CHLORPYRIFOS

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

STCC NUMBER

4941125 (insecticides, other than agricultural not elsewhere classified)
4941124 (agricultural insecticides, not elsewhere classified, other than liquid)
4941123 (agricultural insecticides, not elsewhere classified, liquid)

DESIGNATIONS

BEILSTEIN REFERENCE NUMBER:1545756
IMO CLASSIFICATION:6.1 /1615 (>2.5%); 9/1615 (<2.5%)
STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:51631

MOLECULAR FORMULA

C9-H11-Cl3-N-O3-P-S C9H11Cl3NO3PS C5NHCL3PO3S2

ERG GUIDE NUMBER

152-SUBSTANCES - TOXIC (COMBUSTIBLE)

SYNONYM REFERENCE

(Ariel GlobalView, 2001; Bingham et al, 2001a; Budavari, 2000; Budavari, 1996; CHRIS , 2001; EXTOXNET, 1996; Hartley & Kidd, 1990; Hayes, 1982; HSDB , 2001; Lewis, 2000; Lewis, 1996; NTP , 1991; OHM/TADS , 2001; RTECS , 2001)

USES/FORMS/SOURCES

USES

In 1965, chlorpyrifos was introduced for use in agriculture and to control mosquito larvae. Today, it is primarily used as a broad spectrum organophosphate insecticide and acaricide. Chlorpyrifos is the most widely used insecticide for nonagricultural purposes (ACGIH, 1991a; Bingham et al, 2001a; Harbison, 1998).
The EPA revised the risk assessment associated with chlorpyrifos and established an agreement with registrants. The modification for usage is intended to reduce exposure to the chemical. Use for apples and tomatoes ended December 31, 2000 (EPA, 2000).

Applications for home lawn and most other outdoor uses, crack and crevice and most other indoor uses, full barrier post- construction, spot and local post-construction, preconstruction, indoor areas where children could be exposed (such as schools), and outdoor areas where children could be exposed (such as parks) has been banned (EPA, 2000).
The following uses are allowed to continue, but with some restrictions: agricultural, termiticides, residential use of containerized baits, indoor use where children will not be exposed, including only ship holds, railroad boxcars, industrial plants, manufacturing plants, or food processing plants, golf courses, road medians, industrial plant sites, non- structural wood treatments including fence posts, utility poles, railroad ties, landscape timbers, logs, pallets, wooden containers, poles, posts, and processed wood products (EPA, 2000).
Use for fire ant mounds and mosquito control is permitted for professional use only (EPA, 2000).

FORMS

It is available as an emulsifiable concentrate, wettable powder, dustable powder, granules, controlled release polymers, ULV liquid, seed treatment, baits, flowable pellets, spray, microcapsule, and impregnated plastics (EPA, 1988a; EXTOXNET, 1996; Hartley & Kidd, 1990a; HSDB, 2001).

Commercial formulations are often mixed with petroleum products to increase the dispersal rate, or are sometimes combined with synthetic clays and talc (HSDB, 2001).

SOURCES

Chlorpyrifos is manufactured by combining 3,5,6-trichloro-2-pyridone + O,O-diethyl phosphorochlorothioate by dehydrochlorination (Ashford, 1994).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

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

USES: Chlorpyrifos, an organophosphate insecticide, is registered for use to control foliage and soil-born insect pests on a variety of foods and feed crops. It is also used as an acaricide and miticide.

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

EPIDEMIOLOGY: Exposure 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. One patient developed acute renal failure after ingesting chlorpyrifos.
DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy has been reported in some cases following intentional exposure to chlorpyrifos. It may rarely develop 6 to 21 days following exposure. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete.
CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (i.e., secretions, bradycardia, fasciculations and miosis) as compared to adults.
INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.

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

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

ACUTE CLINICAL EFFECTS

Chlorpyrifos is absorbed by ingestion, skin contact (the main route of exposure) and inhalation (Hathaway et al, 1991; Harbison, 1998a). It is difficult to wash off once adsorbed by the skin (Harbison, 1998a).

In humans, 3 percent of a dermal dose of 5 mg/kg penetrated the skin; erythrocyte and plasma cholinesterase remained unchanged after single dermal dose of 5 mg/kg (Nolan et al, 1984). Chlorpyrifos was one of the most rapidly absorbed insecticides when applied to the shaved skin of mice. The half-life for absorption of radioactive chlorpyrifos was 6 to 25 minutes (Shah et al, 1981).

The hallmark of organophosphorus poisoning is the inhibition of plasma pseudocholinesterase, erythrocyte acetylcholinesterase, or both (Namba, 1972).

Chlorpyrifos seems to be one of the 'safer' organophosphates. Exposures characteristically cause selective depression of plasma, but not red blood cell, cholinesterase activity without other systemic effects (Eliason et al, 1969; (Hayes, 1982). A single oral dose of 0.5 mg/kg produced an 85% depression of plasma cholinesterase activity without affecting red blood cell acetylcholinesterase (Nolan et al, 1984).

However, given a large enough dose, chlorpyrifos is capable of inducing cholinergic signs and symptoms typical of organophosphorus compounds (Hayes & Laws, 1991). The severity of symptoms for any organophosphorus compound depends on the route and intensity of exposure, as well as individual conditions of susceptibility.

Based on its acute oral toxicity in rats, chlorpyrifos would be in the moderately toxic group of organophosphates (Morgan, 1989). There are considerable differences in susceptibility to chlorpyrifos, as measured by LD50 doses, between different species (Hayes & Laws, 1991). This may be due, at least in part, to different levels of deactivating paraoxonase in different species (Costa et al, 1990).

Depending on the extent and duration of exposure, signs and symptoms of organophosphate poisoning may include any or all of the following (AH Hall , 1995; Harbison, 1998a; Zenz, 1994; Sittig, 1991):

Nausea, vomiting, abdominal cramps, diarrhea, increased urinary frequency and urgency
Headache, giddiness, vertigo, mental confusion, disorientation, drowsiness, generalized profound weakness, loss of muscle coordination, slurring of speech, fasciculations and twitching of muscles (particularly of tongue and eyelids), random jerky movements, incontinence, paresthesia, muscle pain, hyporeflexia, distal numbness, ataxia, convulsions, coma, death
Sensation of tightness in the chest (after inhalation exposure), difficulty breathing, respiratory distress, excessive salivation and respiratory mucus, oronasal frothing, cyanosis, pulmonary rales and rhonchi, pulmonary edema, hypertension
Excessive tearing, loss of accommodation, ocular pain, blurring or dimness of vision, miosis (pinpoint pupils)

Symptoms may be DELAYED BY SEVERAL HOURS after an acute exposure because chlorpyrifos requires metabolic activation to the more toxic oxon form. Complete symptomatic recovery usually occurs within 1 week; increased susceptibility to the effects of anticholinesterase agents persists for up to several weeks after exposure (Proctor et al, 1988).

CHOREOATHETOSIS (ceaseless jerky, sinuous, involuntary movements) was responsive to atropine developed in a 23-year-old female after ingestion of chlorpyrifos (Joubert et al, 1984).

Death from organophosphate poisoning occurs mainly from respiratory arrest arising from excessive secretion of the respiratory tract, intense bronchoconstriction, paralysis of respiratory muscles, failure of the respiratory center, or all four; there is often a secondary cardiac component (HSDB , 2001). In very severe cases in which the patient has been unconscious for some time, brain damage can occur from lack of oxygen (ILO, 1998).

Some signs and symptoms of acute organophosphate poisoning, based on experience with parathion, can persist for days to months afterwards. These include fatigue, ocular symptoms, EEG abnormalities, gastrointestinal complaints, excessive dreams, and intolerance to exposure to organophosphates (ILO, 1998).

Delayed effects may be produced with the phosphorothioates such as chlorpyrifos. After an initial period of apparent recovery, clinical effects may recur for up to several weeks after an acute exposure (Minton & Murray, 1988).

Some organophosphates can induce delayed neuropathy of a combined sensory-motor type. Sensation of numbness or tingling in the extremities may appear several weeks after acute exposure. Recovery requires weeks to months, and may never be complete (Done, 1979).

It is not clear if all organophosphates have this activity (Cherniack, 1986; Wadia et al, 1987). An expert panel review of chlorpyrifos and other organophosphates concluded that acute and severe poisoning in humans from suicidal ingestion were the only known cases of organophosphate-induced delayed neurotoxicity (Clegg & van Gemert, 1999).
Sensory-motor polyneuropathy caused by severe organophosphate poisoning typically demonstrates a milder sensory component than motor component. Other causes should be investigated in cases in which the patient experienced peripheral sensory neuropathy and did NOT show severe cholinergic toxicity (Moretto & Lott, 1998).
Chlorpyrifos was, in the past, generally regarded as not inducing delayed neurotoxic effects (EPA, 1988a). As this conclusion was evidently based on animal data, some considered it needed to be re-evaluated in view of at least two cases of delayed peripheral neuropathy from chlorpyrifos reported in the literature (Moses, 1989).

In one case, a 3-year-old boy developed paralysis of the vocal cord 11 days after ingestion; reflexes disappeared on day 18 (Aiuto et al, 1993).
In another case, delayed peripheral sensory neuropathy was reported in an office worker three weeks after an acute exposure when the office was sprayed with a mixture of chlorpyrifos and methylcarbamic acid (Hodgson et al, 1986). Because of the mixed exposure, this case of delayed neuropathy could not be conclusively attributed to chlorpyrifos.

However, the expert panel (Clegg & van Gemert, 1999) were doubtful that the case reported by Aiuto (1993) was an organophosphate poisoning. They suspected that brainstem encephalitis or Guillian-Barre syndrome was the probable etiology, because of the patient's rapid recovery and the spatial distribution of the neuropathy.
Moreover, in the second case (Hodgson et al, 1986), blood samples obtained for erythrocyte and plasma cholinesterase were "mishandled", and testing was not conclusive for chlorpyrifos etiology (Albers et al, 1999).
In a case of suicidal ingestion of approximately 300 mg/kg chlorpyrifos, weakness and paresthesia of the legs developed about 6 weeks after exposure, despite treatment with atropine and 2-PAM during the patient's 17 days in a coma and on a respirator immediately after the ingestion (Clayton & Clayton, 1993).
Eight cases of peripheral sensory neuropathy were reported that developed after exposure to professionally applied chlorpyrifos. Memory loss and cognitive dysfunction were also present in five of these cases (Kaplan et al, 1993).
Moretto and Lotti (1998) reviewed 11 cases of patients poisoned by organophosphates, who developed polyneuropathy. The sensory component was preceded by cholinergic effects and was mild compared with the motor deficit. These authors found little evidence for a causal link to exposure in the cases reported by Kaplan (1993), as the information was based almost entirely on medical history (Moretto & Lotti, 1998).

The standard assay for predicting delayed neurotoxicity is a test for paralysis and/or neurotoxic esterase inhibition in hens. A subcutaneous dose of 200 mg/kg, but not 100 mg/kg, induced delayed ataxia in the standard atropinized hen assay; however, the effects were completely reversible (Gaines, 1969).

Oral administration of 60 to 90 mg/kg (4 to 6 times the estimated LD50) produced delayed neuropathy in hens. This threshold dose required pralidoxime and atropine to protect the birds from cholinergic toxicity (Capodicasa et al, 1991).
Delayed neurotoxicity (ataxia in the hindlimbs) was produced in cats receiving 300 mg/kg of chlorpyrifos (a supralethal dose), followed by atropine and 2-PAM to control cholinergic symptoms. Average onset of delayed neuropathy was 19 days after exposure, and the effects produced by chlorpyrifos were similar to those from the positive control, DFP (Fikes et al, 1992). Chlorpyrifos did not produce delayed ataxia in mice (El-Sebae et al, 1977).
Another measure of delayed neurotoxicity is inhibition of the neurotoxic esterase. Chlorpyrifos did not inhibit this enzyme in the brains of hens and did not induce delayed neurotoxicity at a non-lethal oral dose of 10 mg/kg/day (Richardson et al, 1993).
High single doses of up to 100 mg/kg produced a range of cholinergic signs in rats, with motor dysfunction predominating in acute exposures. Females were more sensitive than males. No treatment-related histopathological lesions were apparent (Mattsson et al, 1996).

From these limited reports in humans and animals, it seems that chlorpyrifos can induce delayed sensory or motor peripheral neuropathy at high doses. Moretto and Lotti (1998) found that their review of the literature showed that animal exposures must be in the lethal range, and human organophosphate doses must be high enough to cause severe cholinergic toxicity (suicidal ingestion of concentrated organophosphates) (Moretto & Lotti, 1998).

Immunologic changes including autoantibodies, atopy, antibiotic sensitivities, elevated CD26 cells, and a decreased percentage of T cells were found in a group of 12 persons 1 to 4.5 years after exposure to chlorpyrifos (Thrasher et al, 1993). This study did not prove any duration or quantification of exposure, onset of signs and symptoms, or information that exposures could be associated with complaints of illness; it was considered a limited study (Albers et al, 1999).

Aspiration of commercial organophosphate preparations which contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986).

CHRONIC CLINICAL EFFECTS

Organophosphorus compounds have CUMULATIVE TOXICITY: daily exposure can cause progressive cholinesterase inhibition until the threshold for development of clinical signs and symptoms has passed. Continued daily exposure may produce increasingly severe effects.

Subchronic and chronic exposure to organophosphorus compounds can lead to cumulative depression of cholinesterase levels until a critical lack of activity causes signs and symptoms of organophosphate poisoning to appear, in a pattern similar to that of acute poisoning (Coye et al, 1986). The level of chronic exposure which can be tolerated depends on the rate of uptake and degradation of the organophosphate in the body, in relation to its potency in inhibiting acetylcholinesterase and the rate of replenishment of acetylcholinesterase activity.

Damage to the nervous system and liver can occur with repeat exposure (Sittig, 1991). However, available evidence indicates that repeated exposure to low doses of chlorpyrifos does not produce severe effects.

A group of 6 termite-control applicators had decreased plasma cholinesterase levels during the spraying season. The levels were below the range of normal or pre-exposure levels, but no signs or symptoms of cholinesterase inhibition were evident. Red blood cell cholinesterase levels averaged 30 percent lower than pre-exposure values but were still within the normal range, and no other adverse effects were reported (Jitsunari et al, 1990).
An oral dose of 0.03 mg/kg/day for 3 weeks did not lower plasma or red cell cholinesterase in human volunteers. Nine doses of 0.1 mg/kg/day reduced plasma cholinesterase, but were generally without other clinical effects (Griffin et al, 1976; ACGIH, 1991; HSDB , 1995). Ingestion of 0.1 mg/kg/day for 4 weeks depressed plasma cholinesterase but otherwise did not produce clinical effects in human volunteers (Hathaway et al, 1991).
Repeated doses of 0.014 mg/kg for up to 28 days did not inhibit plasma pseudocholinesterase in human volunteers. A slight reduction was seen at a dose of 0.03 mg/kg/day for 21 days. A dose of 0.1 mg/kg/day for 9 days produced a 34 percent inhibition relative to pre-exposure values (McCollister SB, 1989).

There were no significant differences in illness or prevalence of symptoms between 175 employees involved in manufacturing chlorpyrifos and 335 matched controls (Brenner, 1989).

In a chronic dietary study on dogs and rats, levels as high as 0.1 mg/kg/day produced no apparent effects; levels of 1 and 3 mg/kg/day produced reversible depression of plasma and red cell cholinesterase (McCollister et al, 1974).

"Normalization" of neurotoxic signs in rats given doses of chlorpyrifos up to 15 mg/kg/day for 13 weeks in the diet was an indication of lack of cumulative toxicity and possible tolerance with repeated exposure. No treatment-related histopathological lesions were apparent (Mattsson et al, 1996).

Co-administration of chlorpyrifos at 10 mg/kg/day, along with DEET at 500 mg/kg/day and pyridostigmine bromide at 5 mg/kg/day for 2 months produced greater neurotoxicity than either agent alone in the hens. Gulf war personnel were potentially exposed to this combination of agents (Abou-Donia et al, 1996).

In the Abou-Donia study, 70 percent of the hens died from exposures to chlorpyrifos and DEET, and to chlorpyrifos and pyridostigmine, and DEET. The doses used do not reflect the doses received by Gulf War personnel. Moreover, none of the soldiers died or were acutely poisoned from the mixed exposures.

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

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

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

FIRST AID

PREHOSPITAL DECONTAMINATION

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

PERSONNEL PROTECTION

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

DECONTAMINATION OF SPILLS/SUMMARY

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

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

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

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

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

SMALL SPILL DECONTAMINATION

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

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

LARGE SPILL DECONTAMINATION

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

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

FURTHER CONTACT INFORMATION

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

MANAGEMENT OF MILD TOXICITY

A patient who is either asymptomatic or presents with mild clinical symptoms (i.e. normal vitals, pulse oximetry and an acetylcholinesterase greater than 80% of lower reference range), and remains stable for 12 hours can be discharged. Obtain appropriate psychiatric evaluation if an intentional exposure.

MANAGEMENT OF MODERATE TO SEVERE TOXICITY

Immediate assessment and evaluation. Airway management is likely to be necessary. Simple decontamination (i.e. skin and gastrointestinal, removal of contaminated clothes). Administer antidotes: atropine for muscarinic manifestations (e.g. salivation, diarrhea, bronchorrhea), pralidoxime for nicotinic manifestations (e.g. weakness, fasciculations). Treat seizures with benzodiazepines. Admit to intensive care with continuous monitoring, titration of antidotes, ventilation, and inotropes as needed. Consult a medical toxicologist and/or poison center.

AIRWAY MANAGEMENT

Immediately assess airway and respiratory function. Administer oxygen. Suction secretions. Endotracheal intubation may be necessary because of respiratory muscle weakness or bronchorrhea. Avoid succinylcholine for rapid sequence intubation as prolonged paralysis may result.

ANTIDOTES

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.

SEIZURES

IV benzodiazepines are indicated for seizures or agitation, diazepam 5 to 10 mg IV, lorazepam 2 to 4 mg IV; repeat as needed.

HYPOTENSIVE EPISODE

IV fluids, dopamine, norepinephrine.

BRONCHOSPASM

Inhaled ipratropium or glycopyrrolate may be useful in addition to intravenous atropine.

MONITORING OF PATIENT

Cardiac monitoring, pulse oximetry. Monitor clinical exam for evidence of muscarinic (e.g. bronchospasm, bronchorrhea, salivation, lacrimation, defecation, urination, miosis) nicotinic (e.g. muscle weakness or fasciculations, respiratory insufficiency) or CNS (e.g. seizures, coma) manifestations of cholinergic toxicity.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ROUTE OF EXPOSURE

A toxic dose has not been established; however, the lowest published toxic dose for a human is 300 mg/kg (RTECS , 2001).
Chlorpyrifos has moderate toxicity and a reported oral LD50 ranging from 80 to 250 mg/kg (Bingham et al, 2001b).
Oral LD50 for humans ranges from 50 to 500 mg/kg (grade 3) (CHRIS , 2001).
ACUTE DERMAL: 1505 mg/kg, Toxicity Category II (EPA, 1988)
ACUTE ORAL: 163 mg/kg, Toxicity Category II (EPA, 1988)

PESTICIDE CLASSIFICATION

The World Health Organization (WHO) has classified chlorpyrifos, technical grade, as pesticide class II (moderately hazardous) (World Health Organization, 2006).

MAXIMUM TOLERATED EXPOSURE

GENERAL/SUMMARY

A single oral dose of 5 mg/kg of chlorpyrifos followed by a single dermal dose of 0.5 or 5 mg/kg two weeks later produced blood concentrations of less than 30 ng/mL (Hayes & Law, 1991; (Nolan et al, 1984).
A single oral dose of 0.5 mg/kg produced an 85% depression of plasma cholinesterase activity without affecting red blood cell acetylcholinesterase (Nolan et al, 1984).
A single dermal dose of 5 mg/kg did not affect plasma or erythrocyte cholinesterase (Nolan et al, 1984).
EPA (1988) has designated this compound as having moderate mammalian toxicity and is not considered to be onocogenic, mutagenic, or teratogenic.
This compound is not teratogenic at levels up to 25 mg/kg/day (EPA, 1988).

OCCUPATIONAL

A study involving spray workers exposed to a 0.5% chlorpyrifos emulsion had decreases in plasma and red blood cell cholinesterase levels. Five of seven sprayers had greater than a 50% reduction in cholinesterase levels within two weeks after the beginning of the spraying program. No symptoms were reported (ACGIH, 1991; Hathaway et al, 1996).
Laborers who packaged chlorpyrifos in an Indonesian manufacturing facility had 70% reduction in blood cholinesterase after one week of exposure. Mild symptoms of anorexia, nausea, and muscular weakness were reported, but there were no severe intoxications. Cholinesterase activity recovered to 62% of preexposure values between weeks 6 and 9 (Pinem et al, 1982).
In occupational exposure assessments, the mean 8-hour air sampling exposure level for chlorpyrifos was 0.008 mg/m(3). The highest single value 0.028 mg/(3). In twenty-four-hour urine samples analyzed for alkyl phosphates, pesticide metabolites were found. The physical examination detected no apparent toxic effect in this study group, although the biological sampling results revealed a need for using personal protective equipment during the handling and application of this pesticide (ACGIH, 1991).

Employees engaged in the manufacture of this compound did not show a greater incidence of illness or symptoms in an 8.5-year morbidity survey (Hathaway et al, 1996).

CASE REPORTS

Human volunteers who ingested 0.03 mg/kg/day for 3 weeks did not have statistically significant plasma cholinesterase depression (ACGIH, 1991).
Doses of chlorpyrifos at 0.1 mg/kg/day, volunteers showed no effects except for plasma cholinesterase depression (ACGIH, 1991).
Similar studies involving the ingestion of chlorpyrifos daily for 4 weeks at doses of 0.014, 0.03, and 0.1 mg/kg revealed inhibition of plasma cholinesterase only at the 0.1 mg/kg dose; these volunteers were otherwise asymptomatic (ACGIH, 1991; Hathaway et al, 1996).
Male volunteers receiving a single oral dose of 0.5 mg/kg had 85% depression of plasma cholinesterase activity with complete recovery in 30 days. These volunteers, however, did not have any signs of disturbed erythrocyte acetylcholinesterase activity or other signs or symptoms of toxicity (Clayton & Clayton, 1993).

ANIMAL DATA

In a 2-year chronic feeding study in rats, plasma and red blood cell cholinesterases were depressed at doses of 1 and 3 mg/kg/day, but no other clinical effects were seen. The no-effect level for cholinesterase depression was 0.1 mg/kg/day (McCollister et al, 1974).
In dogs, inhibition of the plasma enzyme was evident at 0.1 mg/kg/day. The no-effect level for cholinesterase depression was 0.03 mg/kg/day (McCollister et al, 1974).
In a 13-week nose-only inhalation study of chlorpyrifos in rats showed no effects at 287 mcg/m(3); the highest attainable level because of its low vapor pressure (Calhoun et al, 1989).
Rats fed chlorpyrifos at 3.0 mg/kg/day for 2 years was noncarcinogenic (Hathaway et al, 1996).

Carcinogenicity Ratings for CAS2921-88-2 :

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

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): Not Assessed under the IRIS program. ; Listed as: Chlorpyrifos
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Chlorpyrifos
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 CAS2921-88-2 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD: 3x10(-3) mg/kg-day

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

References: ACGIH, 1991 Bingham et al, 2001 Budavari, 2000 CHRIS, 2001 Clayton & Clayton, 1993 EXTOXNET, 1996 Hartley & Kidd, 1990 HSDB, 2001 Lewis, 2000 NTP, 1991 OHM/TADS, 2001 RTECS, 2001
- LC50- (INHALATION)RAT:
- LD50- (ORAL)CHICKEN:
- LD50- (ORAL)GOAT:
- LD50- (ORAL)GUINEA_PIG:
- LD50- (ORAL)HUMAN:
- LD50- (INHALATION)MOUSE:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)MOUSE:
- LD50- (ORAL)RABBIT:
- LD50- (SKIN)RABBIT:
- LD50- (INHALATION)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LD50- (ORAL)SHEEP:
- LDLo- (SUBCUTANEOUS)GUINEA_PIG:
- TDLo- (ORAL)CHICKEN:
- TDLo- (ORAL)DOG:
- TDLo- (ORAL)HUMAN:
- TDLo- (ORAL)MOUSE:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (ORAL)RAT:
- TDLo- (SUBCUTANEOUS)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS2921-88-2 (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

Chlorpyrifos

TLV:

TLV-TWA: 0.1 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: BEI(A), 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(A): The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational. Substances identified as Acetylcholinesterase Inhibiting Pesticides are part of this notation.
IFV: Inhalable fraction and vapor.
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: 350.57

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 CAS2921-88-2 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS2921-88-2 (National Institute for Occupational Safety and Health, 2007):

Listed as: Chlorpyrifos
REL:

TWA: 0.2 mg/m(3)
STEL: 0.6 mg/m(3)
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: Not Listed

OSHA PEL Values for CAS2921-88-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS2921-88-2 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS2921-88-2 (U.S. Environmental Protection Agency, 2010):

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

1 (0.454)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS2921-88-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS2921-88-2 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS2921-88-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS2921-88-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS2921-88-2 (49 CFR 172.101 - App. B, 2005):

Listed as Chlorpyriphos
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS2921-88-2 (EPA, 2005):

Not Listed

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS2921-88-2 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

Potential exposure to chlorpyrifos exists for those involved in the manufacture, formulation, and application of this compound. It is heat sensitive and decomposes in moisture (NTP , 1991; Sittig, 1991).

HANDLING

Unless wearing appropriate personal protective equipment, do not handle broken packages (AAR, 2000; Sittig, 1991).

Avoid ingestion, inhalation, and contact with skin and eyes (OHM/TADS , 2001).

STORAGE

CONTAINER

Store in tightly sealed containers away from water and heat (OHM/TADS , 2001; Sittig, 1991).
Appropriate containers for chlorpyrifos are glass, composition and earthenware jars, metal drums, or boxes made of chipboard, fibre, wood, or pasteboard (OHM/TADS , 2001).

ROOM/CABINET RECOMMENDATIONS

Under normal storage conditions chlorpyrifos is stable (Hayes & Law, 1991).
Store chloropyrifos in a cool or refrigerated area that is protected from moisture and is well-ventilated. If possible, it is best stored in an inert atmosphere (NTP , 1991; Sittig, 1991).
Store away from strong acids and their fumes such as hydrochloric, nitric, and sulfuric (Sittig, 1991).

INCOMPATIBILITIES

Avoid contact with strong acids such as hydrochloric, sulfuric, and nitric acids, or acid fumes since violent reactions may occur (Sittig, 1991).
The rate of hydrolysis in water increases with the temperature and pH (NTP , 1991).
Chlorpyrifos is unstable under alkaline conditions (NTP , 1991).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

Contaminated clothing should be removed and sealed in a vapor-tight container for disposal (NTP , 1991).

EYE/FACE PROTECTION

Unless full facepiece respiratory protection is worn, personnel should wear splash-proof chemical goggles and face shield when working with liquid chlorpyrifos. When working with powders or dust, personnel should wear dust-proof goggles and face shields unless full face piece respiratory protection is worn (Sittig, 1991).

RESPIRATORY PROTECTION

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

Use a MSHA/NIOSH approved full facepiece respirator with a organic vapor/acid gas (specific for hydrochloric acid, organic vapors, acid gas, and sulfur dioxide) or pesticide cartridge with a dust/mist filter (NTP , 1991; Sittig, 1991).

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 2921-88-2.

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

CPF 2

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): None detected
Notes: Not Listed
Citation: (DuPont, 2002)

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

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

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- Combustible material: may burn but does not ignite readily.
- Containers may explode when heated.
- Runoff may pollute waterways.
- Substance may be transported in a molten form.
Chlorpyrifos does not readily ignite or burns with difficulty. However, commercial formulations may be combined with flammable mixtures such as No 2 diesel oil and kerosene (AAR, 2000; HSDB , 2001; NIOSH , 2001).
Prevent run-off water from draining into water sources and sewers (AAR, 2000).
Keep away from ignition sources. During combustion, poisonous gases are emitted, including organic sulfides and heated containers may explode (AAR, 2000; Sittig, 1991).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS2921-88-2 (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 CAS2921-88-2 (NFPA, 2002):

Not Listed

Extinguish fires using a dry chemical, foam CO2 or Halon extinguishers or an agent suitable for the type of surrounding fire (AAR, 2000; NTP , 1991; Sittig, 1991).

COMBUSTION TOXICITY

Chlorpyrifos, when heated to decomposition, emits very toxic fumes of chlorides, organic sulfides, and oxides of nitrogen, phosphorus, and sulfur (AAR, 2000; Lewis, 2000; OHM/TADS , 2001; Sittig, 1991).

EXPLOSION HAZARD

Containers of chlorpyrifos may rupture violently due to a build-up of heat and pressure (Sittig, 1991).

DUST/VAPOR HAZARD

Chlorpyrifos does not pose a vapor hazard due to its low vapor pressure; however, if chlorpyrifos is used as a mist, particulate inhalation is possible (ACGIH, 1991; Hathaway et al, 1996).

Avoid breathing dusts and fumes from burning chlorpyrifos. When heated to decomposition, it emits toxic fumes of organic sulfides, chlorides, and oxides of nitrogen, phosphorus, and sulfur (AAR, 2000; Lewis, 2000; Sittig, 1991).

REACTIVITY HAZARD

Violent reactions occur when chlorpyrifos is in contact with strong acids such as hydrochloric, sulfuric, and nitric acids, or acid fumes. It is also incompatible with caustics and amines (Pohanish & Greene, 1997; NIOSH , 2001; NTP , 1991; Sittig, 1991).

This compound is corrosive to copper, copper alloys, and brass (NTP , 1991).

Strong alkalis solutions cause chlorpyrifos to hydrolyze (NTP , 1991; Pohanish & Greene, 1997).

Chlorpyrifos is incompatible with alkaline materials (Hartley & Kidd, 1990; HSDB , 2001; OHM/TADS , 2001).

It is reactive to hydrogen compounds and water. The rate of hydrolysis increases with temperature, pH, and the presence of metals that can form chelates (NTP , 1991; OHM/TADS , 2001).

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 CAS2921-88-2 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS2921-88-2 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Chlorpyrifos (dursban)
TEEL-0 (units = mg/m3): 0.1
TEEL-1 (units = mg/m3): 0.6
TEEL-2 (units = mg/m3): 15
TEEL-3 (units = mg/m3): 20
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 CAS2921-88-2 (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):

Not Listed

NIOSH IDLH Values for CAS2921-88-2 (National Institute for Occupational Safety and Health, 2007):

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.
Persons not wearing protective equipment should be restricted from area of the spill or leak until clean-up is complete (Sittig, 1991).
Keep this compound out of water sources and sewers (AAR, 2000).
Deposit spilled material in sealed containers for reclamation or disposal in an approved facility (Sittig, 1991).

SMALL LEAK/SPILL

Remove all sources of ignition (NTP , 1991).
Pour acetone on chlorpyrifos solids until moist, and transfer the moistened compound to an appropriate container. Any substance remaining can be cleaned up with an absorbent paper dampened with acetone. Seal the contaminated paper in a container to prevent the release of vapors (NTP , 1991).
Wash down the contaminated area with acetone, followed by soap and water (NTP , 1991).
Do not reenter the area until a safety officer has determined the area is clean (NTP , 1991).

LARGE LEAK/SPILL

Chlorpyrifos is environmentally hazardous and appropriate measures should be taken to prevent its spread into the environment (AAR, 2000).
Remove all sources of ignition (NTP , 1991).
Large land spills can be contained by digging a holding area such as a pit, pond, or lagoon (AAR, 2000).
- Cover any solids with a plastic sheet to prevent chlorpyrifos from dissolving in the rain or from fire-fighting water (AAR, 2000).
- Pour acetone on chlorpyrifos solids until moist, and transfer the moisten compound to an appropriate container. Any substance remaining can be cleaned up with an absorbent paper dampened with acetone. Seal the contaminated paper in a container to prevent the release of vapors (NTP , 1991).
- Liquid spills can be diked with sand bags, soil, foamed concrete or polyurethane to prevent surface flow. Use vermiculite, dry sand or soil, cement powder, commercial sorbents, or fly ash to absorb excess liquid (AAR, 2000; Sittig, 1991).
For large water spills use excavated lagoons, sand bag barriers, or natural deep water pockets to trap the material at the bottom. Suction hoses, or mechanical dredges or lifts can be used to remove the pollutant (AAR, 2000).

WASTE TREATMENT OPTIONS

RECYCLING/RECLAMATION

Chlorpyrifos granular crystals sink in water and will form a layer at the bottom. The substance can be almost completely recovered by physical means (OHM/TADS , 2001).
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.

CHEMICAL TREATMENT

In an aqueous methanol solution (pH 6), chlorpyrifos is 50% hydrolyzed in 1,930 days and in 7.2 days at a pH of 9.96 (Sittig, 1991).
Spray mixtures containing less than a 1% concentration of this compound are destroyed with an excess of 5.25% sodium hypochlorite in less than 30 minutes at 100 degrees C, and in 24 hours at 30 degrees C (Sittig, 1991).
Concentrated mixtures of chlorpyrifos (61.5%) are destroyed by treatment with 100:1 volumes of sodium hypochlorite solution (5.25%) and steam in 10 minutes (Sittig, 1991).
A caustic soda-methanol or caustic soda-detergent can be used as a decontaminant, but the used rinse solution must be incinerated or buried away from water sources (ATSDR, 1997).

PHYSICAL TREATMENT

Incineration, adsorption , and landfilling are the recommended disposal methods. If an EPA-approved incinerator is not available, material can be buried in an approved chemical waste landfill (ATSDR, 1997; OHM/TADS , 2001).
Small amounts can be absorbed with sand, peat, straw, sawdust, or other similar material. Place material in impervious containers, and bury in an area away from water supplies (ATSDR, 1997; OHM/TADS , 2001).
Bottom pumps or underwater vacuum systems can be used as a countermeasure (OHM/TADS , 2001).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Chlorpyrifos is released in the environment during the manufacture of the end-use products (in minor amounts) and its use as an insecticide. Inhalation and ingestion of contaminated foods exposes the general population to the pesticide (HSDB, 2004; Howard, 1991) .

In June 2000, the Environmental Protection Agency (EPA) entered into agreement with registered chemical manufacturers to cease production and sales of almost all residential products containing chlorpyrifos, and to decrease chlorpyrifos concentrations in residential termiticides. The phase out of additional chlorpyrifos-containing products will continue in US markets through 2005 (EPA, 2002).
The concentration level and persistence of chlorpyrifos vary depending on the type of formulation. Emulsifiable concentrates and wettable powders tend to produce a large increase in concentration. Granules and controlled-release formulations do not produce as rapid an increase in concentration, but the concentration persists longer (EXTOXNET, 1996).
The FDA Total Diet Study, FDA Monitoring Program, and USDA National Residue Program, reported chlorpyrifos is infrequently detected in various foods such as fruit, vegetables, grains, and processed foods (Howard, 1991).
In a study simulating a typical American home, the airborne levels from gradual release pest control strips with chlorpyrifos ranged from 100 to 230 ng/m(3) over a 30 day period (Howard, 1991).

ENVIRONMENTAL FATE AND KINETICS

Chlorpyrifos reacts with photochemically produced hydroxyl radicals, but is not expected to react with ozone (Howard, 1991).
- If released into the atmosphere in the vapor-phase at 25 degrees C, chlorpyrifos will react with photochemically produced hydroxyl radicals with a half-life of 6.34 hours at an atmospheric concentration of 8x10(5) hydroxyl radicals/cm(3) (Howard, 1991).
- From the rate constant, 9.2X10(-11) cm(3)/molecule-sec (at 25 degrees C), the estimated half-life for vapor-phase reaction with hydroxyl radicals is 4 hours (HSDB, 2004).
- Photolysis potentially contributes to transformation of chlorpyrifos (Howard, 1991).
Results of a chemical oxidation chamber study showed that 82 - 92% chlorpyrifos existed in vapor phase at temperatures of 60 - 80 degrees C. Photodegradative loss of chlorpyrifos during the 2-hour irradiation period was ~8%. The experimental hydroxyl radical reactivity rate was similar to predicted rates, with measured half-lives from 1.4 to 2.4 hours. Reaction rates were unaffected by various air temperatures between 60 - 80 degrees C (Hebert et al, 2000).
A vapor pressure of 2X10(-5) mmHg (at 25 degrees C) indicates chlorpyrifos, at ambient air, is expected to exist in both vapor and particulate phases (HSDB, 2004).
A thin film of chlorpyrifos exposed to wavelengths from a UV light had a photodegradation half-life of 52.45 hours (HSDB, 2004).
Photochemical conversion half-life of chlorpyrifos in air is 2.27 hours (Howard, 1991).

WATER

SURFACE WATER
- The hydrolysis half-life is 35-78 days (at 25 degrees C) in neutral conditions (Howard, 1991).
- When chlorpyrifos is released in the water, it partitions from the water and adsorbs to the sediments. The rate of volatilization from a river may be inhibited greatly by this characteristic. The desorption from the sediment can contribute to the persistence in water (Howard, 1991).
- The hydrolysis rate of water is relatively independent of pH from pH 1 to pH 7. The adsorption to sediments in acidic or neutral water does not influence the hydrolysis rate (Howard, 1991).
- Alkaline conditions and the presence of Cu(+2) ions in significant concentrations markedly increase the hydrolysis rate (EXTOXNET, 1996; Howard, 1991).
- Cu(+2) ions added to both distilled water and natural water solution of chlorpyrifos at pH 8.2-8.3 reduced the half-lives from several weeks to less than one day (Howard, 1991).
- A 10 degrees C decrease in temperature will slow the hydrolysis rate by 2 1/2-3 fold (EXTOXNET, 1996; Howard, 1991).
- At the same temperature and pH, canal water containing metal ions hydrolyzed 16 times faster, but metal ions in natural waters is not enough to enhance the hydrolysis rate (Howard, 1991).
- Metal catalysis was not an important factor in the hydrolysis rate in three different types of natural water at 25 degrees C. The half-life was 48 days (Howard, 1991).
- Differences in degradation rates in sterile and non-sterile natural water and natural water and sediment were not significant (Howard, 1991).
- Neutral and acidic conditions did not significantly alter the hydrolysis rate of chlorpyrifos when adsorbed to sediments when compared to hydrolysis to natural water. In the sorbed-state, alkaline conditions may slow down the hydrolysis rate (EXTOXNET, 1996; Howard, 1991).
- The hydrolysis of chlorpyrifos produces 3,5,6-trichloro-2-pyridinol and variations of trichloropyridyl phosphorothioates (Verschueren, 2001; Howard, 1991).
- The surface water photolysis half-life during the midsummer is approximately 3 to 4 weeks. Photolysis also decreases in deep waters, in natural waters with lessened light intensity, and when sunlight exposure is decreased (EXTOXNET, 1996; Howard, 1991).
- Chlorpyrifos degrades faster in non-sterile water versus sterilized water. Microbial degradation may be a contributing factor (Howard, 1991).
- A laboratory freshwater ecosystem intended to mimic drainage ditches was set up to study the fate of chlorpyrifos and its effect on crustaceans and insects. Doses were applied to produce a nominal insecticide concentration of 5 or 35 mcg/L. Two experiments were run, one with the ecosystem dominated by the macrophyte Elodea nuttallii, and another using an open water system. In the vegetative system, the insecticide is largely adsorbed and receives minimal mixing, while in the open water system the insecticide mixes readily. In the open water system, the sediment played an important role as a sink for chlorpyrifos. 50% of the applied dose was removed in 8 days (Brock et al, 1992).

SOIL

TERRESTRIAL

In soil, chlorpyrifos slowly degrades by chemical hydrolysis and microbial degradation (Howard, 1991).
Clay in either dry or moist soil serves as a catalyst for chemical hydrolysis. Chemical hydrolysis was significant on air-dried soil surfaces and soil clays. The primary degradation product is 3,5,6-trichloro-2-pyridinol (Howard, 1991).
Volatilization losses of chlorpyrifos from non-tilled soil were 2 to 4 times greater than the losses from conventionally tilled fields. As much as one half of the pesticide applied was volatilized during the 26 days of the study. The maximum volatilization rates were measured at midday, indicating that soil dryness was not an important factor in the rate (Whang et al, 1993).
Volatilization from soil surfaces contributes to the loss of chlorpyrifos (Howard, 1991).
On moist soils, the volatility half-life was 45 to 163 hours, with 62 to 89% of the applied compound remaining on the soil after 36 hours(EXTOXNET, 1996).
The volatilization from moist treated soils produces enough toxic fumes to kill insects (Howard, 1991).
Chlorpyrifos adsorbed in organic matter and persisted in muck soil at 1 ppm for 16 weeks. Soil with a higher clay or organic content is more stable (OHM/TADS , 2001).
Chlorpyrifos degrades faster in non-sterile soil versus sterilized soil. Microbial degradation may be a contributing factor (Howard, 1991).

Only 5% of an initial 10 ppm concentration remained in non-sterile sandy loam soil after one week and after 8 weeks in non-sterile organic soil. Whereas, 50% remained in sterile sandy loam after 17 weeks and more than 24 weeks later in sterile organic soil (Verschueren, 2001).

Chlorpyrifos adsorbs tightly to soil and is not expected to leach significantly (Howard, 1991).
Photodegradation is not expected to be an important fate process (Howard, 1991).

Photodegradation was not significant on dry treated soil exposed to sunlight for 8 days. Chlorpyrifos under a sunlamp for 12,000 hours had less than 2% decomposition (Howard, 1991).

Persistence of chlorpyrifos in general soil has been reported between 60-120 days (Howard, 1991).
The half-life for this compound is between 60 and 120 days, but depending on soil type, temperature, and other conditions, the half-life can range from 2 weeks to over 1 year (EXTOXNET, 1996).
Between 2.6 and 9.3% of the compound applied to sand or silt loam soil remained after 30 days (EXTOXNET, 1996).

The initial half-life and persistence measurements were taken in the following soil compositions, respectively: (Howard, 1991)

Soil Type	Initial Half-Life	Persistence Measurements
paddy soil:	10 days	residual remaining after 60 days
sandy soil:	14 days	4% remaining after 1 year
muck soil:	8 weeks	9% remaining after 1 year
sandy loam:	not reported	remaining at 2-4 weeks
field soil:	not reported	remaining at 180 days

In silt loam soil, chlorpyrifos disappears 2-3 times faster in surface soil versus applications beneath the surface (Howard, 1991).

In silt loam soil at 25 degrees C, the hydrolysis rate was about 59% in 20 days (Howard, 1991).

Chlorpyrifos in sandy loam soil is relatively immobile (Howard, 1991).
Clay loam and high clay soil, using concentrations of 0.01, 0.1, and 1.0 ppm has soil sorption constants of 2740 and 995, respectively (Howard, 1991).

OTHER

OTHER
- The half-life of chlorpyrifos in an aqueous methanolic solution at a pH of 6 is 1930 days; at a pH of 9.96 the half-life is 7.2 days (Hayes & Lawes, 1991).
- Aqueous alcoholic solution of chlorpyrifos decomposes in 7D at pH 10 to 50% of the original chlorpyrifos concentration(Howard, 1991).

ABIOTIC DEGRADATION

Chlorpyrifos slowly degrades in soil by chemical hydrolysis and microbial degradation. Manure in the soil will increase its persistence. Clay in the soil promotes degradation by chemical hydrolysis. Hydrolysis is also significant in air-dried soil surfaces. Persistence is influenced by soil type, temperature, and other conditions. The material adsorbs strongly to soil and will not likely leach. It adsorbs to organic matter in muck soil and is relatively immobile in sandy loam soil. Losses from soil occur by volatilization from the surface. Incorporation of the material to lower soil layers by tilling reduces volatilization losses. Photodegradation is not important in soil. Absorption through roots and leaves is not significant (OHM/TADS, 2001; EXTOXNET, 1996; Whang et al, 1993; Howard, 1991).

In water systems, chlorpyrifos partitions to sediment, hydrolyzes, volatilizes, or photodegrades. Sediment can act as a sink for chlorpyrifos. Desorption from sediment may contribute to its persistence in water. Sorption under alkaline conditions may slow hydrolysis. Decreases in water temperature also slows hydrolysis. Combined alkaline conditions and the presence of metal ions may affect the hydrolysis rate in certain waters. Volatilization is the main source of loss from pond water. Volatilization from rivers may be highly inhibited by its tendency to partition. Photolysis decreases with depth or with decreased sunlight (EXTOXNET, 1996; Brock et al, 1992; Howard, 1991).

In the atmosphere, chlorpyrifos is photodegraded by reaction with hydroxyl radicals or photolytic conversion. It can exist as a vapor or in particulate phase in ambient air, based on the vapor pressure of 2 x 10(-5) mmHg (at 25 degrees C). The atmospheric half-life ranges from 2-6H (HSDB, 2004; Howard, 1991).

BIODEGRADATION

This compound biodegrades significantly. In non-sterile soils, a measured half-life of 4 weeks for clay loam and 12 weeks for silt loam was found. This compares to the sterile soil measurements 24 weeks for both soil types. Pretreating the soil with a hydrolysis product of 3,4,5-trichloro-2-pyridinol did not enhance degradation rates. Manuring appears to increase the persistence of chlorpyrifos (Howard, 1991).

In aerobic soils, the half-life was from 11 to 141 days in seven soils of various textures (loamy sand to clay) and with soil pHs from 5.4 to 7.4. Soil half-life was unaffected by soil texture or organic matter content. The persistence of this compound was lower in soils with higher pH. In anaerobic soils, the half-life of chlorpyrifos was 15 days in loam and 58 days in clay (EXTOXNET, 1996).

There was no significant difference in the degradation rate in natural water versus sterilized natural water (Howard, 1991).

The half-life of chlorpyrifos in a seawater-sediment was 24 days; when sterilized with formalin, the half-life was over 28 days (Howard, 1991).

In a shake-flask test, chlorpyrifos degraded about 40% faster in active natural water than in water sterilized with formalin (Howard, 1991).

Soils with a short history of chlorpyrifos application had a half-life of 42 days, and fields previously treated (8 years) had a half-live of 15 days. This suggest the degradation product, 3,4,5-trichloro-2-pyridinol, does not effect the process (Howard, 1991).

Biodegradation half-life for various soil types tested in greenhouse conditions for 50D, at 23-26 degrees C, constant light, and initial concentration of 5-10 mg/kg (Verschueren, 2001):

sandy soil - 7D
organic rich orchard soil - 12D
agricultural soil - 9D
volcanic soil - 15D
field test - 30D dissipation half-life

The degradation rate in non-sterile sandy loam soil and muck soils is significantly faster than sterile soils. The rate decreased with when the temperature was lowered, and moisture was also a variable (Howard, 1991).

Chlorpyrifos in clay and silt soils sterilized by autoclaving had a half-life of 24 weeks. The half-life is significantly shorter in non-sterile soils, 4 weeks (clay loam) and 12 weeks (silt loam) (Howard, 1991).

In non-sterile sandy loam soil its half-life was 1 week, versus 17 weeks when the soil was sterile. In non-sterile organic soil it had a half-live of 2.5 weeks, versus 40 weeks in sterile soil (Howard, 1991).

The half-lifes in seven soils, varying in texture (loamy sand to clay) and with pHs 5.4-7.4, were 11 to 141 days. Soil half-life was unaffected by soil texture or organic matter content. The persistence was lower in soils with higher pH (Howard, 1991).

The half-life anaerobic in soils containing chlorpyrifos was 15 days in loam and 58 days in clay (EXTOXNET, 1996).

BIOACCUMULATION

HUMANS

Chlorpyrifos does not have potential to bioaccumulate (EXTOXNET, 1996).

FISH

This compound accumulates in the tissues of aquatic organisms (EXTOXNET, 1996).
If the chemical is absorbed by fish, it seldom persists for longer than a week (OHM/TADS , 2001).
Chlorpyrifos is highly toxic to fish and would most likely be lethal to the fish before it accumulated in the tissues (OHM/TADS , 2001).

BIRDS

Due to the highly toxic nature of organophosphates, chlorpyrifos would probably be lethal to the animal before it accumulated in the tissues (OHM/TADS , 2001).

PLANTS

AQUATIC
- Absorption of the chemical through the roots and leaves is insignificant (OHM/TADS , 2001).
- This compound may be toxic to some plants (i.e. head lettuce). Research indicates that residues can remain on plant surfaces for approximately 10 to 14 days, and chlorpyrifos and its metabolites can accumulate in certain crops (EXTOXNET, 1996).

MAMMALS

Chlorpyrifos rapidly metabolizes in rats, dogs, and other mammals following ingestion. It does not have a significant bioaccumulation potential (EXTOXNET, 1996; Hartley & Kidd, 1990).
- One case reported chlorpyrifos was found unchanged in cow feces, but was not found in the urine or milk. Four days following spray dipping (0.15% emulsion), chlorpyrifos was detected in the milk (EXTOXNET, 1996).
- Chlorpyrifos did not accumulate in any rat tissue except the fat (EXTOXNET, 1996).

BIOCONCENTRATION FACTOR

The estimated log bioconcentration factors (BCFs) of 3.08 (based on the water solubility) and 3.54 (based on the log Kow) indicate chlorpyrifos can bioaccumulate in various aquatic organisms (Howard, 1991).
In a 35 day flowing water study, the log BCF in mosquito fish was 2.67 (Verschueren, 2001; Howard, 1991).
In a static ecosystem study, the log BCF in mosquito fish was 2.50 (Howard, 1991).
BCF values ranging from 2.50 to 3.54 suggest significant bioconcentration (Howard, 1991).
BCF values of 58 to 5100 have been seen in fish with continuous exposure, from the embryonic through fry stages (EXTOXNET, 1996).

ENVIRONMENTAL TOXICITY

Chlorpyrifos is very highly toxic to freshwater fish, aquatic invertebrates, estuarine, marine organisms, birds, honey bees, and other wildlife (EXTOXNET, 1996; EPA, 1988) Willson & Eisley, 1997).

Acute toxicity tests of fish exposed to very low concentrations of this insecticide revealed cholinesterase inhibition. Fish and aquatic invertebrate deaths have occurred at application concentrations as low as 0.01 pounds of active ingredient per acre (EXTOXNET, 1996).

Due to the high acute toxicity and its persistence in sediments, chlorpyrifos is a hazard to sea bottom dwellers. It also appears that smaller organisms are more sensitive to chlorpyrifos than larger ones (EXTOXNET, 1996).

Decreased survival and growth and increased deformities were seen in first generation offspring of fathead minnows exposed to chlorpyrifos, at 2.68 mcg/L for 30 days, during a 200-day period which in they reproduced (EXTOXNET, 1996).

AQUATIC TOXICITY

EC50 - (SALTWATER) EASTERN OYSTER: 0.27 ppm for 24H (OHM/TADS , 2001; OHM/TADS , 2001)
LC50 - (WATER) BLUEGILL: 0.01 mg/L for 96H (EXTOXNET, 1996)
LC50 - (SALTWATER) BLUE CRAB: 0.12 ppm for 24H (OHM/TADS , 2001)
LC50 - (FRESHWATER) BLUEGILL SUNFISH: 0.004 ppm for 24H (OHM/TADS , 2001)
LC50 - (FRESHWATER) BLUEGILL SUNFISH: 0.0033 ppm for 96H (OHM/TADS , 2001)
LC50 - (FRESHWATER) CHANNEL CATFISH: 0.0198 ppm for 24H (OHM/TADS , 2001)
LC50 - (FRESHWATER) CHANNEL CATFISH: 0.0134 ppm for 96H (OHM/TADS , 2001)
LC50 - (WATER) CRUSTACEAN (Gammarus lacustris): 0.11 mcg/L for 96H (conditions of bioassay not specified) (HSDB, 2004)
LC50 - (WATER) CRUSTACEAN (Gammarus fasciatus): 0.32 mcg/L for 96H (conditions of bioassay not specified) (HSDB, 2004)
LC50 - (WATER) FATHEAD MINNOW: 0.331 mg/L for 96H (EXTOXNET, 1996)
LC50 - (FRESHWATER) GOLDFISH: 0.18 ppm for 24H (OHM/TADS , 2001)
LC50 - (FRESHWATER) GOLDFISH: 0.32 ppm for 24H (OHM/TADS , 2001)
LC50 - (WATER) GOLDFISH: 0.806 mg/L for 96H (EXTOXNET, 1996)
LC50 - (WATER) GUPPY (Poecilia reticulata): 220 mcg/L for 48H (conditions of bioassay not specified) (HSDB, 2004)
LC50 - (WATER) LAKE TROUT: 0.098 mg/L for 96H (EXTOXNET, 1996)
LC50 - (FRESHWATER) LONGNOSE KILLIFISH: 0.0068 ppm for 24H (OHM/TADS , 2001)
LC50 - (FRESHWATER) LONGNOSE KILLIFISH: 0.0032 ppm for 48H (OHM/TADS , 2001)
LC50 - (WATER) LONGNOSE KILLIFISH (Fundulus similis): 3.2 mcg/L for 48H (at a salinity of 24 g/kg, conditions of bioassay not specified) (HSDB, 2004)
LC50 - (FRESHWATER) KOREAN SHRIMP (Palaemon macrodactylus): 0.25 mcg/L for 96H (conditions of bioassay not specified) (HSDB, 2004)
LC50 - (WATER) MOSQUITO FISH: < 1,000 mcg/L for 24H (HSDB, 1996)
LC50 - (FRESHWATER) MOSQUITO FISH: 0.23 ppm for 36H (OHM/TADS , 2001)
LC50 - (WATER) RAINBOW TROUT, mature: 0.009 mg/L for 96H (EXTOXNET, 1996)
LC50 - (FRESHWATER) RAINBOW TROUT: 0.02 ppm for 48H (CHRIS, 2001; OHM/TADS , 2001)
LC50 - (FRESHWATER) RAINBOW TROUT: 0.0075 ppm for 24H (OHM/TADS , 2001)
LC50 - (FRESHWATER) RAINBOW TROUT: 0.003 ppm for 96H (OHM/TADS , 2001)
LC50 - (WATER) RAINBOW TROUT: 0.003 mg/L for 96H (Hartley & Kidd, 1990a)
LC50 - (WATER) RAINBOW TROUT: 0.110 ppm for 24H (CHRIS, 2001)
LC50 - (WATER) RAINBOW TROUT (Salmo gairdneri): 15 mcg/L for 96H (at 7.2 degrees C) (HSDB, 2004)
LC50 - (WATER) SHEEPSHEAD MINNOW (Cyprinodon variegatus), juvenile: >1000 mcg/L for 24H (at a salinity of 24 g/kg, conditions of bioassay not specified) (HSDB, 2004)
LC50 - (WATER) SHINER PERCH (Cymatogaster aggregata): 3.5; 3.7 mcg/L for 96H (static lab bioassay) (HSDB, 2004)
LC50 - (WATER) SPOT (Leiostomus xanthurus), juvenile: 7 mcg/L for 48H (at a salinity of 26 g/kg, conditions of bioassay not specified) (HSDB, 2004)
LC80 - (FRESHWATER) FATHEAD MINNOW: 1.0 ppm for 72H (OHM/TADS , 2001)
LC90/95 - (WATER) TRICHLOPTERA (Hydropsyche pellucidula): >0.5 ppm for 1H (conditions of bioassay not specified) (HSDB, 2004)
LC90/95 - (WATER) TRICHLOPTERA (Hydropsyche pellucidula): 0.2-0.5 ppm for 1H (conditions of bioassay not specified) (HSDB, 2004)
LC90/95 - (WATER) DIPTERA (Simulium ornatum): 0.05-0.1 ppm for 1H (conditions of bioassay not specified) (HSDB, 2004)
LC90/95 - (WATER) EPHIMETOPTERA (Bactis rhodani): 0.01 to 0.02 ppm for 1H (conditions of bioassay not specified) (HSDB, 2004)
LC100 - (FRESHWATER) FATHEAD MINNOW: 5.0 ppm for 24H (OHM/TADS , 2001)
LD50 - (ORAL) BULLFROGS (Rana catesbiana) Male: >400 mg/kg (conditions of bioassay not specified) (HSDB, 2004)
LD50 - (SALTWATER) GRASS SHRIMP: 0.00281 for 24H (OHM/TADS , 2001)
LD50 - (SALTWATER) GRASS SHRIMP: 0.0024 for 48H (OHM/TADS , 2001)
LD50 - (SALTWATER) RAMSHORN SNAIL: 2.0 ppm for 72H (OHM/TADS , 2001)
TL50 - (FRESHWATER) KOREAN SHRIMP: 0.00025 ppm for 96H (static lab bioassay) (OHM/TADS , 2001)
TL50 - (FRESHWATER) KOREAN SHRIMP: 0.0001 ppm for 96H (intermittent flow lab bioassay) (OHM/TADS , 2001)
TL50 - (FRESHWATER) KOREAN SHRIMP (Palaemon macrodactylus): 0.002-0.046 ppm for 96H (HSDB, 2004)
TL50 - (FRESHWATER) SCUD: 0.0056 ppm for 24H (OHM/TADS , 2001)
TL50 - (FRESHWATER) SCUD: 0.0032 ppm for 96H (OHM/TADS , 2001)
TLm - (WATER) BLUEGILL FISH: 0.038 ppm for 36H (acclimated) (CHRIS, 2001)
TLm - (WATER) BLUEGILL FISH: 0.125 ppm for 36H (laboratory) (CHRIS, 2001)
TLm - (WATER) MOSQUITO FISH: 0.23 ppm for 36H (CHRIS, 2001)
TLm - (WATER) MOSQUITO FISH: 0.595 ppm for 36H (laboratory) (CHRIS, 2001)
TLm - (SALTWATER) SHINER PERCH: 0.0035 for 96H (static lab bioassay) (OHM/TADS , 2001)
TLm - (SALTWATER) SHINER PERCH: 0.0037 for 96H (flowing water lab bioassay) (OHM/TADS , 2001)

FOWL TOXICITY

LD50 - (ORAL) JAPANESE QUAIL (Coturnix): 293 ppm (95% confidence limit) (HSDB, 2004)
LC50 - (ORAL) JAPANESE QUAIL (Coturnix), Male, 2.5 months old: 15.9 mg/kg (HSDB, 2004)
LC50 - (ORAL) JAPANESE QUAIL (Coturnix), Male, 2 months old: 17.8 mg/kg (HSDB, 2004)
LD50 - (ORAL) CANADIAN GEESE (Branta canadensis) Male and Female: >80 mg/kg (HSDB, 2004)
LD50 - (ORAL) CHUKAR, Male, 3-5 months old: 60.7 mg/kg (HSDB, 2004)
LD50 - (ORAL) CHUKAR, Female, 3-5 months old: 61.6 mg/kg (HSDB, 2004)
LD50 - COMMON GRACKLE (Quiscalus quiscula), Adult: 13 mg/kg (HSDB, 2004)
LD50 - (ORAL) CROW (Corvus brachyrhynchos), Adult: >32 mg/kg (HSDB, 2004)
LD50 - (ORAL) HOUSE SPARROW, Male: 21.0 mg/kg (HSDB, 2004)
LD50 - (ORAL) LESSER SANDHILL CRANE, Male: 25-50 mg/kg (HSDB, 2004)
LD50 - (ORAL) MALLARD, Female: 75.6 mg/kg (HSDB, 2004)
LD50 - (UNREPORTED) MALLARD: 70-80 mg/kg (CHRIS, 2001)
LD50 - (ORAL) MALLARD DUCKLING (Anas platyrhynchos), Male and Female, 15-19 days old: 167 mg/kg (HSDB, 2004)
LD50 - (ORAL) PHEASANT, Male, 3-5 months old: 8.41 mg/kg (HSDB, 2004)
LD50 - (ORAL) PHEASANT SP Pheasant, Female, 3-5 months old: 17.7 mg/kg (HSDB, 2004)

INSECT TOXICITY

LC50 - (WATER) MOSQUITO (Culex pipens), 4th instar: 1.2 mcg/L for 24H (HSDB, 2004)
LC50 - (WATER) MOSQUITO (Aedes species), 4th instar: 0.5-3.5 mcg/L for 24H (HSDB, 2004)
LC50 - (WATER) MOSQUITO (Aedes aegypti), 2nd instar: 0.0011 mcg/L for 24H (HSDB, 2004)
LC50 - (WATER) MOSQUITO (Aedes aegypti), 4th instar: 0.0014 mcg/L for 24H (HSDB, 2004)
LC50 - (WATER) MOSQUITO (Aedes aegypti), 3rd and 4th instar: 10 mcg/L for 18H (HSDB, 2004)
LD50 - (TOPICAL) AMERICAN COCKROACH (Periplaneta americana), Nymph: 5.7 mcg/g for 24H (HSDB, 2004)
LC50 - (WATER) MOSQUITO (Anopheles freeborni), 4th instar: 0.9-7.0 mcg/L for 24H (HSDB, 2004)
LD50 - (TOPICAL) AMERICAN COCKROACH (Periplaneta americana), Adult: 0.67 mcg/insect for 24H (HSDB, 2004)
LD50 - (TOPICAL) ASSASSIN BUG (Sinea diadema): <0.5 mcg/insect for 24H (HSDB, 2004)
LD50 - (TOPICAL) BOXELDER BUG (Leptocoris trivittatus), Nymph: > 4.9 mcg/g for 24H; >0.2 mcg/insect nymph (HSDB, 2004)
LD50 - (TOPICAL) COLORADO POTATO BEETLE (Leptinotarsa decemlineata), Larva: >2.0 mcg/insect for 24H (HSDB, 2004)
LD50 - (TOPICAL) GERMAN COCKROACH (Blatella germanica) Male, adult: 1.92 mcg/g (0.092 mcg/insect) for 24H (HSDB, 2004)
LD50 - (TOPICAL) GREEN BUG (Schizaphis graminum), Adult: < 41.6 mcg/g for 24H; <0.5 mcg/insect (HSDB, 2004)
LD50 - (TOPICAL) HONEY BEE (Apis mellifera), Adult worker: approximately 1.14 mcg/bee (as dust) (HSDB, 2004)
LD50 - (TOPICAL) HOUSEFLY (Musca domestica), Female, adult: 2.2 mcg/g for 24H; 0.075 mcg/fly (HSDB, 2004)
LD50 - (TOPICAL) STABLE FLY (Stomoxys calcitrans), Male, adult: 1.13 mcg/g for 24H; 0.093 mcg/fly (HSDB, 2004)
LD50 - (TOPICAL) STABLE FLY (Stomoxys calcitrans) Female, adult: 1.5 mcg/g for 24H; 0.024 mcg/fly (HSDB, 2004)
LC50 - PREDACEOUS DIVING BEETLE (Hygrotus sp.), Adult: 40 mcg/L for 24H (HSDB, 2004)
LC50 - PREDACEOUS DIVING BEETLE (Laccophilus decipiens), adult: 4.6 mcg/L for 24H (HSDB, 2004)
LC50 - PREDACEOUS DIVING BEETLE (Thermonectus basillaris): 6 mcg/L for 24H (HSDB, 2004)
LC50 - WATER SCAVENGER BEETLE (Berosus styliferus), Adult: 9 mcg/L for 24H (HSDB, 2004)
LC50 - WATER SCAVENGER BEETLE (Hydrophilus triangularis), Larva: 20 mcg/L for 24H (HSDB, 2004)
LC50 - WATER SCAVENGER BEETLE (Hydrophilus triangularis), Adult: 30 mcg/L for 24H (HSDB, 2004)
LC50 - WATER SCAVENGER BEETLE (Tropisternus lateralis), Larva: 52 mcg/L for 24H (HSDB, 2004)
LC50 - WATER SCAVENGER BEETLE (Tropisternus lateralis), Adult: 8 mcg/L for 24H (HSDB, 2004)
LC50 - CLADOCERAN (Daphnia sp.): 0.88 mcg/L for 4H (encapsulated formulation, conditions of bioassay not specified) (HSDB, 2004)
LC50 - AMPHIPOD (Hyalella azteca): 1.28 mcg/L for 24H (encapsulated formulation) (HSDB, 2001)
LC50 - MAYFLY (Ephemerella sp): 0.33 mcg/L for 72H (encapsulated formulation) (HSDB, 2001)
LC50 - PYGMY BACKSWIMMER (Neoplea striola): 0.97 mcg/L for 144H (encapsulated formulation) (HSDB, 2001)

The snail Biomphalaria alexandrina, infected with the parasite Schistosomo-masoni cercariae, was exposed to sublethal concentrations (0.125, 0.25 and 0.5 ppm) of chlorpyrifos. The exposure induced a reduction in egg production and egg hatchability. This result suggests this system may be a useful monitor for low insecticide concentrations in aquatic environments (Ibrahim et al, 1992).

SOIL MICROFLORA: Chlorpyrifos reduced the count of aerobic nitrogen fixing bacteria and nitrogen fixation, when added to soil at concentrations of 10 to 300 mcg/g. Fungal populations and denitrifying bacteria were not affected (Martineztoledo et al, 1992).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

350.58

DESCRIPTION/PHYSICAL STATE

Chlorpyrifos is white granular crystalline solid with a mild mercaptan-type or sulfur odor. Technical grades are an amber solid cake with amber oil (AAR, 2000; ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; EXTOXNET, 1996; Hathaway et al, 1996; HSDB , 2001; Lewis, 2000; EPA, 1990).

The diethyl sulfide and diethyl disulfide content of chlorpyrifos contributes to the persistent mercaptan odor the technical product (Bingham et al, 2001; Hathaway et al, 1996). This insecticide contains o,o-diethyl-o-3,5 phosphorothioate (AAR, 2000).

Chlorpyrifos granular crystals sink in water and will form a layer at the bottom (OHM/TADS , 2001).

No information found at the time of this review.

VAPOR PRESSURE

1.87x10(-5) mmHg (at 20 degrees C) (ACGIH, 1991; Bingham et al, 2001) EPA, 1988; OHM.TADS, 2001)

1.87x10(-5) mmHg (at 25 degrees C) (Budavari, 2000; Hayes, 1982) Hayes & Law, 1991 NTP, 1991)

2.5 mPa (at 25 degrees C) (EXTOXNET, 1996; Hartley & Kidd, 1990)

1.9x10(-5) mmHg (Clayton & Clayton, 1993) Howard, 1991)

0.00002 mmHg (NIOSH , 2001)

2.02X10(-5) mmHg (at 25 degrees C) (HSDB , 2001)

8.87X10(-5) mmHg (at 35 degrees C) (OHM/TADS , 2001)

SPECIFIC GRAVITY

OTHER TEMPERATURE AND/OR PRESSURE

1.40 (liquid at 110 degrees F) (NIOSH , 2001)
1.398 (at 43.5 degrees C) (liquid) (HSDB , 2001; OHM/TADS , 2001)

TEMPERATURE AND/OR PRESSURE NOT LISTED

12.09 (calculated) (gas) (CHRIS , 2001)

DENSITY

OTHER TEMPERATURE AND/OR PRESSURE

LIQUID: 1.398 g/mL (at 43.5 degrees C) (HSDB, 1990)
1.398 g/cm(3) (at 43.5 degrees C) (Bingham et al, 2001)

VAPOR DENSITY

12.09 (calculated) (CHRIS , 2001)

FREEZING/MELTING POINT

FREEZING POINT

108 degrees F (NIOSH , 2001)
41.5-43.5 degrees C;106.7-110.3 F; 314.7-316.7 K (CHRIS , 2001)

MELTING POINT

41.5-43.5 degrees C (EPA, 1988)
41-42 degrees C (Budavari, 2000) Howard, 1991)
41.5-44 degrees C (EXTOXNET, 1996)
42-43 degrees C (Sittig, 1991)
42-43.5 degrees C (Hartley & Kidd, 1990; Lewis, 2000; NTP , 1991)
42.5-43 degrees C (ACGIH, 1991; Bingham et al, 2001; Hayes, 1982; Hayes & Laws, 1991)
45.5-46.5 degrees C (Clayton & Clayton, 1993)
42 degrees C (OHM/TADS , 2001)

BOILING POINT

160 degrees C (decomposes) (OHM/TADS , 2001)

320 degrees F (decomposes) (NIOSH , 2001)

approximately 200 degrees C (Bingham et al, 2001)

SOLUBILITY

IN WATER

very slightly soluble in water (Lewis, 2000)
It is insoluble in water (AAR, 2000).
1.12 ppm (at 24 degrees C) (Howard, 1991)
2 ppm (at 35 degrees C) (Hayes & Law, 1991)
2 ppm (at 25 degrees C) (Budavari, 2000; OHM/TADS , 2001)
2 mg/L (at 25 degrees C) (EXTOXNET, 1996; Hartley & Kidd, 1990)
approximately 2 mg/L (NTP , 1991)
0.0002% (NIOSH , 2001)
0.4 mg/L (at 23 degrees C) (HSDB , 2001)
1.4 mg/L (at 25 degrees C) (HSDB , 2001)
0.00013 g/100 mL (Bingham et al, 2001)

IN ORGANIC SOLVENTS

soluble in most organic solvents (ACGIH, 1991; Budavari, 2000; Lewis, 2000)
acetone: 650 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
benzene: 790 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
carbon disulfide: 590 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
carbon tetrachloride: 310 g/100 g (at 25 degrees C) (Budavari, 2000)
chloroform: 630 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
diethyl ether: 510 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
ethanol: 63 g/100 g (at 25 degrees C) (Budavari, 2000)
ethyl acetate: > 200 g/100 g (at 25 degrees C) (Budavari, 2000)
isooctane: 79 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990) Hayes & Law, 1991; (NTP , 1991)
kerosene: 60 g/100 g (at 25 degrees C) (Budavari, 2000)
methanol

45 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
43% w/w (Budavari, 2000) Hayes & Law, 1991)

methylene chloride

714 g/100 g (at 25 degrees C) (Budavari, 1996)
400 g/100 g (at 25 degrees C) (Budavari, 2000)

propylene glycol: 4 g/100 g (at 25 degrees C) (Budavari, 2000)
toluene: 150 g/100 g (at 25 degrees C) (Budavari, 2000)
1,1,1-trichloroethane: 400 g/100 g (at 25 degrees C) (Budavari, 2000)
triethylene glycol: 5 g/100 g (at 25 degrees C) (Budavari, 2000)
xylene

400 g/100 g (at 25 degrees C) (Budavari, 2000; Hartley & Kidd, 1990; NTP , 1991)
645 g/100 g (at 25 degrees C) (Budavari, 1996)
5.0 kg/L (at 25 degrees C) (HSDB , 2001)

dichloromethane: 4000 g/kg (at 25 degrees C) (Hartley & Kidd, 1990; NTP , 1991)

OCTANOL/WATER PARTITION COEFFICIENT

log Kow = 4.96 (Howard, 1991)

log Kow = 5.27 (HSDB , 2001)

HENRY'S CONSTANT

7.8x10(-5) atm-m(3)/mol (at 25 degrees C) (calculated) (Howard, 1991)

2.9X10(-6) atm m(3)/mol (at 20 degrees C) (HSDB , 2001)

SPECTRAL CONSTANTS

UV Maxima: 208, 230, 290 (HSDB , 2001)

OTHER/PHYSICAL

ORGANIC CARBON PARTITION COEFFICIENT

Koc = 995-31,000, reported in a variety of soils (HSDB , 2001).

-REFERENCES

GENERAL BIBLIOGRAPHY

40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.

40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.

49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.

49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.

62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.

65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.

67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.

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Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents