Ethyl p-nitrophenyl benzenethiophosphonate

H300: Fatal if swallowed [Danger Acute toxicity, oral]

H310: Fatal in contact with skin [Danger Acute toxicity, dermal]

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P262, P264, P270, P273, P280, P301+P316, P302+P352, P316, P321, P330, P361+P364, P391, P405, and P501 (click each P-code to see the statement)

H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]

H310 (100%): Fatal in contact with skin [Danger Acute toxicity, dermal]

H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (100%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

Aggregated GHS information provided per 42 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H311: Toxic in contact with skin [Danger Acute toxicity, dermal]

H330: Fatal if inhaled [Danger Acute toxicity, inhalation]

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

P203, P260, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P308+P316, P316, P318, P319, P320, P321, P330, P361+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

H320: Causes eye irritation [Warning Serious eye damage/eye irritation]

P203, P260, P262, P264, P264+P265, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P308+P316, P316, P318, P319, P320, P321, P330, P337+P317, P361+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer immediately for medical attention. Wear protective gloves when administering first aid. Put clothes in sealable container.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer immediately for medical attention.

Rinse mouth. Give a slurry of activated charcoal in water to drink. Refer immediately for medical attention.

Warning: Extremely hazardous by skin contact. Effects may be delayed up to 12 hours. Caution is advised.

Signs and Symptoms of Acute EPN Exposure: Acute exposure to EPN may produce the following signs and symptoms: pinpoint pupils, blurred vision, headache, dizziness, muscle spasms, and profound weakness. Vomiting, diarrhea, abdominal pain, seizures, and coma may also occur. The heart rate may decrease following oral exposure or increase following dermal exposure. Hypertension (high blood pressure) is not uncommon. Respiratory symptoms include dyspnea (shortness of breath), respiratory depression and respiratory paralysis. Giddiness, slurred speech, confusion, and psychosis may also be observed.

Emergency Life-Support Procedures: Acute exposure to EPN may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination.

Inhalation Exposure:

1. Move victims to fresh air. Emergency personnel should avoid self-exposure to EPN.

2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.

3. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

4. Transport to a health care facility.

Dermal/Eye Exposure:

1. Remove victims from exposure. Emergency personnel should avoid self- exposure to EPN.

3. Remove contaminated clothing as soon as possible.

4. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes.

5. Wash exposed skin areas three times with soap and water.

6. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

7. Transport to a health care facility.

Ingestion Exposure:

1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.

2. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

3. Vomiting may be induced with syrup of Ipecac. If elapsed time since ingestion of EPN is unknown or suspected to be greater than 30 minutes, do not induce vomiting and proceed to Step

4.Ipecac should not be administered to children under 6 months of age.Warning: Ingestion of EPN may result in sudden onset of seizures or loss of consciousness. Syrup of Ipecac should be administered only if victims are alert, have an active gag-reflex, and show no signs of impending seizure or coma. If ANY uncertainty exists, proceed to Step

4.The following dosages of Ipecac are recommended: children up to 1 year old, 10 mL (1/3 oz); children 1 to 12 years old, 15 mL (1/2 oz); adults, 30 mL (1 oz). Ambulate (walk) the victims and give large quantities of water. If vomiting has not occurred after 15 minutes, Ipecac may be readministered. Continue to ambulate and give water to the victims. If vomiting has not occurred within 15 minutes after second administration of Ipecac, administer activated charcoal.

4. Activated charcoal may be administered if victims are conscious and alert. Use 15 to 30 g (1/2 to 1 oz) for children, 50 to 100 g (1-3/4 to 3-1/2 oz) for adults, with 125 to 250 mL (1/2 to 1 cup) of water.

5. Promote excretion by administering a saline cathartic or sorbitol to conscious and alert victims. Children require 15 to 30 g (1/2 to 1 oz) of cathartic; 50 to 100 g (1-3/4 to 3-1/2 oz) is recommended for adults.

6. Transport to a health care facility. (EPA, 1998)

(General first aid procedures)

Eye: Irrigate immediately - If this chemical contacts the eyes, immediately wash (irrigate) the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately.

Skin: Soap wash immediately - If this chemical contacts the skin, immediately wash the contaminated skin with soap and water. If this chemical penetrates the clothing, immediately remove the clothing, wash the skin with soap and water, and get medical attention promptly.

Breathing: Respiratory support

Swallow: Medical attention immediately - If this chemical has been swallowed, get medical attention immediately.

(Non-Specific -- Organophosphorus Pesticide, n.o.s.) Stay upwind; keep out of low areas. Move containers from fire area if you can do it without risk. Fight fire from maximum distance. Dike fire control water for later disposal; do not scatter the material. Wear positive pressure breathing apparatus and special protective clothing.

(Non-Specific -- Organophosphorus Pesticide, n.o.s.) For small fires, use dry chemical, carbon dioxide, water spray, or foam. For large fires, use water spray, fog, or foam. (EPA, 1998)

Use powder, alcohol-resistant foam, water spray, carbon dioxide.

Self contained breathing apparatus with a full facepiece operated in pressure demand, or other positive pressure mode /should be used in firefighting/. /Parathion/

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use "alcohol" foam, dry chemical or carbon dioxide. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic/

If material on fire or involved in fire: Use water in flooding quantities as fog. Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) /Organophosphorus pesticides, solid, toxic/

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]:

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.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank 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. (ERG, 2024)

Personal protection: complete protective clothing including self-contained breathing apparatus. Do NOT wash away into sewer. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting.

1) Ventilate area of spill. 2) Cover with soda ash, mix and spray with water. Place in container of water and allow to stand for two days, then neutralize with 6 molar hydrogen chloride.

Do NOT wash away into sewer. Sweep spilled substance into containers; if appropriate, moisten first to prevent dusting. Carefully collect remainder, then remove to safe place. Chemical protection suit including self-contained breathing apparatus.

An explosion damaged the EPN section of manufacturing plant. Unknown quantities were flushed (due to firefighting) into a drainage ditch, sanitary sewer, and waste treatment plant. At water treatment plant, initial EPN level (5.8 mg/l) was reduced to zero following treatment with sodium hydroxide and about 2 wk of aeration. Sodium hydroxide was applied at various locations in the drainage ditch until pH was raised to about 11.0. After treatment, affected water was pumped into abandoned gypsum lagoon system.

Environmental considerations: Air spill: Apply water spray or mist to knock down vapors. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/

For more Cleanup Methods (Complete) data for EPN (6 total), please visit the HSDB record page.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Hydrolysis: Treat EPN with alkali... . Peer-review: Large amount, incinerate in a unit with effluent gas scrubbing. (Peer-review conclusions of an IRPTC expert consultation (May 1985))

The worker should immediately wash the skin when it becomes contaminated.

Work clothing that becomes wet or significantly contaminated should be removed and replaced.

Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics, and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

For more Preventive Measures (Complete) data for EPN (11 total), please visit the HSDB record page.

Ventilate area of spill. Cover with soda ash, mix, and spray with water. Place in container of water and allow to stand for 2 days, then neutralize with 6 molar hydrochloric acid. (EPA, 1998)

Separated from strong oxidizers and food and feedstuffs. Well closed. Provision to contain effluent from fire extinguishing. Store in an area without drain or sewer access.

Keep away from heat and open flame. Keep container closed. Store at 65-100 °F.

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

0.5 [mg/m3], inhalable fraction[German Research Foundation (DFG)]

0.20 [mg/m3]

5.0 [mg/m3]

50 [mg/m3]

0.5 mg/m³

TWA 0.5 mg/m3 [skin]

0.5 [mg/m3]

5 mg/m3 (NIOSH, 2024)

5 mg/cu m

See: 2104645

0.1 [mg/m3], inhalable fraction and vapor

8 hr Time Weighted Avg (TWA): 0.1 mg/cu m (inhalable fraction), skin.

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded.

A4; Not classifiable as a human carcinogen.

Biological Exposure Index (BEI): Determinant: cholinesterase activity in red blood cells; Sampling Time: discretionary; BEI: 70% of individual's baseline. The determinant is nonspecific, since it is also observed after exposure to other chemicals. /Acetylcholinesterase inhibiting pesticides/

(inhalable fraction and vapour): 0.1 mg/m

0.1 mg/m³ (inhalable fraction and vapor) [2000]

(inhalable fraction): 0.5 mg/m

A harmful concentration of airborne particles can be reached quickly.

The substance is irritating to the eyes and skin. Cholinesterase inhibition. The substance may cause effects on the nervous system. This may result in convulsions and respiratory failure. Exposure could cause unconsciousness and death. The effects may be delayed. Medical observation is indicated.

Cholinesterase inhibition. Cumulative effects are possible. See Acute Hazards/Symptoms.

Excerpt from NIOSH Pocket Guide for EPN:

Skin: PREVENT SKIN CONTACT - Wear appropriate personal protective clothing to prevent skin contact.

Eyes: PREVENT EYE CONTACT - Wear appropriate eye protection to prevent eye contact.

Wash skin: WHEN CONTAMINATED - The worker should immediately wash the skin when it becomes contaminated.

Remove: WHEN WET OR CONTAMINATED - Work clothing that becomes wet or significantly contaminated should be removed and replaced.

Change: DAILY - Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises.

Provide:

• EYEWASH - Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substances; this is irrespective of the recommendation involving the wearing of eye protection.

• QUICK DRENCH - Facilities for quickly drenching the body should be provided within the immediate work area for emergency use where there is a possibility of exposure. [Note: It is intended that these facilities provide a sufficient quantity or flow of water to quickly remove the substance from any body areas likely to be exposed. The actual determination of what constitutes an adequate quick drench facility depends on the specific circumstances. In certain instances, a deluge shower should be readily available, whereas in others, the availability of water from a sink or hose could be considered adequate.] (NIOSH, 2024)

Rubber gloves, protective clothing, goggles, respirators.

Wear appropriate personal protective clothing to prevent skin contact.

Wear appropriate eye protection to prevent eye contact.

Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substance; this is irrespective of the recommendation involving the wearing of eye protection.

For more Personal Protective Equipment (PPE) (Complete) data for EPN (8 total), please visit the HSDB record page.

NIOSH/OSHA

Up to 5 mg/m3 :

(APF = 10) Any supplied-air respirator

(APF = 50) Any self-contained breathing apparatus with a full facepiece

Light yellow crystalline powder with an aromatic odor. Used as an insecticide for cotton and an acaricide. (EPA, 1998)

Yellow solid with an aromatic odor. [pesticide] [Note: A brown liquid above 97 degrees F.] [NIOSH]

YELLOW CRYSTALLINE POWDER WITH CHARACTERISTIC ODOUR.

Yellow solid with an aromatic odor.

Yellow solid with an aromatic odor. [pesticide] [Note: A brown liquid above 97 °F.]

Light yellow crystals

Yellow crystals

White crystalline solid

For more Color/Form (Complete) data for EPN (6 total), please visit the HSDB record page.

Aromatic odor

215 °C @ 5 mm Hg

at 0.667kPa: 215 °C

97 °F (EPA, 1998)

Insoluble (NIOSH, 2024)

Miscible with isopropanol, benzene, toluene, xylene, acetone, methanol

Very sol in ether, ethanol

In water, 3.11 mg/l @ 20-25 °C

Solubility in water: none

Insoluble

1.268 at 77 °F (EPA, 1998) - Denser than water; will sink

Specific gravity: 1.270 @ 25 °C

1.3 g/cm³

1.268 @25 °C

(77 °F): 1.27

0.0003 mmHg at 212 °F (EPA, 1998)

0.00000095 [mmHg]

9.50X10-7 mm Hg @ 25 °C

Vapor pressure, Pa at 25 °C:

0.0003 mmHg

(212 °F): 0.0003 mmHg

log Kow= 4.78

Stable in neutral and acidic media but hydrolyzed by alkali to liberate p-nitrophenol.

Stable at ordinary temperatures.

The substance decomposes under influence of alkalies (hydrolysis) forming p-nitrophenol

When heated to decomposition, emits highly toxic fumes of /sulfur oxides, phosphorus oxides, nitrogen oxides, and phosphine/.

DT50 70 days (pH 4), 22 days (pH 7), 3.5 days (alkaline)

Non-corrosive

Specific gravity: 1.27 at 25 °C/4 °C; index of refraction: 1.5978 at 30 °C/D /Technical EPN/

Index of refraction: 1.6021 @ 25 °C/D

168.87 Ų [M+H]+ [CCS Type: TW; Buffer gas: N2; Ionization: GC-APCI+]

Insoluble in water. Hydrolyzed by alkali [EPA, 1998].

Nitro, Nitroso, Nitrate, and Nitrite Compounds, Organic

Sulfonates, Phosphonates, and Thiophosphonates, Organic

Organophosphates, such as EPN, are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrides. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides.

Strong oxidizers

Incompatible with alkaline pesticides.

Contact with strong oxidizers may cause fires & explosions; hydrolyzes slowly at pH values above seven.

Ethyl p-nitrophenyl phenylphosphorothioate (EPN)

1 x 10 ^-5 mg/kg-day

A4; Not classifiable as a human carcinogen.

The substance can be absorbed into the body by inhalation of its aerosol, through the skin and by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

Dizziness. Pupillary constriction. Muscle cramps. Excessive salivation. Sweating. Muscle twitching. Nausea.

MAY BE ABSORBED! Redness. Pain. Further see Inhalation.

Redness. Blurred vision.

Nausea. Abdominal cramps. Vomiting. Diarrhoea. Drowsiness. Further see Inhalation.

irritation eyes, skin; miosis, lacrimation (discharge of tears); rhinorrhea (discharge of thin nasal mucus); headache; chest tightness, wheezing, laryngeal spasm; salivation; cyanosis; anorexia, nausea, abdominal cramps, diarrhea; paralysis, convulsions; low blood pressure, cardiac irreg

Eyes, skin, respiratory system, cardiovascular system, central nervous system, blood cholinesterase

Chemical: EPN

Neurotoxin - Predominantly motor

Other Poison - Organophosphate

ACGIH Carcinogen - Not Classifiable.

Oral RfD: 0.00001 mg/kg/day (Uncertainty Factor: 1000, Modifying Factor: 1)

IRIS Current

LD50 Rabbit dermal 30 mg/kg

LD50 Rat (female) oral 8 mg/kg

LD50 Rat (male) oral 36 mg/kg

LD50 Dog oral 20 mg/kg

For more Non-Human Toxicity Values (Complete) data for EPN (21 total), please visit the HSDB record page.

... Hens treated concurrently with EPN, n-hexane and methyl isobutyl ketone. Methyl isobutyl ketone alone or in combination with O-ethyl O-nitrophenyl phenylphosphonothioate and n-hexane induced liver microsomal cytochrome p450 content and phoenobarbital inducible cytochrome p450 enzyme activities. Microsomes from hens treated with EPN, n-hexane, methyl isobutyl ketone or mixtures of EPN, n-hexane and methyl isobutyl ketone significantly enhanced the biotransformation of EPN to the more neurotoxic oxidation metabolite EPN. The results indicate that increased neurotoxicity after concurrent exposure to EPN, n-hexane and methyl isobutyl ketone is related to methyl isobutyl ketone induction of phenobarbital inducible cytochrome p-450 isozymes and the subsequent metabolic activation of EPN.

The anticholinesterase action of parathion and EPN was significantly potentiated by carbon disulfide /in ddY mice/, while that of dimethoate and diazinon was significantly reduced. Carbon disulfide had no significant effect or was slightly suppressive on the action of the other organophosphorus cmpd. In an in vitro experiment, liver microsomes isolated 1 hour after carbon disulfide were incubated with parathion or EPN. Effects on detoxication and activation of parathion and EPN by liver microsomes were evaluated by determining the degree of p-nitrophenol production and extent of cholinesterase inhibition, respectively. Liver microsomal detoxification and activation of parathion and EPN were decreased by carbon disulfide. The authors suggest that the diverse effects of carbon disulfide on the toxicity of various organophosphorus insecticides may reflect quantitative and qualitative differences in the metabolism of each cmpd.

...In vivo studies with rat and dog showed that EPN affects metabolism /of malathion/ by inducing change from carboxy ester hydrolysis to phosphate hydrolysis.

Basic treatment: Establish a patent airway. Suction if necessary. Aggressive airway control may be needed. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Organophosphates and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or has severe pulmonary edema. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Administer atropine. Correct hypoxia before giving atropine ... . Administer pralidoxime chloride (2 PAM). USE UNDER DIRECT PHYSICIAN ORDERS ONLY ... . Treat seizures with adequate atropinization and correction of hypoxia. Rarely is diazepam necessary ... . For hypotension with signs of hypovolemia, administer fluid cautiously and consider vasopressors for hypotension with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organophosphates and related compounds/

Atropine sulfate. Administer atropine sulfate intravenously, or intramuscularly if intravenous injection is not possible. Remember that atropine can be administered through an endotracheal tube if initial IV access if difficult to obtain. Depending on the severity of poisoning, doses of atropine ranging from very low to...high... . The objective of atropine antidotal therapy is to antagonize the effects of excessive concentrations of acetylcholine at end-organs having muscarinic receptors. Atropine does not reactivate the cholinesterase enzyme or accelerate disposition of organophosphate. Recrudescence of poisoning may occur if tissue concentrations of organophosphate remain high when the effect of atropine wears off. Atropine is effective against muscarinic manifestations, but it is ineffective against nicotinic actions, specifically muscle weakness and twitching, and respiratory depression. Despite the limitations, atropine is often a life-saving agent in organophosphate poisonings. Favorable response to a test dose of atropine can help differentiate poisoning by anticholinesterase agents from other conditions. However, lack of response, with no evidence of atropinization (atropine refractoriness) is typical of more severe poisonings. The adjunctive use of nebulized atropine has been reported to improve respiratory distress, decrease bronchial secretions, and increase oxygenation. ...Do not administer atropine or pralidoxime prophylactically to workers exposed to organophosphate pesticides. Prophylactic dosage with either atropine or pralidoxime may mask early signs and symptoms of organophosphate poisoning and thus allow the worker to continue exposure and possibly progress to more severe poisoning. Atropine itself may enhance the health hazards of the agricultural work setting: impaired heat loss due to reduced sweating and impaired ability to operate mechanical equipment due to blurred vision. This can be caused by mydriasis, one of the effects of atropine. /Organophosphate pesticides/

Glycopyrolate has been studied as an alternative to atropine and found to have similar outcomes using continuous infusion. Ampules...of glycopyrolate were added to ...saline and this infusion was titrated to the desired effects of dry mucous membranes and heart rate above 60 beats/min. During this study, atropine was used as a bolus for a heart rate less than 60 beats/min. The other apparent advantage to this regimen was a decreased number of respiratory infections. This may represent an alternative when there is a concern for respiratory infection due to excessive and difficult to control secretions, and in the presence of altered level of consciousness where the distinction between atropine toxicity or relapse of organophosphate poisoning is unclear. /Organophosphate pesticides/

For more Antidote and Emergency Treatment (Complete) data for EPN (19 total), please visit the HSDB record page.

The assessment of exposure to the organophosphate pesticides, bromophos and dicrotophos, can be accomplished through measurement of these compounds in the blood. However, since organophosphate pesticides are rapidly cleared from the blood, it is difficult to be able to detect the pesticides in blood unless very large quantities have been absorbed. This test may be useful for identification of the compound in cases of severe exposure, although documented tests for measurement of specific organophosphate pesticides in blood are very limited. Blood Reference Ranges: Normal - None detected; Exposed - Not established; Toxic - Not established. Serum or Plasma Reference Ranges: Normal - Not established; Exposed - Not established; Toxic - Not established. Urine: The assessment of organophosphate pesticide exposure can be accomplished through measurement of the following alkyl phosphate metabolites: dimethylphosphate, diethylphosphate, dimethylthiophosphate, diethylthiophosphate, dimethyldithiophosphate, and diethyldithiophosphate. ... The one limitation to measurement of urinary alkyl metabolites is that this test is only useful for assessing recent exposure, due to the short half-life of organophosphate pesticides. Urine Reference Ranges: Normal - Note established; Exposed - Not established; Toxic - Not established. /Organophosphate Pesticides/

Determination of RBC and Serum (Plasma) Cholinesterase Levels. ... BAT for acetylcholinesterase inhibitors (sampling time is end of exposure or end of shift, or for long-term exposures sampling time is after several shifts: both measured as acetylcholinesterase in erythrocytes): reduction of activity to 70% of reference value. ... BEI (sampling time is discretionary): 70% of individual's baseline. /Organophosphate Pesticides/

Measurement of whole blood-AChE is the most widely adopted method for monitoring the effects of occupational exposure to organophosphorus insecticides. Physiological variations in blood ChE levels occur in a healthy person and are seen among a population. It has been estimated that the coefficient of variation for AChE activity in samples from an individual is 8-11%, and that a decrease of 23% below pre-exposure level may, therefore, be considered significant. If the average of several pre-exposure values were available, then a decrease of 17% would be significant. It has been recommended that, if measured activity is reduced by 30% or more of the pre-exposure value, AChE measurements should be repeated at appropriate intervals to confirm the results. Depressions of AChE or ChE in excess of 20-25% are considered diagnostic of exposure but not, necessarily, indicative of hazard. Depressions of 30-50% or more are considered indicators for removal of an exposed individual from further contact with pesticides until levels return to normal. /Organophosphorus Pesticides/

...Organophosphorus pesticides may undergo hydrolysis in vivo to yield substituted phosphoric acids that are subsequently excreted in urine. Advances in gas chromatography and combined gas chromatography/mass spectrometry (GC/MS) have made it possible to analyse the urine of exposed persons for the presence of appropriate metabolites. It is usually necessary to preserve the sample by the addition of chloroform, to concentrate or extract the metabolite(s), and to convert them to suitably-volatile derivatives that can be detected by GC. Obviously, access to a well-equipped analytical laboratory, capable of the quick processing of samples, is a necessary factor if monitoring by urine analysis is proposed. However, in some cases, simpler and sensitive colorimetric tests are available for screening the urine of exposed persons. Thus, 4-nitrophenol can be measured directly in the urine of workers exposed to parathion. Consideration of the concentration of metabolite(s) in the urine can be helpful in determining patterns of exposure, and these concentrations can be calibrated against the effects on AChE for a particular pesticide. However, the time-course and peak of excretion of metabolites appears to vary according to dose, so that serial sampling and analyses of urine are desirable. Levels of metabolite alone cannot be considered a guide to hazard. This is obvious when it is realized that pesticides that have very different toxicities may yield identical acidic metabolites. Thus, the level of metabolites in urine, after exposure to sufficient amounts of the very toxic parathion-methyl to depress blood-AChE to 50%, will be much lower than that of the identical metabolites, following exposure to the related fenitrothion, which is about 40 times less toxic. /Organophosphorus Pesticides/

SRP: Workers should undergo an annual medical exam. Contraindications for work with organophosporous pesticides are organic diseases of the CNS, mental disorders and epilepsy, and pronounced endocrine disorders. Blood cholinesterase, both plasma and RBC, must be determined before work starts. In the event of prolonged work periods, this activity should be determined at intervals of 3-4 days. Persons exhibiting a fall in cholinesterase activity of 25% or more must be transferred to other work where they are not exposed until cholinesterase activity is restored. /Organophosphorous pesticides/

/HUMAN EXPOSURE STUDIES/ Poisonous if inhaled; ingestion may be fatal. Rapidly absorbed through skin. Repeated exposure may, without symptoms, be increasingly hazardous.

/HUMAN EXPOSURE STUDIES/ Signs and symptoms of acute intoxication by organophosphorus insecticides include muscarinic, nicotinic, and central nervous system (CNS) manifestations. Symptoms may develop rapidly, or there may be a delay of several hours after exposure before they become evident. The delay tends to be longer in the case of more lipophilic compounds, which also require metabolic activation. Symptoms may increase in severity for more than one day and may last for several days. In severe cases, respiratory failure is a dominant effect. /Organophosphorus Pesticides/

/HUMAN EXPOSURE STUDIES/ ...A 500 mL suspension that contained EPN was obtained from the GI tract of a 46 yr old farmer who died following generalized convulsions and cardiorespiratory arrest.

/HUMAN EXPOSURE STUDIES/ Agricultural chemicals are also important allergens responsible for allergic dermatitis. These include insecticides (... EPN ...) ... .

For more Human Toxicity Excerpts (Complete) data for EPN (9 total), please visit the HSDB record page.

LD50 ANAS PLATYRHYNCHOS (MALLARD DUCK) ORAL 3.08 MG/KG (95% CONFIDENCE LIMIT 2.38-4.00), 3 MO OLD FEMALES /SAMPLE PURITY = 91%/

LD50 PHEASANT ORAL 53.4 MG/KG (95% CONFIDENCE LIMIT 38.5-74.1), 3-5 MO OLD FEMALES /SAMPLE PURITY = 91%/

LD50 ALECTORIS CHUKAR (CHUKAR) ORAL 14.3 MG/KG (95% CONFIDENCE LIMIT 10.3-19.8), 3 MO OLD FEMALES /SAMPLE PURITY = 91%/

LD50 COTURNIX ORAL 5.25 MG/KG (95% CONFIDENCE LIMIT 3.79-7.28), 2 MO OLD FEMALES

For more Ecotoxicity Values (Complete) data for EPN (25 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ .../Symptoms appearing in mallards, pheasants, chukars, coturnix, pigeons, and house sparrows from acute oral LD50 dose were/ ataxia, prostration, salivation, lacrimation, tenesmus, diarrhea, dyspnea, tremors, wings thrust at right angles to body axis, tetany, terminal wing-beat convulsions, or opisthotonos.

/BIRDS and MAMMALS/ Injection of duck eggs ...causes deformity of feet of ducklings.

/AQUATIC SPECIES/ EPN was acutely toxic to crustaceans and fish, with commercial pink shrimp being most sensitive species tested. In chronic toxicity studies using M. bahia, significant mortality and fewer young were produced at EPN exposure level of 4.13 ug/L.

/OTHER TERRESTRIAL SPECIES/ Toxic to bees.

/PLANTS/ Non-phytotoxic except to some varieties of apple.

6.30e-01

8.20e+00

8.90e-02

2.00e+00

2.80e-03

Volatile

1.90e+00

2.50e+01

2.70e-01

The substance is very toxic to aquatic organisms. Bioaccumulation of this chemical may occur in fish. The substance may cause long-term effects in the aquatic environment. This substance does enter the environment under normal use. Great care, however, should be taken to avoid any additional release, for example through inappropriate disposal.

EPN's production may have resulted in its release to the environment through various waste streams; its former use as an insecticide and acaricide would have resulted in its direct release to the environment. If released to air, a vapor pressure of 9.5X10-7 mm Hg at 25 °C indicates EPN will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase EPN will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 5.1 hours. EPN in p-dioxane exhibits slight absorption of UV light in the environmentally relevant range (>290 nm), suggesting that EPN may be susceptible to direct photolysis by sunlight. Particulate-phase EPN will be removed from the atmosphere by wet and dry deposition. If released to soil, EPN is expected to have low mobility based upon a mean Koc of 1,327. Volatilization from moist soil surfaces is not expected to be an important fate process based upon a Henry's Law constant of 4.44X10-7 atm-cu m/mole. EPN is not expected to volatilize from dry soil surfaces based upon its vapor pressure. The half-life of EPN in soil under field conditions ranges from about 2 weeks to 1 month. In laboratory studies, biodegradation half-lives of 30 to 90 days in upland soils and 3 to 15 days in submerged soils have been reported. If released into water, EPN is expected to adsorb to suspended solids and sediment based upon the Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. BCF values ranging from 358 to 7,700 in fish suggest bioconcentration in aquatic organisms is high to very high; however, EPN is rapidly depurated. EPN is stable in neutral and acidic media, but hydrolyzed by alkali to liberate p-nitrophenol. Half-lives for EPN in water are 70 days (pH 4); 22 days (pH 7); 3.5 days (alkaline). Occupational exposure to EPN may have occurred through inhalation and dermal contact with this compound at workplaces where EPN was produced or used. Monitoring data indicate that the general population may be exposed to EPN via ingestion of food. (SRC)

EPN's production may have resulted in its release to the environment through various waste streams; its former use as an insecticide and acaricide(1) would have resulted in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), a mean Koc value of 1,327(2), indicates that EPN is expected to have low mobility in soil(SRC). Volatilization of EPN from moist soil surfaces is not expected to be an important fate process(SRC), given a Henry's Law constant of 4.44X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 9.5X10-7 mm Hg(3), and water solubility, 3.11 mg/l(4). EPN is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). The half-life of 14C-labeled EPN in field tests with Dundee silt loam (pH 5.5, organic matter 1.3%) and Keyport silt loam (pH 6.4, organic matter 2.75%) were 2 weeks and 1 month, respectively(5) Greater than 90% of the residual radiolabeled carbon was found in the top 3 inches of soil, after 18 months, indicating no leaching of EPN or its degradation products had occurred(5). Under greenhouse conditions 14C-labeled EPN has a half-life of 5-6 weeks in Fallsington sandy loam soil (pH 5.6, organic matter 1.4%)(5). In a biometer study with Keyport silt loam half-lives were 5 and 6 weeks at 2 and 10 ppm, respectively(5). Breakdown of EPN in soil proceeded primarily through hydrolysis and oxidation to phenylphosphonic acid, followed by further degradation of the phenyl ring to CO2(5). Under laboratory conditions, the half-lives of 1 ppm EPN in upland soils were 30-90 days and in submerged soils, 3-15 days(6). In upland soils degradation products were EPN-oxon, desethyl EPN-oxon, O-ethyl S-methylphenylphosphonothiolate, p-nitrophenol, O-ethyl O-methylphenylphosphonate, O-ethylphenylphosphonate, and phenylphosphonic acid(6).

AQUATIC FATE: Based on a classification scheme(1), a mean Koc value of 1,327(2), indicates that EPN is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon a Henry's Law constant of 4.44X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 9.7X10-7 mm Hg(4) and water solubility, 3.11 mg/l(5). According to a classification scheme(6), BCF values of 358(7) to 7,700(8) in fish suggest the potential for bioconcentration in aquatic organisms is high to very high(SRC); however, EPN is rapidly depurated(9). Based on results of persistence studies done on EPN in soil(10,11), EPN is expected to degrade primarily through hydrolysis and oxidation to phenylphosphonic acid(SRC). Photodegradation half-lives for EPN in aqueous solution without humic acids, containing humic acids, containing humic acids from soil and containing humic acid sodium salt were 38.5, 28.9, 34.6, and 49.5 days, respectively; EPN at 10-15 ppm plus humic acids at 5 ppm were irradiated in Pyrex-glass vessels with artificial sunlight(12). Half-lives for EPN in water are 70 days (pH 4); 22 days (pH 7); 3.5 days (alkaline)(13).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), EPN, which has a vapor pressure of 9.5X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase EPN is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 5.1 hours(SRC), calculated from its rate constant of 7.5X10-11 cu cm/molecule-sec at 25 °C(SRC), that was derived using a structure estimation method(3). Particulate-phase EPN may be removed from the air by wet and dry deposition(SRC). EPN in p-dioxane exhibits slight absorption of UV light in the environmentally relevant range (>290 nm)(4), suggesting that EPN may be susceptible to direct photolysis by sunlight(SRC).

AEROBIC: EPN, present at 100 mg/l, reached 3% of its theoretical BOD in 4 weeks using an activated sludge inoculum at 30 mg/l and the Japanese MITI test(1). Field dissipation half-lives ranging from 28 to 56 days have been reported(2). The half-life of 14C-labeled EPN in field tests with Dundee silt loam (pH 5.5, organic matter 1.3%) and Keyport silt loam (pH 6.4, organic matter 2.75%) were 2 weeks and 1 month, respectively(3) Greater than 90% of the residual radiolabeled carbon was found in the top 3 inches of soil, after 18 months, indicating no leaching of EPN or its degradation products had occurred(3). Under greenhouse conditions 14C-labeled EPN has a half-life of 5-6 weeks in Fallsington sandy loam soil (pH 5.6, organic matter 1.4%)(3). In a biometer study with Keyport silt loam half-lives were 5 and 6 weeks at 2 and 10 ppm, respectively(3). Breakdown of EPN in soil proceeded primarily through hydrolysis and oxidation to phenylphosphonic acid, followed by further degradation of the phenyl ring to CO2(3). Under laboratory conditions, the half-life of 1 ppm EPN in upland soil was 30-90 days and in submerged soil it was 3-15 days(4). In upland soils, degradation products were EPN-oxon, desethyl EPN-oxon, O-ethyl S-methylphenylphosphonothiolate, p-nitrophenol, O-ethyl O-methylphenylphosphonate, O-ethylphenylphosphonate, and phenylphosphonic acid(4).

The rate constant for the vapor-phase reaction of EPN with photochemically-produced hydroxyl radicals has been estimated as 7.5X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 5.1 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Half-lives for EPN in water are 70 days (pH 4); 22 days (pH 7); 3.5 days (alkaline)(2). EPN in p-dioxane exhibits slight absorption of UV light in the environmentally relevant range (>290 nm)(3), suggesting that EPN may be susceptible to direct photolysis by sunlight(SRC). Photodegradation half-lives for EPN in aqueous solution without humic acids, containing humic acids, containing humic acids from soil, and containing humic acid sodium salt were 38.5, 28.9, 34.6, and 49.5 days, respectively; EPN at 10-15 ppm plus humic acids at 5 ppm were irradiated in pyrex-glass vessels with artificial sunlight(4).

BCF values of 2,346(1), 700(2), 2,100 to 7,700(3), 358 to 1590(4), 1682(5), 495(6) to 1205(7), 929 to 1116(7), 641(7), 376(7) in topmouth gudgeon, pinfish, adult sheepshead minnow, carp, willow shiner, killifish, guppy, goldfish, and white cloud mountain fish, respectively, have been reported. According to a classification scheme(8), these BCF values suggest the potential for bioconcentration in aquatic organisms is high to very high(SRC). Although EPN can be bioconcentrated in aquatic organisms, it is also rapidly depurated(2). Pinfish exposed to 2.4 ug/l EPN, bioconcentrated the compound rapidly, reaching an apparent steady-state in approximately 2 days(2). After a 4-day post-exposure period only 1 out of 4 pinfish had detectable levels of EPN (0.04 g/g) in its tissues and after 8 days EPN was not detected in any fish(2). EPN was applied to sorghum leaves in a terrestrial-aquatic model ecosystem containing salt marsh catepillars, mosquito larvae, plankton, alga, snails and fish. After 33 days the values for bioaccumulation or ecological magnification in snail and fish were reported as 12,561 and 346, respectively(3).

Koc values, measured at concentrations of 0.01, 0.1 and 1.0 ppm EPN, were 1,997 and 706 for a clay loam and a high clay soil, respectively, with a mean of 1,327(1). According to a classification scheme(2), these Koc values suggest that EPN is expected to have low mobility in soil. In field tests with Dundee silt loam (pH 5.5, organic matter 1.3%) and Keyport silt loam (pH 6.4, organic matter 2.75%), greater than 90% of the residual radiolabeled carbon was found in the top 3 inches of soil, after 18 months, indicating no leaching of EPN or its degradation products had occurred(3).

The Henry's Law constant for EPN is 4.44X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 9.5X10-7 mm Hg(1), and water solubility, 3.11 mg/l(2). This Henry's Law constant indicates that EPN is expected to be essentially nonvolatile from water and moist soil surfaces(3). EPN is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

GROUNDWATER: EPN was not detected in groundwater samples collected in CA; the detection limit was 0.6 ppb(1).

DRINKING WATER: EPN was not detected in tap water from Ottawa, Canada; the detection limit was 1 ng/l(1).

SURFACE WATER: Water samples from tailwater pits in Haskell County, KS, used to collect irrigation runoff were analyzed for herbicide and insecticide residue(1). Concentrations of EPN in water from May-Dec 1974 were reported as zero for May-Jul, 1 ppb for Aug, and as trace (<0.5 ppb) for Nov-Dec(1). EPN was found in water samples collected from the Minaga River and the Minaga Reservoir, Japan during Jul-Oct 1997 and Sept-Nov 1998; concentrations were not given(2).

SEDIMENT: Soil sediment samples from tailwater pits in Haskell County, KS, used to collect irrigation runoff were analyzed for herbicide and insecticide residue(1). Concentrations of EPN measured from May-Dec 1974 were reported as 0 ppb for May-Jul and 27 and 2 ppb, for Aug and Nov-Dec, respectively(1).

URBAN/SUBURBAN: During ambient air monitoring at 10 U.S. locations (Columbia, SC, Lubbock, TX, Huntsville, AL, Pasadena, CA, Miss. State, MS, Harlington, TX, Houston, TX, Fresno, CA, Helena, MT, and Perkin, IL) during 1980, EPN was detected in 1 of 123 samples at a concn of 4.6 ng/cu m(1).

EPN was identified during the 1975 FDA Total Diet Study in large fruit, nuts, and infant and junior foods(1). The FDA's Total Diet Study in 1970-76 reported 1.4% of 148 peanut samples contained detectable residues of EPN; EPN concentrations ranged from 0.11-0.5 ppm(1). In a review of the chemicals reported in the FDA's Revised Market Basket Study from 1982 to 1991, representing 37 market baskets each containing 234 food items that represented about 5000 food types, EPN was reported 3 times in 2 foods at an average concentration of 0.005 ug/g(2). Only 1 of 13,980 and 0 of 13,085 samples of foods collected and analyzed in 10 state food laboratories in 1988 and 1989, respectively, contained detectable levels of EPN(3). The FDA's pesticide residue monitoring program in fiscal year 1988/1989 monitored 18,798 samples of domestically-produced food and imported food from 88 countries; EPN was identified although concentrations and percent positive detects were not reported(4). The FDA's pesticide residue monitoring program in fiscal year 1989/1990 monitored 19,962 samples of domestically-produced food and imported food from 92 countries; EPN was identified although concentrations and percent positive detects were not reported(5). 3 of 457 domestic samples of mixed feed rations collected by the FDA for pesticide surveillance during fiscal years 1989 to 1994 contained EPN; concentrations ranged from trace amounts to 0.030 ppm(6).

Many of the organophosphorus insecticides are excreted in the milk ... /Organophosphorus insecticides/

Occupational exposure to EPN may have occurred through inhalation and dermal contact with this compound at workplaces where EPN was produced or used(SRC). Workers involved in the manufacture or use of the pesticide EPN are exposed to this compound primarily by inhalation and dermal contact(SRC). Applicator personnel (pilots, loaders, ground applicators, and flagmen) monitored during aerial and ground application of EPN to cotton fields averaged 11, 15, 39, and 317 ug per 8-hr workday, respectively, due to respiratory exposure; dermal exposure averaged 2.1, 6.3, 7.5, and 117.7 mg per 8-hr workday for pilots, loaders, ground applicators, and flagmen, respectively(1). The levels of exposure were affected by route of exposure, body region, method of application, job function, attitude and experience, duration of exposure, weather conditions, and accidents(1). Some workers may ingest small amounts of this compound as a result of incidental contact resulting from such habits as smoking and eating with unwashed hands(1,2) or via contaminated foods(2). Monitoring data indicate that the general population may be exposed to EPN via ingestion of food, and dermal contact via products containing EPN(SRC).

Secondary exposure of children through contact with their parents' contaminated clothing can also occur. /Organophosphorus pesticides/

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Hydrolysis: Treat EPN with alkali... . Peer-review: Large amount, incinerate in a unit with effluent gas scrubbing. (Peer-review conclusions of an IRPTC expert consultation (May 1985))

/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Health: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Fire or Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Public Safety: CALL Emergency Response Telephone Number ... . As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Protective Clothing: 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. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

For more DOT Emergency Guidelines (Complete) data for EPN (16 total), please visit the HSDB record page.

UN 2783; Organophosphorus pesticide, solid,

UN 2784; Organophosphorus pesticide, liquid, flammable, toxic, flash point less than 23 °C

UN 3017; Organophosphorus pesticide, liquid, toxic, flammable, flash point between 23 °C and 61 °C

UN 3018; Organophosphorus pesticide, liquid, toxic

For more Shipping Name/ Number DOT/UN/NA/IMO (Complete) data for EPN (6 total), please visit the HSDB record page.

49 216 74; Organophosphorus pesticide, liquid, not otherwise specified (compounds and preparations) (insecticides, other than agricultural, NEC)

49 216 75; Organophosphorus pesticide, liquid, not otherwise specified (compounds and preparations) (agricultural insecticides, NEC, liquid)

49 105 44; Organophosphorus pesticide, liquid, not otherwise specified (compounds and preparations) (insecticides, other than agricultural, NEC)

49 105 45; Organophosphorus pesticide, liquid, not otherwise specified (compounds and preparations) (agricultural insecticides, NEC, liquid)

49 216 76; Organophosphorus pesticide, solid, not otherwise specified (compounds and preparations) (insecticides, other than agricultural, NEC)

49 216 77; Organophosphorus pesticide, solid, not otherwise specified (compounds and preparations) (agricultural insecticides, NEC, other than liquid)

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

Do not transport with food and feedstuffs. Severe marine pollutant.

Symbol: T+, N; R: 27/28-50/53; S: (1/2)-22-36/37-45-60-61

UN Hazard Class: 6.1; UN Pack Group: I