred in a 3-year-old boy who was exposed to parathion (Zadik et al, 1983). The reported incidence of hyperglycemia in children following organophosphate or carbamate poisoning is about 22% (Zwiener & Ginsburg, 1988a), and may be the result of acute pancreatitis (Weizman & Sofer, 1992).
GLYCOSURIA: Glycosuria (without ketosis) can occur following severe poisoning (Namba, 1972). In one case, glycosuria occurred in a 3-year-old boy who was exposed to parathion (Zadik et al, 1983).
KETOACIDOSIS: Keto-acidosis occurred in a 3-year-old boy who was exposed to parathion (Zadik et al, 1983).
HYPOGLYCEMIA: Hypoglycemia has also been described in organophosphate poisoning (Hruban et al, 1963). Cholinergic agents stimulate insulin secretion by the islets of Langerhans (Kajinuma et al, 1968).

FLUID ELECTROLYTE

DEHYDRATION: Severe vomiting and diarrhea may cause significant dehydration (Hantson et al, 1995).
HYPOKALEMIA: A 40-year-old man developed protracted diarrhea and hypokalemia after ingesting parathion. Urinary potassium levels were elevated (more than 30 mmol/L) and represented the major source of potassium loss (Hantson et al, 1995).

GASTROINTESTINAL

Nausea, vomiting, diarrhea, abdominal cramps and hypersalivation are common muscarinic signs of organophosphate poisoning (Bardin et al, 1987).
FECAL INCONTINENCE: Fecal incontinence occurs in severe poisoning (Hayes, 1965).
PANCREATITIS: Acute pancreatitis has been reported following ingestion of parathion (Lankisch et al, 1990) and other organophosphates (Weizman & Sofer, 1992).

GENITOURINARY

URINARY INCONTINENCE: Involuntary urination can occur in more severe poisonings, and changes in urinary frequency may also become evident (Done, 1979).

HEENT

MIOSIS: Intense miosis is a typical manifestation, and is useful diagnostically (Hantson et al, 1995; De Bleecker et al, 1992), but is not always present following exposure. In one study, miosis occurred in 50/61 patients (82%) (Bardin et al, 1987).
MYDRIASIS: Even with the probable occurrence of miosis, mydriasis can occur in severely poisoned individuals (Dixon, 1957).
BLURRED VISION: Lacrimation and blurred vision are commonly present, and blurred vision may persist for several months (Milby, 1971; Whorton & Obrinsky, 1983).
OPSOCLONUS: A 29-year-old man developed opsoclonus 8 hours after ingesting parathion (De Bleecker, 1992).
EXCESSIVE SALIVATION: Excessive salivation, a muscarinic effect, has occurred following exposure. In one study, the adverse effect was reported in more than 50% of patients (Bardin et al, 1987).

HEMATOLOGIC

PROTHROMBIN TIME ABNORMALITIES: Alterations in prothrombin time (shortened or prolonged), and increased or decreased factor VII levels have been described, but clinically significant bleeding or hypercoagulability are rare (Von Kaulla & Holmes, 1961).
BLEEDING: Tendency to bleeding, probably related to platelet dysfunction, may occur (Ziemen, 1984).

HEPATIC

REDUCED LIVER FUNCTION: Parathion-poisoned patients showed the greatest disturbance in liver function, as judged by BSP retention and elevated bilirubin, SGOT, and SGPT, in a group of 52 patients hospitalized for exposure to insecticides, rodenticides, and drugs (Hayes, 1982). Liver function changes appeared to have no relationship to the clinical outcome of these cases (Hayes, 1982).

IMMUNOLOGIC

DERMAL SENSITIZATION: Dermal sensitization to some organophosphates has been reported following skin exposure (Milby et al, 1964), although a majority have not been adequately evaluated for this activity (Coye, 1984).

METABOLIC

CHOLINESTERASE SUPPRESSION: Delayed and prolonged suppression of acetylcholinesterase (AChE) levels developed in a 29-year-old man after ingesting 50 to 100 mL (12 to 24 g) of methyl parathion (Isbister et al, 2007).

MUSCULOSKELETAL

TOXIC MYOPATHY: Areas of necrosis were seen in the diaphragm in a case of lethal parathion poisoning (De Reuck & Willems, 1975).
RHABDOMYOLYSIS: A 22-year-old woman developed rhabdomyolysis (peak CPK 5290 IU/L), myalgia and muscle weakness after ingesting parathion (Yeh et al, 1993).

NEUROLOGIC

The earliest manifestations of poisoning are often referable to the central nervous system (CNS): giddiness, uneasiness, restlessness, anxiety and tremulousness. The initial CNS effects are commonly followed by headache, ataxia, drowsiness, difficulty in concentrating, mental confusion, and slurred speech (Grob & Garlick, 1950).
NEUROLOGICAL TEST DEFICITS: Patients occupationally exposed to organophosphate poisoning had poorer performance on subtests dealing with verbal attention, visual memory, motor function, and problem solving when compared with controls. Psychiatric symptoms were not different. Neuropsychological evaluations were performed 10 to 34 months after exposure (Ruckart et al, 2004; Rosenstock et al, 1991).
SEIZURE: Seizure may be an early symptom after a significant exposure (Joy, 1982), with children appearing to be more susceptible to seizures than adults (Zwiener & Ginsburg, 1988a). Additionally, EEG changes following mild organophosphate poisoning have appeared similar to interictal EEG's of temporal lobe epileptics (Brown, 1971).
DISTURBED CONSCIOUSNESS: Changes in mental cognition can occur following exposure. In one study, more than 50% of patients in one study had a disturbed level of consciousness. Five of 61 patients were confused; 16/61 were confused and unable to sit or stand; 16/61 were stuporous without reaction to speech (Bardin et al, 1987).
COMA: In severe poisonings, coma can supervene. Rarely, generalized convulsions can follow (Grob & Garlick, 1950).
MUSCLE WEAKNESS: Muscle weakness and fatigability occur commonly (De Bleecker et al, 1992).
FASCICULATIONS: Muscle fasciculations occur commonly (De Bleecker et al, 1992), and in one study, fasciculations were present in 54% (33/61) of patients with organophosphate poisoning (Bardin et al, 1987). Muscle paralysis occasionally supervenes (Done, 1979).
INTERMEDIATE SYNDROME/PARALYSIS: Type II neurological effects, also known as "intermediate syndrome," can appear from 12 to 72 hours following exposure and does involve paralysis. The paralysis is unresponsive to atropine and may be due to excess acetylcholine at nicotinic receptors. Paralytic signs include: inability to lift the neck or sit up, ophthalmoparesis, slow eye movement, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis and death (Wadia et al, 1987). In rare cases, paralysis of the diaphragm has occurred (Rivett & Potgieter, 1987).
DELAYED PERIPHERAL NEUROPATHY: Peripheral neuropathy has been reported following repeated exposure to parathion. Paresthesia developed approximately 11 weeks after the last exposure, and loss of the use of the legs after another 3 weeks. Weakness and other neurological problems were still evident almost 2 years later. However, a clear association to parathion cannot be made because of the long delay of symptom development (Hayes, 1982). Typically, it appears 6 to 21 days after acute exposure and can involve progressive distal weakness and ataxia in the lower limbs. Flaccid paralysis, spasticity, ataxia, or quadriplegia may ensue (Cherniack, 1988). Recovery requires weeks to months, and the recovery may never be complete (Done, 1979a).
ATAXIA: Following acute bromophos exposure, a cerebellar disorder manifested as ataxia developed approximately 5 weeks after acute exposure with no acute cholinergic effects and no other delayed neuropathy evident (Michotte et al, 1989).
DYSKINESIA: Dyskinesias can result following exposure. These effects can present in multiple forms including choreoathetosis (ceaseless jerky, sinuous, involuntary movements) (Joubert et al, 1984), opisthotonos (type of spasm where the head and heels are drawn backward while the trunk is forward) (Smith, 1977), and opsoclonus (rapid, uncontrolled eye movements) (Pullicino & Aquilina, 1989).
DROWSINESS: Acute or chronic exposure to organophosphates may impair concentration and induce confusion and drowsiness and may be a factor in plane crashes by agricultural pilots doing cropdusting (Levin & Rodnitzky, 1976).
REDUCED COGNITION: Persons with other signs of organophosphate poisoning have shown reduced cognitive efficiency and slowness of thought related to the degree of cholinesterase inhibition (Levin & Rodnitzky, 1976).
IMPAIRED MEMORY: Impaired memory is a major CNS effect of organophosphate exposure and may occur in the absence of other overt clinical signs. It has been found in workers chronically exposed to organophosphates (Levin & Rodnitzky, 1976).
SPEECH IMPAIRMENT: Slowed speech, problems in finding words, slurring, intermittent pauses, and perseveration have been seen in persons who have other clinical signs of organophosphate poisoning (Levin & Rodnitzky, 1976).

PSYCHIATRIC

HALLUCINATIONS: Visual and auditory hallucinations may occur during the acute stage of parathion poisoning (Namba et al, 1971).
PSYCHOSIS: Psychosis and a variety of other personality and behavioral disorders have been described from exposure to organophosphates (Dille & Smith, 1964; Conyers & Goldsmith, 1971; Joubert & Joubert, 1988). These effects are more common with chronic exposure. Organophosphates may exacerbate psychotic symptoms in persons with preexisting schizophrenic tendencies; it is not clear if these symptoms can be induced by organophosphates in the absence of preexisting abnormality (Levin & Rodnitzky, 1976).
ANXIETY: Anxiety and/or irritability have frequently occurred in persons exposed to organophosphates (Levin & Rodnitzky, 1976).
DEPRESSION: Depression, correlated with the severity of cholinesterase inhibition, has occurred in cases of acute organophosphate poisoning (Levin & Rodnitzky, 1976).

RESPIRATORY

Increased bronchial secretions, bronchospasm, chest tightness, heartburn, and dyspnea occur in severe and moderately severe organophosphate poisonings (Hayes, 1965).
ACUTE LUNG INJURY: Acute lung injury can occur as a manifestation of severe organophosphate poisoning (Chhabra & Sepaha, 1970).
ASTHMA EXACERBATION: Asthma exacerbations may occur after the inhalation of nontoxic amounts of some organophosphates in sensitive patients with preexisting asthma (Bryant, 1985). Bronchospasms following exposure may be a pharmacologic effect from the muscarinic activity of organophosphates (Lund & Monteagudo, 1986).
TACHYPNEA: Tachypnea has been reported following exposure with one study reporting a respiratory rate greater than 30 breaths/minute in 39% of patients (Bardin et al, 1987).
RESPIRATORY FAILURE: Acute respiratory insufficiency, due to any combination of depression of the respiratory center, respiratory paralysis, bronchospasm or increased bronchial secretions, is the main cause of death in many acute organophosphate poisonings (Lerman & Gutman, 1988; Anon, 1984). Respiratory crisis may be delayed by 2 to 3 weeks after acute exposure to parathion (Kokkas, 1985).
CHEMICAL PNEUMONITIS: Aspiration of commercial organophosphate preparations which contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986).

VITAL SIGNS

FEVER: Fever occurred in a 5-year-old boy who had ingested a small amount of a mixture of parathion, diazinon and chlordane; it persisted for two days (DePalma et al, 1970).

CHRONIC CLINICAL EFFECTS

Chronic parathion exposures are of particular concern, as persons may become more susceptible to the toxic effects after repeated exposure (NIOSH/OSHA). Parathion binds irreversibly to and inhibits the activity of cholinesterases (ILO, 1983), and is expected to have cumulative toxicity. Decreased tolerance with chronic exposure has been demonstrated in rats. Sublethal doses fed over several weeks produced an increased sensitivity to a lethal challenge dose (Kurtz, 1979).

Many fatal chronic occupational parathion poisonings have been reported (Osorio et al, 1991).

Occupational exposure to 4.88 mg/day did not cause clinical symptoms in men; the no-effect level in adults is considered to be approximately 0.07 mg/kg/day (Hayes & Laws, 1991).

Sensitization is not a significant problem with parathion (Hayes & Laws, 1991).

Parathion was not stored in the tissues of rats in subacute feeding studies (Clayton & Clayton, 1993).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

ORAL EXPOSURE

Prehospital gastrointestinal decontamination is NOT recommended because of the potential for early coma or seizures and aspiration.

DERMAL EXPOSURE

Remove contaminated clothing. Wash skin thoroughly with soap and water.

EYE EXPOSURE

Copious eye irrigation.

INHALATION EXPOSURE

Immediately assess airway and respiratory function. Administer oxygen.

PERSONNEL PROTECTION

Universal precautions should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids.
Vomiting containing organophosphates should be placed in a closed impervious container for proper disposal.

DECONTAMINATION OF SPILLS/SUMMARY

A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a).

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

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

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

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

SMALL SPILL DECONTAMINATION

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

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

LARGE SPILL DECONTAMINATION

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

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

FURTHER CONTACT INFORMATION

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

ANTIDOTES

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

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

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

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

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

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

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

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

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

FIRST AID

ORAL EXPOSURE

Prehospital gastrointestinal decontamination is NOT recommended because of the potential for early coma or seizures and aspiration.

DERMAL EXPOSURE

Remove contaminated clothing. Wash skin thoroughly with soap and water.

EYE EXPOSURE

Copious eye irrigation.

INHALATION EXPOSURE

Immediately assess airway and respiratory function. Administer oxygen.

PERSONNEL PROTECTION

Universal precautions should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids.
Vomiting containing organophosphates should be placed in a closed impervious container for proper disposal.

DECONTAMINATION OF SPILLS/SUMMARY

A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a).

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

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

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

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

SMALL SPILL DECONTAMINATION

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

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

LARGE SPILL DECONTAMINATION

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

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

FURTHER CONTACT INFORMATION

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

ANTIDOTES

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

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

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

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

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

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

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

Oral doses in the range of 120 to 900 milligrams have been fatal; however, humans have survived much higher reported doses. Three individuals survived estimated doses of 20,000 to 40,000 mg of parathion (Hayes & Laws, 1991).

Much interindividual variation in susceptibility to parathion is possible.

A dose of 2 milligrams of parathion was lethal to a child (Lewis, 1998).

The estimated minimum lethal oral parathion dose ranges from less than 10 mg to 120 mg (Hathaway, 1996).

It is estimated that ingestion or inhalation of 10 to 300 milligrams of parathion is fatal in adults (Baselt, 1997).

The lowest published lethal dose for a human was 171 micrograms/kilogram by the oral route (RTECS , 1999).

The lowest published lethal dose for a human by the dermal route was 7143 micrograms/kilogram (RTECS , 1999).

The lowest published lethal dose for a human by the intratracheal route was 714 micrograms/kilogram (RTECS , 1999).

The lethal dose of parathion for children has been estimated to be between 0.1 mg/kg and 2.0 mg/kg (Etzel et al, 1987).

CASE REPORTS

Death was reported in a tractor-sprayer driver who had been applying 0.125 percent parathion spray to almond orchards for 3 weeks, despite the use of full protective clothing and a respirator. Large amounts were found in gastric contents, and it was concluded that a large exposure occurred during one hour of driving the rig from a combination of dermal and/or ingestion. It was suspected that the exposure was accidental, and may have occurred while trying to clear a clogged nozzle (Osorio et al, 1991).
Fourteen people died from acute parathion poisoning after ingesting bread baked with flour contaminated with parathion during transport from the mill. Investigators estimated that 10 to 15 milliliters of parathion may have spilled onto a 22.5 kilogram bag of flour in the truck during transport. One month after the incident, a sample taken from the floor of the truck contained 0.87 mg/kg parathion. A loaf of bread baked in the bakery on the same day as the outbreak of illnesses contained 410 mg/kg parathion (Etzel et al, 1987).

MAXIMUM TOLERATED EXPOSURE

The World Health Organization (WHO) has classified parathion as pesticide class Ia (extremely hazardous) (World Health Organization, 2006).

The lowest published toxic dose to a man was 429 micrograms/kilogram/4 days by the oral route based on inhibition of true cholinesterase (RTECS , 1999).

The lowest published toxic dose for a woman was 5670 micrograms/kilogram causing mydriasis, coma, and dyspnea (RTECS , 1999).

The ingestion of 50 to 100 mL (12 to 24 g) of methyl parathion by a 29-year-old man caused delayed suppression of acetylcholinesterase levels but only minimal effects (nausea, vomiting and blurred vision). Following supportive treatment (including early pralidoxime therapy), he became asymptomatic after 12 hours (Isbister et al, 2007).

Aggressive treatment with atropine and oximes has saved some patients with ingestions as high as 50 grams (Hayes, 1982). With the proper treatment, patients can survive even large doses. One patient survived an attempted suicide with 150 grams of parathion; treatment included atropine, obidoxime and charcoal hemoperfusion. Recovery was complete except for residual polyneuropathy (de Monchy et al, 1979).

Three workers in a pesticide-formulating plant developed symptoms of organophosphate poisoning associated with each worker wearing a uniform that was contaminated with 76 percent parathion and then laundered. The uniform had been laundered three times before the third worker wore it and he still developed nausea, vomiting, and red cell cholinesterase activity of 75% of normal (Clifford & Nies, 1989).

"An oral dose of 7.2 mg/parathion/day, 5 days/week, for 6 weeks produced a 33% decrease in whole blood cholinesterase activity (16% and 37% for eyrthrocyte and plasma cholinesterase, respectively) in 4 adult female volunteers. This corresponded to a daily oral intake of 0.078 mg/kg. No significant effects on the activities of cholinesterase in blood were observed as a result of the daily oral ingestion by groups of 4 subjects of either sex of 0.6, 1.2, 2.4, or 4.8 mg of parathion for periods ranging from 25 to 70 days. The results showed that a safe no-effect daily oral dose of parathion in humans was less than 0.078 mg/kg and greater than 0.058 mg/kg" (HSDB , 1999).

ANIMAL DATA

Rats were not affected by a 1 part per million level of parathion in their diet; however, 5 parts per million inhibited red cell cholinesterase; the latter dose corresponded to approximately 0.25 milligram/kilogram/day (Hayes & Laws, 1991).

Carcinogenicity Ratings for CAS56-38-2 :

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

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

EPA (U.S. Environmental Protection Agency, 2011): C ; Listed as: Parathion

C : Possible human carcinogen.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: Parathion

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

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Parathion
MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS56-38-2 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD:

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

References: ACGIH, 1991 Budavari, 1996 Hayes & Laws, 1991 IARC, 1983 ITI, 1995 ) Lewis, 1996 OHM/TADS, 1999 RTECS, 1999 Note: All values are from RTECS, 1999 unless otherwise noted.
- LC50- (INHALATION)DOG:
- LC50- (INHALATION)RAT:
- LCLo- (INHALATION)GUINEA_PIG:
- LCLo- (INHALATION)MOUSE:
- LCLo- (INHALATION)RABBIT:
- LCLo- (INHALATION)RAT:
- LD50- (INTRAPERITONEAL)CAT:
- LD50- (INTRAVENOUS)CAT:
- LD50- (ORAL)CAT:
- LD50- (INTRAPERITONEAL)CHICKEN:
- LD50- (ORAL)CHICKEN:
- LD50- (INTRAPERITONEAL)DOG:
- LD50- (INTRAVENOUS)DOG:
- LD50- (ORAL)DOG:
- LD50- (ORAL)GOAT:
- LD50- (INTRAPERITONEAL)GUINEA_PIG:
- LD50- (ORAL)GUINEA_PIG:
- LD50- (SKIN)GUINEA_PIG:
- LD50- (ORAL)HORSE:
- LD50- (ORAL)HUMAN:
- LD50- (INTRAMUSCULAR)MOUSE:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (INTRAVENOUS)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)MOUSE:
- LD50- (SUBCUTANEOUS)MOUSE:
- LD50- (ORAL)RABBIT:
- LD50- (SKIN)RABBIT:
- LD50- (INTRAMUSCULAR)RAT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (INTRAVENOUS)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LDLo- (INTRAMUSCULAR)GOAT:
- LDLo- (ORAL)GOAT:
- LDLo- (INTRATRACHEAL)HUMAN:
- LDLo- (ORAL)HUMAN:
- LDLo- (SKIN)HUMAN:
- LDLo- (ORAL)MOUSE:
- LDLo- (INTRAMUSCULAR)SHEEP:
- LDLo- (ORAL)SHEEP:
- TDLo- (ORAL)HUMAN:
- TDLo- (ORAL)RAT:
- TDLo- (SUBCUTANEOUS)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS56-38-2 (American Conference of Governmental Industrial Hygienists, 2010):

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

Adopted Value

Parathion

TLV:

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

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: BEI, IFV, Skin
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
IFV: Inhalable fraction and vapor.
Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.

TLV Basis - Critical Effect(s): Cholinesterase inhib
Molecular Weight: 291.27

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

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

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

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

AIHA WEEL Values for CAS56-38-2 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS56-38-2 (National Institute for Occupational Safety and Health, 2007):

Listed as: Parathion
REL:

TWA: 0.05 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: [skin]

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

Note(s):

IDLH:

IDLH: 10 mg/m3
Note(s): Not Listed

OSHA PEL Values for CAS56-38-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Parathion
Table Z-1 for Parathion:

8-hour TWA:

ppm:

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

mg/m3:

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

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

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS56-38-2 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS56-38-2 (U.S. Environmental Protection Agency, 2010):

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

10 (4.54)

Additional Information:
Listed as: Phosphorothioic acid, O,O-diethyl O-(4-nitrophenyl) ester
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS56-38-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS56-38-2 (U.S. Environmental Protection Agency, 2010b):

Listed as: Parathion
P or U series number: P089
Footnote:
Listed as: Phosphorothioic acid, O,O-diethyl O-(4-nitrophenyl) ester
P or U series number: P089
Footnote:
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS56-38-2 (U.S. Environmental Protection Agency, 2010):

Listed as: Parathion
Reportable Quantity, in pounds: 10

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

Threshold Planning Quantity, in pounds:

100
Amount necessary to be covered by this standard. See 40 CFR 355.30.

Note(s): b

b: The calculated TPQ changed after technical review as described in a technical support document for the final rule, April 22, 1987.

EPA SARA Title III, Community Right-to-Know for CAS56-38-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Parathion [Phosphorothioic acid, O,O-diethyl-O-(4-nitrophenyl) ester]
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS56-38-2 (49 CFR 172.101 - App. B, 2005):

Listed as Parathion
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS56-38-2 (EPA, 2005):

Not Listed

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 2783 (49 CFR 172.101, 2005):

Hazardous materials descriptions and proper shipping name: Organophosphorus pesticides, solid, toxic

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN2783
Packing Group: I

I: Packing Group I - indicates the degree of danger presented by the material is great.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB7, IP1, N77, T6, TP33

IB7: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Wooden (11C, 11D and 11F). Additional Requirement: Liners of wooden IBCs must be sift-proof.
IP1: IBCs must be packed in closed freight containers or a closed transport vehicle.
N77: For materials of not more than two percent active ingredients by weight, packagings need not conform to the requirements of part 178 of this subchapter, if liquid contents are absorbed in an inert material.
T6: Minimum test pressure (bar): 4; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: None
Non-bulk packaging: 211
Bulk packaging: 242

Quantity Limitations:

Passenger aircraft or railcar: 5 kg
Cargo aircraft only: 50 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: 40

40: Stow "clear of living quarters".

Hazardous materials descriptions and proper shipping name: Organophosphorus pesticides, solid, toxic

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN2783
Packing Group: II

II: Packing Group II - indicates the degree of danger presented by the material is medium.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB8, IP2, IP4, N77, T3, TP33

IB8: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Fiberboard (11G); Wooden (11C, 11D and 11F); Flexible (13H1, 13H2, 13H3, 13H4, 13H5, 13L1, 13L2, 13L3, 13L4, 13M1 or 13M2).
IP2: When IBCs other than metal or rigid plastics IBCs are used, they must be offered for transportation in a closed freight container or a closed transport vehicle.
IP4: Flexible, fiberboard or wooden IBCs must be sift-proof and water-resistant or be fitted with a sift-proof and water-resistant liner.
N77: For materials of not more than two percent active ingredients by weight, packagings need not conform to the requirements of part 178 of this subchapter, if liquid contents are absorbed in an inert material.
T3: Minimum test pressure (bar): 2.65; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: 153
Non-bulk packaging: 212
Bulk packaging: 242

Quantity Limitations:

Passenger aircraft or railcar: 25 kg
Cargo aircraft only: 100 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: 40

40: Stow "clear of living quarters".

Hazardous materials descriptions and proper shipping name: Organophosphorus pesticides, solid, toxic

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN2783
Packing Group: III

III: Packing Group III - indicates the degree of danger presented by the material is minor.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB8, IP3, N77, T3, TP33

IB8: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Fiberboard (11G); Wooden (11C, 11D and 11F); Flexible (13H1, 13H2, 13H3, 13H4, 13H5, 13L1, 13L2, 13L3, 13L4, 13M1 or 13M2).
IP3: Flexible IBCs must be sift-proof and water-resistant or must be fitted with a sift-proof and water-resistant liner.
N77: For materials of not more than two percent active ingredients by weight, packagings need not conform to the requirements of part 178 of this subchapter, if liquid contents are absorbed in an inert material.
T3: Minimum test pressure (bar): 2.65; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: 153
Non-bulk packaging: 213
Bulk packaging: 240

Quantity Limitations:

Passenger aircraft or railcar: 100 kg
Cargo aircraft only: 200 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: 40

40: Stow "clear of living quarters".

ICAO International Shipping Name for UN2783 (ICAO, 2002):

Proper Shipping Name: Organophosphorus pesticide, solid, toxic
UN Number: 2783

LABELS

NFPA

NFPA Hazard Ratings for CAS56-38-2 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

Workers should be competent, well-trained, and properly supervised (IPCS, 1992).
When handling parathion, workers should wear appropriate personal protective clothing, including boots, overalls, gloves, respirators, and impermeable hoods to prevent contact (IPCS, 1992; NIOSH , 1999). Eye protection also should be worn and eyewash fountains should be provided (NIOSH , 1999).
Smoking or eating around areas of parathion exposure should be prohibited (Shih et al, 1985).
"It is sound practice for the different classes [of pesticides] to be clearly distinguished by background colours on the label and, in the case of compounds of high or extreme hazard, for the appropriate danger symbol to be incorporated. It often occurs that an adequately labelled quantity of pesticide in bulk is locally repacked into smaller containers. Each such small package should bear a similar label, and repacking in containers which have held, or are easily identifiable with, containers used for food should be absolutely forbidden. If small packages are to be transported, the same rules apply as for the carriage of larger packages" (ILO, 1998).
Parathion can be transferred from the hands to cigarettes. More parathion was transferred to cigarettes from hands which had been in contact with the surface of drums containing emulsifiable concentrate (179 mcg average) than by dipping a cigarette directly into a bag of 25% water-wettable powder and brushing it off (109 mcg average) (Wolfe et al, 1975).

STORAGE

CONTAINER

As containers may leak, they must be inspected regularly (Sittig, 1991).
Parathion will reactive with some forms of rubber, plastics, and coatings (HSDB , 1999).
"Temperatures above 100 degrees C (212 degrees F) may cause decomposition so that containers may burst" (HSDB , 1999).
Protect parathion containers from mechanical damage, corrosion, and ignition sources (HSDB , 1999).
Pesticide labels should provide the following information: approved name and trade name; the name of the packager, supplier, or manufacturer; directions for and precautions to be taken during use; protective equipment to be worn; poisoning symptoms and first-aid treatment for suspected poisonings (ILO, 1998).

ROOM/CABINET RECOMMENDATIONS

Store in areas where any spillage from containers will not endanger workers or contaminate other materials (Sittig, 1991).
Parathion storage containers should be protected from corrosion, mechanical damage, and sources of ignition (HSDB , 1999).
Locate outdoor storage facilities a minimum of 20 feet from dwellings/populated areas. When feasible, equip facilities with a sprinkler system (HSDB , 1999).
Parathion should be stored in a well ventilated area (OHM/TADS , 1999).
Rooms used to store parathion should be well constructed and be outfitted with secure locks. "Floors should be kept clear" (ILO, 1998).
If repacking of parathion occurs where it is stored, light and ventilation should be adequate, washing stations should be nearby, and drinking, eating, and smoking in the area should be forbidden (ILO, 1998).

INCOMPATIBILITIES

Keep separate from strong oxidizers and alkaline materials (NIOSH , 1999).

-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.

Prevent skin contact with parathion by wearing appropriate personal protective clothing. Remove and replace wet work clothing or clothing that has become significantly contaminated. Workers wearing contaminated clothing should change clothing before leaving the work premises (NIOSH , 1999).

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

Parathion can penetrate canvas shoes, sneakers, and leather (HSDB , 1999).

A single washing with soap and water can remove from 80 to 92% of an organophosphate on the skin if done immediately (Fredriksson, 1961). If delayed, the same procedure may remove only 50 to 70%.

Following a soap and water wash, a second wash with 95% ethanol will leave only about a 5 to 10% organophosphate residue (Fredriksson, 1961).

"Facilities for quickly drenching the body should be provided within the immediate work area for emergency use where there is a possibility of exposure. [Note: It is intended that these facilities provide a sufficient quantity or flow of water to quickly remove the substance from any body areas likely to be exposed. The actual determination of what constitutes an adequate quick drench facility depends of the specific circumstances. In certain instances, a deluge shower should be readily available, whereas in others, the availability of water from a sink or hose could be considered adequate]" (NIOSH , 1999).

EYE/FACE PROTECTION

Goggles should be worn when working with this material (CHRIS , 1999).

A face shield (8-inch minimum) should be worn to prevent prolonged or repeated skin contact with the compound (HSDB , 1999).

RESPIRATORY PROTECTION

Wear a self-contained positive pressure breathing apparatus when working in the vicinity of spills or leaks or when fighting fires (AAR, 1998).

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 56-38-2.

All data are compiled from published sources and are NOT recommended specifically by Truven Health Analytics. The appearance of specific manufacturers or products in this section does not represent an endorsement by Truven Health Analytics. No attempt has been made to verify the data presented. All product recommendations should be confirmed with the specific manufacturer for verification of product performance.
CLOTHING

Plastic Laminate

DuPont Personal Protection

Tychem 10,000

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.1
Notes: liquid
Citation: (DuPont, 2002)

Tychem 7500

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid
Citation: (DuPont, 2002)

Tychem 9400

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.01
Notes: liquid
Citation: (DuPont, 2002)

Tychem BR

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.01
Notes: Not Listed
Citation: (DuPont, 2002)

Tychem LV

Degradation Rating: Not Listed
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.01
Notes: Not Listed
Citation: (DuPont, 2003)

Tychem QC

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid
Citation: (DuPont, 2002)

Tychem SL

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid
Citation: (DuPont, 2002)

Tychem TK

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.01
Notes: Not Listed
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.01
Notes: liquid
Citation: (DuPont, 2002)

Teflon Laminate

Mar-Mac Manufacturing, Inc.

Commander Ultrapro

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >420
Permeation Rate (mcg/cm2/min): <0.1
Notes: Not Listed
Citation: (Mar-Mac Manufacturing, Inc, 1995)

FOOTWEAR

Specific recommendations and test data for this product type were not found in the available manufacturers' product literature.

GLOVES

Specific recommendations and test data for this product type were not found in the available manufacturers' product literature.

GENERAL INFORMATION

This section provides a compilation of chemical resistance information and test data for specific protective clothing products. Chemical resistance information includes both degradation resistance ratings and permeation resistance data. This information is designed to assist in the selection of appropriate protective clothing. Only data on specific products and manufacturers are included. Generic information or recommendations are not provided since significant differences can exist in the chemical resistance for apparent similar product types.
Specific product information is organized by general product type (gloves, garments, and footwear), material type, and manufacturer. The category 'garments' may include totally encapsulating suits, splash suits, as well as other items (e.g., coveralls, jackets, and aprons). Specific manufacturers should be contacted to determine the features of available styles/models.
In addition to chemical resistance information, there are many critical variables in the selection of protective clothing which cannot be represented in this summary of the literature. Some factors to be considered in choosing protective clothing include, but are not limited to: overall clothing integrity, physical hazard resistance, durability, human factors, ease of decontamination, and cost. Overall clothing integrity refers to a specific design's ability to offer consistent protection for all clothing-covered areas of the body. Physical hazards include resisting the effects of abrasion, cuts, tears, and punctures. Human factors entail effects on wearer mobility, visibility, and hearing for garments; dexterity, tactility, and grip for gloves; ankle support and weight for footwear; and, any effect of the clothing on the function of the wearer. There are several variations in the design for gloves, garments, and footwear that affect these factors. Protective clothing must properly be sized and correctly fit the wearer to ensure its proper use and function.
As required in the U.S.A., protective clothing should be selected based on a risk assessment of the workplace. This risk assessment must account for the identification of existing as well as potential hazards and involve the recommendation of protective clothing appropriate for the identified hazards. Therefore, the recommendations in this section should not be used as the sole basis for decisions on choice of protective clothing, but rather should be used as a tool by qualified occupational health and safety professionals or other technically qualified persons in conjunction with a review of all mitigating factors. Consult the OSHA PPE Standard (29 CFR 1910.132 - 1910.138) for regulations and additional guidance regarding the selection and use of protective clothing and equipment. For general information on protective clothing selection, refer to the "PERSONAL PROTECTIVE EQUIPMENT - OSHA PUB 3077" document.
PROTECTIVE CLOTHING SELECTION

Determine the type of protective clothing item needed based on a risk assessment (e.g., gloves, garments, footwear).
For high risk situations, choose clothing that covers all parts of the body that may be exposed. In many cases, multiple clothing items will be required. Low risk situations may permit partial body protective clothing. Select protective clothing products that have reported chemical resistance data. High risk situations involving full body clothing or extended chemical contact often require permeation resistance data to determine the barrier effectiveness of materials used in the construction of clothing. Relatively low risk situations, where only splash or incidental exposure occur, may allow use of protective clothing based on degradation or penetration resistance data. Specifics on the interpretation of chemical resistance data are presented below.
Other factors must be considered in addition to chemical resistance. The selected chemical protective clothing item should offer the optimal combination of protection against identified hazards while allowing maximum function and comfort.

INTERPRETATION OF DEGRADATION RATINGS

Degradation refers to physical changes in a material as the result of chemical exposure. Degradation may become evident in visible changes, such as discoloration, swelling, delamination, deterioration, or disintegration. Degradation effects may also be measured by weight change or other changes in a material's physical properties (e.g., strength, elasticity, hardness).
Degradation resistance ratings are provided by manufacturers to rate the amount of degradation that occurs for a particular protective clothing material when contacted by a chemical. All degradation ratings are qualitative and include ratings, such as "EXCELLENT," "GOOD," "FAIR," "POOR," and "NOT RECOMMENDED." There is no standard test method for the measurement of chemical degradation resistance; therefore, manufacturer ratings may be based on different testing approaches. This makes comparison of degradation ratings between manufacturers unreliable.
The use of degradation resistance ratings alone to recommend protective clothing, particularly for high hazard situations, should be avoided. Degradation resistance testing does not directly assess the barrier quality of protective clothing, since materials can show relatively little degradation but still allow either permeation or penetration by a chemical. Degradation resistance ratings can be used to exclude protective clothing materials from consideration. Protective clothing materials with a "NOT RECOMMENDED" degradation resistance rating should never be used.
For some products, the rating "NO PENETRATION" is provided. This refers to penetration resistance test results that are based on a different procedure (American Society for Testing and Materials (ASTM) Standard Test Method F 903). Penetration resistance testing involves placing a material sample in a test cell, exposing the exterior side of the material to a chemical, and then observing the interior side of the material for visible signs of liquid penetration. Part of the test is conducted at an elevated pressure. Test results are reported as pass (no penetration) or fail (penetration detected). Unlike degradation testing, penetration testing provides an assessment of protective clothing material barrier performance. Since penetration resistance testing examines only observable amounts of liquid penetration, permeation may still occur. The use of penetration resistance data must be restricted to liquid chemicals, and should be limited to scenarios where there is no reasonable vapor exposure hazard under the conditions of exposure.

INTERPRETATION OF PERMEATION DATA

Permeation is the process of chemical movement through a material on a molecular level. Permeation resistance refers to the ability of a material to retard or prevent chemical movement through it. Permeation may occur without any visible signs of degradation.
Permeation resistance is measured using a test cell which is divided into two halves by a protective clothing specimen. Chemical is placed on the challenge side, while the collection side is periodically monitored for permeating chemical. Permeation data were obtained in accordance with the American Society for Testing and Materials (ASTM) Standard Test Method F 739 (Resistance of Materials Used in Protective Clothing to Permeation by Liquids and Gases), unless stated otherwise. In the case of chemicals that are classified as warfare agents, the data were obtained in accordance with the Military Standard 282 (MIL-STD-282) (Military Standard, Filter Units, Protective Clothing, Gas-Mask Components, and Related Products: Performance Test Methods).
Permeation rate is the amount of chemical that passes through a material for a measured surface area per unit time. In this section, permeation rate is expressed in micrograms per square centimeter per minute (mcg/cm(2)/min). The reported permeation rate is either the steady-state rate or the maximum rate observed during testing. In some cases, very large permeation rates exceed measurement techniques and are reported as ">" (greater than) or "HIGH."
Breakthrough time is the elapsed time, in minutes, from the time the chemical comes in contact with the material exterior surface, to the time that chemical is detected on the interior surface. When no breakthrough is detected, the breakthrough time is report as ">" the testing period. If permeation breakthrough is rapid, results are reported as "<" (less than) the earlier sampling time or as "IMMEDIATELY" (which usually means breakthrough in less than 4 minutes).
The breakthrough time should exceed the expected use period of the selected protective clothing. Additionally, there are several other factors that must be taken into account to provide appropriate protection.
Permeation testing is usually conducted with full strength, undiluted chemical for the duration of the test period. Actual exposures may involve diluted chemical for short or intermittent exposure periods.
Permeation testing is usually conducted at room temperature. Permeation occurs faster at elevated temperatures (short breakthrough times and higher permeation rates) and slower at reduced temperatures (long breakthrough times and lower permeation rates).
Permeation resistance of mixtures cannot usually be determined on the basis of the individual chemicals making up the mixture. Synergistic effects may occur and result in more rapid permeation than accounted for by the individual mixture chemicals.
Permeation rates may be used to calculate potential wearer exposure; however, several assumptions must be made about the extent of exposure and condition of clothing wear. Furthermore, there are few chemicals with dermal exposure limits, making it difficult to determine an acceptable skin exposure level.

COMPANY INFORMATION

DuPont Personal Protection P. O. Box 80705 Wilmington, DE 19880-0705 USA Phone: (302) 774-1000 Toll-Free: (800) 931-3456 Website: http://personalprotection.dupont.com Email: personalprotection@usa.dupont.com
Mar-Mac Manufacturing, Inc. P. O. Box P.O. Box 278 McBee, SC 29101 USA Phone: (843) 335-8211 Fax: (843) 355-8599 Toll-Free: (843) 335-8211 Website: http://www.marmac.com Email: info@marmac.com

REFERENCES

CHEMICAL PROTECTIVE CLOTHING CITATIONS

The following sources were consulted for chemical protective clothing data:

(Ansell-Edmont, 2001)
(Bata Shoe Company, 1995)
(Best Manufacturing, 2002)
(Best Manufacturing, 2004)
(Boss Manufacturing Company, 1998)
(ChemFab Corporation, 1993)
(Comasec Safety, Inc., 2003)
(Comasec Safety, Inc., 2003a)
(DuPont, 2002)
(DuPont, 2002)
(DuPont, 2003)
(Guardian Manufacturing Group, 2001)
(ILC Dover, Inc., 1998)
(Kappler Inc., 2001)
(Kimberly-Clark, 2002)
(LaCrosse-Rainfair, 1997)
(MAPA Professional, 2003)
(MAPA Professional, 2004)
(Mar-Mac Manufacturing, Inc, 1995)
(Marigold Industrial, 2003)
(Memphis Glove Company, 2001)
(Montgomery Safety Products, 1995)
(Nat-Wear, 2001)
(Neese Industries, Inc., 2003)
(North, 2002)
(North, 2002)
(Playtex, 1995)
(River City, 1995)
(Safety 4, 2002)
(Servus, 1995)
(Standard Safety Equipment, 1995)
(Tingley, 2002)
(Trelleborg-Viking, Inc., 2001)
(Trelleborg-Viking, Inc., 2002)
(Wells Lamont Industrial, 2002)
(Workrite, 1997)

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

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.
Parathion is not flammable (CHRIS , 1999).
Parathion "does not burn or burns with difficulty" (AAR, 1998).
The compound in solvents is slightly flammable (OHM/TADS , 1999).
Lewis (1996) states that parathion is combustible when exposed to heat or flame.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS56-38-2 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

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

Dry chemical, CO2 or water spray.

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

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

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

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

NFPA Extinguishing Methods for CAS56-38-2 (NFPA, 2002):

Not Listed

Use water as fog in flooding amounts (AAR, 1988).

Dry chemical, "alcohol" foam, or carbon dioxide can be used to extinguish this material, if on fire (AAR, 1998).

COMBUSTION TOXICITY

When heated to decomposition, parathion releases poisonous carbon monoxide vapors (HSDB , 1999) as well as nitrogen, phosphorus, and sulfur oxide vapors (Lewis, 1996).

EXPLOSION HAZARD

In terms of explosiveness, parathion is considered "stable" (OHM/TADS , 1999).

A parathion-endrin mixture may be violent or explosive (Lewis, 1996; Pohanish & Greene, 1997).

It is possible for containers of parathion, when heated, to explode (CHRIS , 1999).

DUST/VAPOR HAZARD

When parathion is heated to decomposition, it releases poisonous carbon monoxide vapors (HSDB , 1999) as well as nitrogen, phosphorus, and sulfur oxide vapors (Lewis, 1996).

Parathion decomposes slowly in air (Lewis, 1997).

REACTIVITY HAZARD

When heated to decomposition, parathion releases toxic fumes of carbon monoxide (HSDB , 1999) and oxides of nitrogen, phosphorus, and sulfur (Lewis, 1996).

Violent or explosive reactions occur when parathion comes into contact with endrin (Lewis, 1996; Pohanish & Greene, 1997).

"Shock can shatter the container" (Lewis, 1996).

The compound is incompatible or may react with strong oxidizers and alkaline materials (NIOSH , 1999).

When in contact with alkaline substances, parathion hydrolyzes (Lewis, 1997).

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.
Keep unauthorized personnel away.
Stay upwind.
Keep out of low areas.

AIHA ERPG Values for CAS56-38-2 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS56-38-2 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Parathion
TEEL-0 (units = mg/m3): 0.1
TEEL-1 (units = mg/m3): 0.15
TEEL-2 (units = mg/m3): 1.5
TEEL-3 (units = mg/m3): 2.0
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 CAS56-38-2 (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: Parathion
Proposed Value:

AEGL-1

10 min exposure:

ppm:
mg/m3: Not recommended

30 min exposure:

ppm:
mg/m3: Not recommended

1 hr exposure:

ppm:
mg/m3: Not recommended

4 hr exposure:

ppm:
mg/m3: Not recommended

8 hr exposure:

ppm:
mg/m3: Not recommended

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: Parathion
Proposed Value:

AEGL-2

10 min exposure:

ppm:
mg/m3: 2.8 mg/m(3)

30 min exposure:

ppm:
mg/m3: 1.9 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 1.5 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 0.96 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.48 mg/m(3)

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: Parathion
Proposed Value:

AEGL-3

10 min exposure:

ppm:
mg/m3: 3.6 mg/m(3)

30 min exposure:

ppm:
mg/m3: 2.5 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 2 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 1.3 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.63 mg/m(3)

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 CAS56-38-2 (National Institute for Occupational Safety and Health, 2007):

IDLH: 10 mg/m3
Note(s): Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area).
- Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.
- Stop leak if you can do it without risk.
- Prevent entry into waterways, sewers, basements or confined areas.
- Cover with plastic sheet to prevent spreading.
- Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers.
- DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
Containment/Disposal - Land Spill
- Restrict the movement of solids and liquids by digging a pit, pond, lagoon, or other such containment area. To prevent solids from dissolving in a water source (rainwater or fire-fighting water), cover with plastic sheeting (AAR, 1998).
Containment/Disposal - Water Spill
- "Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. If dissolved, in region of 10 ppm or greater concentration, apply activated carbon at ten times the spilled amount. Remove trapped material with suction hoses. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates" (AAR, 1998).
- "If the spill occurs in a waterway and the parathion-containing material is immiscible with water and sinks, dam the waterway to stop the flow and to retard dissipation by water movement. Use a bottom pump, dredging, or underwater vacuum equipment to remove undissolved material" (IPCS, 1992).
Construct a barrier using the most suitable material available (e.g., earth, sand) to prevent liquid from spreading (IPCS, 1992).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and an approved respirator. Get fire-fighting equipment ready (Ford, 1989; EPA, 1975).

WASTE TREATMENT OPTIONS

CHEMICAL TREATMENT

A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978) EPA, 1975a).
Aqueous solutions of parathion (nitrophenyl phosphorothioate) were studied using uv radiation and varying pH values to determine the rate of photodegradation. The results showed that the dark reactions were negligible, and the rate of reaction increased as the pH was increased (Gal et al, 1992).
Absorb spill with a 1:3 combination of sodium carbonate crystals and lime, sand, earth, or damp sawdust. Sweep the mixture into a container that cannot be permeated and that is tightly closed and properly labelled. Transfer the container to a safe place for disposal (IPCS, 1992).
The material can be inactivated with strong detergent (Ford, 1989).
Emptied leaking containers can be decontaminated with a 10% sodium carbonate solution (1 liter solution per 20-liter drum). Rinse the container and mix rinsings with sawdust for appropriate disposal (IPCS, 1992).
For in situ amelioration, use carbon or peat to absorb the material (OHM/TADS , 1999).
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.

PHYSICAL TREATMENT

Place material to be disposed mixed with equal parts of crushed limestone and sand in an open furnace fit with an afterburner and alkaline scrubber. Use a combustible solvent to cover the mixture. Ignite and burn carefully (ITI, 1995; OHM/TADS , 1999).
Combine spilled material with sand and crushed limestone and place in a carton. Burn the carton in a furnace equipped with an alkali scrubber and afterburner (ITI, 1995).
Burn absorbents, containers, or surplus products contaminated with the compound at high temperatures in an incinerator with effluent gas scrubbing capability (IPCS, 1992).
When material cannot be incinerated, bury in an approved area where surface or groundwater will not become polluted. Before burying, mix the material with liberal amounts of sodium carbonate crystals and then mix with soil containing a high amount of organic matter. Abide by all local laws (IPCS, 1992).
Parathion can be incinerated in a rotary kiln. Temperatures range from 820 to 1600 degrees C; the residence time is seconds (HSDB , 1999).
Liquid injection incineration is another potential disposal method. Temperatures range from 650 to 1600 degrees C; the residence time is between 0.1 and 2 seconds (HSDB , 1999).
Parathion also may be disposed using fluidized bed incineration. Temperatures range from 450 to 980 degrees C, with a residence time of seconds (HSDB , 1999).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

ENVIRONMENTAL EXPOSURE

Developed as an insecticide/miticide in the late 1940s, parathion use was initially restricted in 1991. Subsequent review of continued worker exposure and its environmental risk resulted in a voluntary agreement between parathion manufacturers and the US EPA in 2001 to halt parathion production and sale and to phase out existing end-use parathion products. Since October 2003, parathion production and application in the United States, as well as its importation into the US, are illegal. Prior to these restrictions and product-use registration cancellations, parathion was used broadly as an insecticide and acaricide, resulting in its direct release to the environment (HSDB, 2004; 66 FR 36356, 2001).
Parathion is not known to occur as a natural product (HSDB, 2004).

OCCUPATIONAL EXPOSURE

Although parathion is no longer manufactured or used in the United States, worker exposure may occur in other countries where the pesticide is used:

Humans are exposed to the pesticide mainly during its manufacture and application to croplands (Howard, 1991).

ENVIRONMENTAL FATE AND KINETICS

When released to the atmosphere, such as when sprayed during field application, parathion will exist mainly as an aerosol and also as a vapor/aerosol combination (Howard, 1991).
It will exist as both a vapor and a particulate in the atmosphere (HSDB, 2004).
Particulate-phase parathion is removed from the atmosphere through wet and dry deposition (HSDB, 2004).
Parathion vapor undergoes rapid photolysis to paraoxon (5 minute half-life in summer sunlight and much slower conversion after sunset) (Howard, 1991).
- Parathion's photolysis half-life in air was measured at 41 minutes in tests using laboratory photoreactors (HSDB, 2004).
- The potential for direct photolysis is expected, since parathion absorbs radiation with wavelengths <320 nm (HSDB, 2004).
Atmospheric degradation of parathion occurs through reaction with photochemically-produced hydroxyl radicals with a calculated half-life of 4.2 hours. The rate constant for this reaction is estimated at 9.2 x 10(-11) cm(3)/molecule-sec at 25 degrees C (HSDB, 2004).
In studies of parathion's degradation in sun light, parathion was irradiated with a mercury low pressure lamp producing light of 290 nanometer wavelengths in water, methanol, 2-propanol, and various aqueous solvent mixtures for 2, 5, or 10 hours. Aqueous solvent mixtures included titanium-oxide, magnesium-oxide, and zinc-oxide. The identity of the compounds obtained was confirmed with gas chromatography. Nitrophenol and paraoxon were produced. Nitrophenol was produced in all solutions at all time intervals in amounts ranging from a trace to 10 percent of the original parathion. Paraoxon was produced in water, methanol, water and methanol, and water and propanol solutions in amounts ranging from a trace to 2% of the original parathion. Dinitrophenol and trinitrophenol could not be identified. The relative amounts of the photo products produced were dependent on the reaction time. The reaction proceeded more slowly in apolar solvents such as n-hexane and cyclohexane. The reaction rate with the oxides depended on the polarity of the oxide. Two principal reactions are involved in the photochemical decomposition of parathion: a free radical mechanism in apolar solvents and an ionic break down in aqueous solvents (Mansour et al, 1983).

WATER

SURFACE WATER
- Parathion is slowly hydrolyzed in water to form p-nitrophenol and diethyl orthothiophosphoric acid. Fifty percent hydrolysis will occur in 120 days, but will proceed more rapidly in alkaline solutions (HSDB, 2004).
- All organophosphate esters undergo hydrolysis in water. Generally, the water-soluble by-products of hydrolysis are less toxic than the parent compound (Minton & Murray, 1988).
- Parathion exists in surface waters for approximately 1 week following its release. It is removed via biodegradation or chemical hydrolysis following adsorption to sediment and particulate matter (Howard, 1991).
- In water, parathion photooxidizes with a <1-10 days half-life. This process is more rapid in eutrophic waters due to the presence of radicals and sensitizers (Howard, 1991).
- In sterile seawater, the chemical hydrolysis parathion half-life is approximately 1 year at 4 degrees C (Howard, 1991).
- Parathion does not volatilize readily from water surfaces (Howard, 1991).
- In distilled water and after 18 hours, only 20% of parathion was lost by photolysis. In swamp water, the same loss occurred in 2 hours. It has been shown that algae's presence can increase the rate of photolysis by a factor of 27 (Howard, 1991).
- In aerated distilled water, 88% of parathion was degraded following 10 hours of irradiation (HSDB, 2004).
- In natural water systems, parathion is 2 to 3 times more persistent than methyl parathion (HSDB, 2004).
- At pH 7.4, and with temperature increased from 20 to 37.5 degrees C, the parathion half-life decreased in water from 19 weeks to 3.8 weeks. When temperature was increased from 20 to 40 degrees C at pH 9, the half-life decreased from 22 days to 5 days (Howard, 1991).

SOIL

TERRESTRIAL
- Parathion binds securely to soil and degrades in several weeks via chemical and biological hydrolysis. By-products formed from this process are p-nitrophenol, diethylthiophosphoric acid, and paraoxon (Howard, 1991).
- When amounts of parathion applied to soil or foliage are in the moderate range, it will degrade within weeks. When applied at high levels, the compound remains for longer periods (Howard, 1991).
- Parathion photolysis can occur on the surface of the soil (Howard, 1991).
- In 3 soils containing various amounts of water, the half-life for parathion photodecomposition ranged from 31 to 70 hours (HSDB, 2004).
- Volatilization is not thought to be an important fate process as indicated by a Henry's Law constant of 5.65 X 10(-7). Studies simulating parathion volatilization from soil showed only 0.1-0.3% losses in 30 days when incorporated the chemical was incorporated into soil at a depth of 10 cm (Howard, 1991).
- Little, if any, volatilization of parathion is expected from moist or dry soil surfaces (HSDB, 2004).
- Organic carbon partition coefficient (Koc) values ranging from 314 to 15860 indicate that parathion should have moderate to no mobility in soil (HSDB, 2004).
- The substance degrades at a moderate rate in soil, plants, and other substrates. Initially, parathion may convert to paraoxon, a more toxic metabolite. This conversion occurs most often under conditions that are dry and hot (IPCS, 1992).
- During the first year, residue levels from spills will decrease markedly; however, residual concentrations may persist in the environment for many years (Howard, 1991).
- In a study comparing the persistence of parathion applied as emulsifiable concentrate and as encapsulated formulations, parathion was applied at a rate of 0.28 kilograms per hectare to mature cotton in a Mississippi field. The 50% disappearance time (DT50) for parathion was 5.2 hours for the emulsifiable concentrate and 70.8 hours for encapsulated formulations (Smith et al, 1987).

ABIOTIC DEGRADATION

When released to the environment, parathion exists in the atmosphere in both vapor and particulate form where it degrades through reaction with photochemically-produced hydroxyl radicals or is removed through wet and dry deposition. In soils and water, parathion undergoes hydrolysis or microbial degradation, with half-lives ranging from 31 hours for photodecomposition in soils to a few weeks for biodegradation in acclimated waters. It may also undergo direct photolysis in all media (HSDB, 2004).

It is not expected to volatilize from water or soil surfaces, nor is it very mobile in soils. Some adsorption to suspended solids and sediment in the water column is expected (HSDB, 2004).

BIODEGRADATION

Parathion typically biodegrades with a half-life of a few weeks. In well acclimated water, however, the compound can degrade completely in as little as 2 weeks (Howard, 1991).

BIOACCUMULATION

FISH

Parathion did not bioaccumulate after 38 days in any of the organisms in a terrestrial aquatic ecosystem, including fish (Howard, 1991).

PLANTS

TERRESTRIAL
- Residues of the compound existing on foliage have a 1 day half-life and will reach low levels in 1 or 2 weeks (Howard, 1991).
- Parathion does not build up in the food chain (CHRIS, 2004; IPCS, 1992).

MAMMALS

Parathion does not build up in the food chain (CHRIS, 2004; IPCS, 1992).
No evidence exists showing that parathion bioaccumulates in cattle, sheep, or rabbits (HSDB, 2004).

OTHER

INVERTEBRATES
- Parathion did not bioaccumulate after 38 days in any of the organisms in a terrestrial aquatic ecosystem. Organisms in the ecosystem included snails, algae, daphnia, and mosquito larvae (Howard, 1991).

BIOCONCENTRATION FACTOR

BIOCONCENTRATION FACTORS (BCF) (Howard, 1991):
- Tadpole: 64 (average)
- American oyster: 300 after 84D
- Fathead minnow: 30 (average) after 70D; 219 (average) after 82-138 days
- Bluegill: 81, 187, 253, 27 (average values) after 12H, 29H, 46H, 504D, respectively
- Bluegill: 63-462 after 0.5 and 3D; 510 and 640 mcg/L, respectively (HSDB, 2004)
- Brook trout muscle: 89, 247, 315 (average values) after 8H, 6D, and 180D, respectively
- Brook trout: 68-344 after 0.33 and 5.83 D; 3180 and 270 mcg/L, respectively (HSDB, 2004)
The average BCF in killifish following 24 to 72 hours exposure to parathion was 98. The average BCF was 88 following exposure to a mixture of pesticides that included parathion for the same time period (HSDB, 2004).
Based on classification of BCF values for various species, bioconcentration in aquatic systems is considered to be low to moderate (Howard, 1991).

ENVIRONMENTAL TOXICITY

The substance is very toxic to birds (IPCS, 1992).

Parathion is extremely toxic to fish and lower aquatic organisms (IPCS, 1992).

Even very low concentrations of parathion are harmful to aquatic life (CHRIS, 2004).

Parathion is extremely toxic to wild animals (IPCS, 1992).

Species that experienced extreme adverse effects are aquatic beetles and mosquito larvae at 0.05 lb/acre (OHM/TADS, 2004).

Chronic exposure of fathead minnows to 4 mcg/L of parathion resulted in deformation and reproductive impairment (Council on Scientific Affairs, 1985) .

Concentrations of 0.04 to 5 ppb are toxic to most invertebrate species (EPA, 1988).

AQUATIC ORGANISMS

ALGAE

NOEC - Chlorophyta: 200 mcg/L (Verschueren, 2001)
NOEC - Cyanophyta: 15 mcg/L (Verschueren, 2001)

CRUSTACEANS

EC (immobilization) - SIMOCEPHALUS SERRULATUS: 0.00037 ppm for 48H -- at 60 degrees F (OHM/TADS, 2004)
EC (immobilization) - DAPHNIA MAGNA: 0.0008 ppm for 50H -- 25% active in xylene (OHM/TADS, 2004)
EC (immobilization) - DAPHNIA PULEX: 0.00037 ppm for 48H -- at 60 degrees F (OHM/TADS, 2004)
EC50 (immobilization) - DAPHNIA MAGNA: 0.8 mcg/L for 50H (HSDB, 2004)
EC50 (immobilization) - DAPHNID (Simocephalus serrulatus): 0.37 mcg/L for 48H (HSDB, 2004)
EC50 - DAPHNID (Simocephalus), first instar: 0.47 mcg/L for 48H -- at 21 degrees C, (confidence limit 0.34-0.66 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
EC50 - DAPHNID (Daphnia pulex), first instar: 0.60 mcg/L for 48H -- at 15 degrees C, (confidence limit 0.45-0.79 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC - BRINE SHRIMP: 0.43 ppm for <24H (CHRIS, 2004; OHM/TADS, 2004)
LC50 - SPOT: 0.018 ppm for 48H (OHM/TADS, 2004)
LC50 - SOWBUG (Asellus brevicaudus), mature: 2130 mcg/L for 96H -- at 15 degrees C, (95% confidence limit 1450-3120 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - SCUD (Gammarus lacustris), mature: 3.4 mcg/L for 96H -- at 21 degrees C, (95% confidence limit 2.6-4.8 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - DAPHNIA MAGNA: 0.0008 ppm for 50H -- 25% active in xylene (OHM/TADS, 2004)
LC50 - SCUD (Gammarus fasciatus), mature: 1.3 mcg/L for 96H -- at 21 degrees C, (95% confidence limit 0.60-1.9 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - CRAYFISH (Orconectes nais), early instar: 0.04 mcg/L for 96H -- at 21 degrees C, (95% confidence limit 0.01-0.20 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - GRASS SHRIMP (Palaemonetes kadiakensis), mature: 1.5 mcg/L for 96H -- at 21 degrees C, (95% confidence limit 0.82-2.7 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - CRAYFISH (Procambarus), mature: <250 mcg/L for 96H -- at 12 degrees C/static bioassay without aeration technical material 98.7% (HSDB, 2004)
LC50 - Gammarus lacustris: 3.5 mcg/L for 96H (Verschueren, 2001)
LC50 - Gammarus fasciatus: 2.1 mcg/L for 96H (Verschueren, 2001)
LC50 - Gammarus fasciatus: 1.6 mcg/L for 120H (Verschueren, 2001)
LC50 - Palaemonetes kadiakensis: 1.5 mcg/L for 96H (Verschueren, 2001)
LC50 - Simocephalus serrulatus: 0.37 for 48H (Verschueren, 2001)
LC50 - Daphnia pulex: 0.60 mcg/L 48H (Verschueren, 2001)
LC50 - Orconectes nais: 0.04 mcg/L for 96H (Verschueren, 2001)
LC50 - Asellus brevicaudus: 600 mcg/L for 96H (Verschueren, 2001)
LC50 - Daphnia magna: 0.8 mcg/L for 24H (Verschueren, 2001)
LC50 - Daphnia magna: 0.37 mcg/L for 48H (Verschueren, 2001)
NOEC - Branchiopoda: 0.02 mcg/L (Verschueren, 2001)
NOEC - Malacostraca: 1 mcg/L (Verschueren, 2001)

FISH

EC (acute toxicity) - Mosquitofish: 0.32 ppm (EPA, 1988)
EC (acute toxicity) - CHANNEL CATFISH: 2.65 ppm (EPA, 1988)
EC (26% enzyme activity) - SHEEPSHEAD MINNOW: 0.01 ppm (OHM/TADS, 2004)
LC33 - MOSQUITO FISH: 0.004 ppm for 24H (OHM/TADS, 2004)
LC50 - RAINBOW TROUT: 2 ppm for 24H (OHM/TADS, 2004)
LC50 - BLUEGILL: 0.056 ppm for 24H (OHM/TADS, 2004)
LC50 - CUTTHROAT TROUT (Salmo clarki): 1560 mcg/L for 48H -- at 12 degrees C, (95% confidence limit 985-2470 mcg/L)/wt 0.3 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - RAINBOW TROUT (Salmo gairdneri): 1430 mcg/L for 96H -- at 12 degrees C, (95% confidence limit 962-2110 mcg/L)/wt 1 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - LAKE TROUT (Salvelinus namaycush): 1920 mcg/L for 96H -- at 12 degrees C, (95% confidence limit 1750-2100 mcg/L)/wt 0.7 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - GOLDFISH (Carassius auratus): 1830 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 1350-2470 mcg/L)/wt 0.9 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - FATHEAD MINNOW (Pimephales promelas): 2350 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 1760-3120 mcg/L)/wt 0.8 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - CHANNEL CATFISH (Ictalurus punctatus): 2650 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 2160-3260 mcg/L)/wt 1.4 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - MOSQUITOFISH (Gambusia affinis): 320 mcg/L for 96H -- at 17 degrees C, (95% confidence limit 156-647 mcg/L)/wt 0.6 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - GREEN SUNFISH (Lepomis cyanellus): 930 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 675-1282 mcg/L)/wt 1.1 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - BLUEGILL (Lepomis macrochirus): 400 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 295-543 mcg/L)/wt 1.0 g/static bioassay without aeration technical material 98.7% (HSDB, 2004)
LC50 - LARGEMOUTH BASS (Micropterus salmoides): 620 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 462-830 mcg/L)/wt 0.7 g/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - RAINBOW TROUT (Salmo gairdneri): 750 mcg/L for 96H -- at 12 degrees C, (confidence limit 520-1100 mcg/L)/wt 1.5 g/static bioassay without aeration/thioate analog/100% technical grade (HSDB, 2004)
LC50 - CHANNEL CATFISH (Ictalurus punctatus): 3300 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 3090-3520 mcg/L)/wt 1.4 g/static bioassay without aeration/thioate analog/100% technical grade (HSDB, 2004)
LC50 - BLUEGILL (Lepomis macrochirus): 24 mcg/L for 96H -- at 18 degrees C, (95% confidence limit 15-38 mcg/L)/wt 1.4 g/static bioassay without aeration/thioate analog/100% technical grade (HSDB, 2004)
LC50 - Pimephales promelas: 1410 mcg/L for 96H (Verschueren, 2001)
LC50 - Lepomis macrochirus: 65 mcg/L for 96H (Verschueren, 2001)
LC50 - Lepomis cyanellus: 426 mcg/L for 96H (Verschueren, 2001)
LC50 - Micropterus salmoides: 190 mcg/L for 96H (Verschueren, 2001)
LC50 - Mosquito fish: 0.20 mg/L for 72H -- static bioassay (Verschueren, 2001)
LC50 - Green sunfish: 0.02 mg/L for 72H -- static bioassay (Verschueren, 2001)
LC100 - GOLDFISH: 2.0 ppm (OHM/TADS, 2004)
LC100 - CARP: 1 ppm for 96H (OHM/TADS, 2004)
LC100 - TILAPIA: 0.5 ppm for 96H (OHM/TADS, 2004)
LC100 - MULLET: 0.125 ppm for 96H (OHM/TADS, 2004)
NOEC - Pisces: 3.2; 3.3; 4.0 mcg/L (Verschueren, 2001)
TLm - BLUEGILL: 0.71 ppm for 96H (OHM/TADS, 2004)
TLm - GOLDFISH: 1.5 ppm (OHM/TADS, 2004)
TLm - MINNOW: 1.6 ppm for 96H -- hard water (OHM/TADS, 2004)
TLm - MINNOW: 1.4 ppm for 96H -- soft water (OHM/TADS, 2004)
TLm - TROUT: 2 ppm for 24H (OHM/TADS, 2004)
TLm - FATHEAD MINNOW: 1.3 ppm for 96H -- soft water (OHM/TADS, 2004)
TLm - BLUEGILL: 0.095 ppm for 96H -- soft water (OHM/TADS, 2004)
TLm - GOLDFISH: 2.7 ppm for 96H -- soft water (OHM/TADS, 2004)
TLm - GUPPY: 0.056 ppm for 96H -- soft water (OHM/TADS, 2004)

TERRESTRIAL ORGANISMS

BIRD

LD50 - (ORAL) BOHBWHITE (Colinus virginianus): 194 ppm for 5D in diet -- (95% confidence limit 150-245 ppm) (HSDB, 2004)
LD50 - (ORAL) CHUKAR PARTRIDGE (Alectoris chukar), 3-12 month old males and females: 24 mg/kg -- (95% confidence limit 16.8-34.2 mg/kg)/sample purity 98.76% (HSDB, 2004)
LD50 - (ORAL) FULVOUS WHISTLING DUCK (Dendrocygna bicolor): 0.125 to 0.250 mg/kg -- sample purity 98.76% (HSDB, 2004)
LD50 - (ORAL) GRAY PARTRIDGE (Perdix perdix), 3-10 month old females: 16 mg/kg -- (95% confidence limit 4-64 mg/kg)/sample purity 98.76% (HSDB, 2004)
LD50 - (ORAL) HOUSE SPARROW (Passer domesticus), females: 3.36 mg/kg -- (95% confidence limit 2.43-4.66 mg/kg)/sample purity 98.86% (HSDB, 2004)
LD50 - (ORAL) JAPANESE QUAIL (Coturnix japonica): 238 ppm for 5D in diet -- (95% confidence limit 152-373 ppm)/technical grade in corn oil, 95% active ingredient (HSDB, 2004)
LD50 - (ORAL) MALLARD (Anas platyrhynchos), 3-4 month old males: 2.13 mg/kg -- 98.76% technical grade (HSDB, 2004)
LD50 - (ORAL) MALLARD (Anas platyrhynchos), 2-3 month old females: 1.90 mg/kg -- (95% confidence limit 1.37-2.64 mg/kg)/sample purity 98.76% (HSDB, 2004)
LD50 - (ORAL) PHEASANT (Phasianus colchicus), 2-3 month old males: 12.4 mg/kg -- sample purity 98.76% (HSDB, 2004)
LD50 - (ORAL) PHEASANT (Phasianus sp.): 365 ppm for 5D in dirt -- (95% confidence limit 316-420 ppm) (HSDB, 2004)
LD50 - (ORAL) SHARP-TAILED GROUSE (Tympanuchus phasianellus), 12-36 month old females: 5.66 mg/kg -- (95% confidence limit 3.46 to 9.24 mg/kg)/sample purity 98.6% & 99.5% (HSDB, 2004)
LC50 - (ORAL) QUAIL (Coturnix coturnix): 44 ppm in 5D diet -- (95% confidence limit 36-53 ppm) (HSDB, 2004)

GASTROPODS

LC100 - LYMNAEID SNAILS: 2.5 ppm -- ditchwater (OHM/TADS, 2004)

INSECT

LC50 - MIDGE (Tanypos grodhausi), larvae: 0.5 mcg/L for 24H -- static bioassay without aeration (HSDB, 2004)
LC50 - STONEFLY (Pteronarcys californica), naiad: 5.4 mcg/L for 96H -- at 15 degrees C, (95% confidence limit 4.7-6.2 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - STONEFLY (Claassenia sabulosa), second year class: 1.5 mcg/L for 96H -- at 15 degrees C, (95% confidence limit 1-2.2 mcg/L)/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - MAYFLY (Hexagenia bilineata), juvenile: 15 mcg/L for 96H -- at 24 degrees C/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - DAMSELFLY (Ischnura venticalis), juvenile: 0.64 mcg/L for 96H -- at 24 degrees C/static bioassay without aeration/technical material 98.7% (HSDB, 2004)
LC50 - Pteronarcys californica: 36 mg/L for 96H (Verschueren, 2001)
LC50 - Pteronarcys dorsata: 3.0 mg/L for 96H (Verschueren, 2001)
LC50 - Pteronarcella badia: 4.2 mg/L for 96H (Verschueren, 2001)
LC50 - Claassenia sabulosa: 1.5 mg/L for 96H (Verschueren, 2001)
LC50 - Acroneuria pacifica: 3.0 mg/L for 96H (Verschueren, 2001)
LC50 - Acroneuria lycorias: 0.013 mcg/L for 30D (Verschueren, 2001)
LC50 - Ephemerella subvaria: 0.16 mg/L for 96H (Verschueren, 2001)
LC50 - Ophigomphus rupinsulensis: 3.25 mg/L for 96H (Verschueren, 2001)
LC50 - Hydropsyche bettoni: 0.45 mcg/L for 30D (Verschueren, 2001)
LC50 - Chironomus riparius, fourth instar larval: 2.5 mcg/L for 24H (Verschueren, 2001)
LC50 - Pteronarcys: 5.4 mcg/L for 48H (Verschueren, 2001)
LC50 - Pteronarcys californica: 2.2 mcg/L for 30D (Verschueren, 2001)
LC50 - Pteronarcys dorsata: 0.9 mcg/L for 30D (Verschueren, 2001)
LC50 - Acroneuria pacifica: 0.44 mcg/L for 30D (Verschueren, 2001)
LC50 - Ephemerella subvaria: 0.056 mcg/L for 30D (Verschueren, 2001)
LC50 - Ophigomphus rupinsulensis: 0.22 mcg/L for 30D (Verschueren, 2001)
NOEC - Diptera: 0.1 mcg/L (Verschueren, 2001)
TLm - CADDISFLY (Hydropsyche californica), larva: 0.43 mcg/L for 96H (HSDB, 2004)
TLm - PTERONARCYS CALIFORNICA: 0.0032 ppm for 96H -- 25% in xylene (OHM/TADS, 2004)
TLm - ARCTOPSYCHE GRANDIS: 0.001 ppm for 96H -- 25% active in xylene (OHM/TADS, 2004)
TLm - SCUD (GAMMARUS LACUSTRIS): 0.0128 ppm for 96H -- in acetone (OHM/TADS, 2004)
TLm - ACRONEURIA PACIFICA: 0.0028 ppm for 96H (OHM/TADS, 2004)
TLm - EPHEMERELLA GRANDIS: 0.003 ppm for 96H (OHM/TADS, 2004)
TLm - SCUD (GAMMARUS LACUSTRIS): 0.0128 ppm for 96H (OHM/TADS, 2004)
TLm - PTERONARCYS CALIFORNICA: 0.032 ppm for 96H (OHM/TADS, 2004)
TLm - ACRONEURIA PACIFICA: 0.0001 ppm for 96H -- 25% active in xylene (OHM/TADS, 2004)

MAMMAL

LD50 - (ORAL) MULE DEER (Odocoileus hemionus hemiomus), 10 month old males: 22 to 44 mg/kg -- sample purity 99.5% (HSDB, 2004)

WORMS

LD50 - EARTHWORM: 34 ng/g (HSDB, 2004)
LD50 - WORMS (Tubifex and limnodrilus spp.): 2-5 ppm for 96H (OHM/TADS, 2004)

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

291.26 (Budavari, 1996)

291.27 (ACGIH, 1991)

291.28 (RTECS , 1999)

DESCRIPTION/PHYSICAL STATE

Parathion is a pale yellow to yellow liquid in pure form (Lewis, 1996) Sittig, 1995). The technical grade of parathion is clear or medium to dark brown and possesses a garlic-like odor (Clayton & Clayton, 1993; NIOSH , 1999).

In its pure form and at temperatures above 6 degrees C, parathion exists as a yellowish liquid (Hayes & Laws, 1991).

It is an oily liquid with an aromatic, sweet odor (Lewis, 1996).

Its odor is phenol-like (HSDB , 1999).

The compound is a solid below 43 degrees F (NIOSH , 1999).

No information found at the time of this review.

VAPOR PRESSURE

3.78 x 10(-5) mmHg (at 20 degrees C) (Budavari, 1996)

9.65 X 10(-6) mmHg (at 25 degrees C) (Howard, 1991)

0.003 mmHg (at 24 degrees C) (Lewis, 1997)

0.00003 mmHg (24 degrees C) (Clayton & Clayton, 1993)

0.00066 mmHg (at 54.5 degrees C) (Clayton & Clayton, 1993)

0.0028 mmHg (at 70.7 degrees C) (Clayton & Clayton, 1993)

5 mPa (at 20 degrees C) (IPCS, 1992)

6.68 X 10(-6) mmHg (at 20 degrees C) (HSDB , 1999)

DENSITY

OTHER TEMPERATURE AND/OR PRESSURE

1.26 g/cm(3) at 25/4 degrees C (Budavari, 1996; Lewis, 1997)

FREEZING/MELTING POINT

FREEZING POINT

6 degrees C; 43 degrees F; 279 degrees K (CHRIS , 1999; NIOSH , 1999)

MELTING POINT

Pure material: 6 degrees C; 43 degrees F (Budavari, 1996; Howard, 1991)
Technical grade: 0 degrees C; 32 degrees F (NIOSH , 1985)

BOILING POINT

375 degrees C; 707 degrees F (at 760 mmHg) (Budavari, 1996; Howard, 1991; Lewis, 1996)

157-162 degrees C (at 0.6 mmHg) (Budavari, 1996; Clayton & Clayton, 1993)

150 degrees C (at 0.6 mmHg) (Hartley & Kidd, 1987)

FLASH POINT

392 degrees F (NIOSH , 1999)

200 degrees C (open cup) (IPCS, 1992)

Flash point at 120-160 degrees C until flammable impurities of technical materials are removed. Residues support combustion when temperature reaches 221 degrees C (HSDB , 1999).

EXPLOSIVE LIMITS

LOWER

Unknown (NIOSH , 1999)

UPPER

Unknown (NIOSH , 1999)

SOLUBILITY

IN WATER

Parathion is practically insoluble in water (Budavari, 1996; EPA, 1985; Lewis, 1997). Parathion's solubility in water is 12.4 mg/L at 20 degrees C (EPA, 1985).
Parathion's solubility in water is 24 mg/L at 25 degrees C (Clayton & Clayton, 1993) and 77 mg/L at 40 degrees C (IPCS, 1992).
6.54 mg/L (at 24 degrees C); 24 mg/L (Howard, 1991)
0.001% (NIOSH , 1999)

IN ORGANIC SOLVENTS

The compound is nearly insoluble in petroleum ether, kerosene, and spray oils (Budavari, 1996; Lewis, 1997).
Parathion is freely soluble in alcohols, esters, ethers, ketones, aromatic hydrocarbons (Budavari, 1996; Lewis, 1997) and animal and vegetable oils (Lewis, 1997). Parathion is soluble in chloroform (HSDB , 1990).

OTHER

Parathion is completely miscible with most organic solvents (Clayton & Clayton, 1993).

OCTANOL/WATER PARTITION COEFFICIENT

3.83 (Howard, 1991)

HENRY'S CONSTANT

5.65 X 10(-7) atm-m(3)/mol (approximate - determined from water solubility and vapor pressure) (Howard, 1991)

1.21 x 10(-6) atm-m(3)/mol (Ehrenfeld et al, 1986)

0.0302 Pa/m(3)/mol (HSDB , 1999)

SPECTRAL CONSTANTS

1036 (HSDB , 1999)

1-348 (HSDB , 1999)

MASS

4788 (HSDB , 1999)

OTHER/PHYSICAL

ODOR THRESHOLD

0.04 ppm (ACGIH, 1991)
4 X 10(-2) ppm (detection in water; purity not specified) (HSDB , 1999)
0.470 mg/m(3) (HSDB , 1999)
0.476 mg/m(3)(low); 0.4760 mg/m(3) (high) (HSDB , 1999)

SURFACE TENSION

39.2 dynes/cm (at 25 degrees C) (Budavari, 1996)

INDEX OF REFRACTION

1.5367 (at 25 degrees C) (Lewis, 1997)

VISCOSITY

15.3 CP (at 25 degrees C) (Budavari, 1996)

-REFERENCES

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Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents