Methyl Parathion

H226: Flammable liquid and vapor [Warning Flammable liquids]

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

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

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

H373 **: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

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]

P210, P233, P240, P241, P242, P243, P260, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P303+P361+P353, P304+P340, P316, P319, P320, P321, P330, P361+P364, P370+P378, P391, P403+P233, P403+P235, P405, and P501 (click each P-code to see the statement)

H226 (93.3%): Flammable liquid and vapor [Warning Flammable liquids]

H300+H330 (32.2%): Fatal if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]

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

H311 (93.3%): Toxic in contact with skin [Danger Acute toxicity, dermal]

H330 (100%): Fatal if inhaled [Danger Acute toxicity, inhalation]

H373 (93.3%): May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

H400 (93.3%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (93.3%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

Aggregated GHS information provided per 90 reports by companies from 6 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.

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

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

H341: Suspected of causing genetic defects [Warning Germ cell mutagenicity]

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, 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)

H316: Causes mild skin irritation [Warning Skin corrosion/irritation]

P203, P260, P262, P264, P264+P265, P270, P271, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P308+P316, P316, P318, P319, P320, P321, P330, P332+P317, P337+P317, P361+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Induce vomiting (ONLY IN CONSCIOUS PERSONS!). Give a slurry of activated charcoal in water to drink. Refer immediately for medical attention.

Note: Parathion-methyl is a cholinesterase inhibitor.

Signs and Symptoms of Acute Parathion-Methyl Exposure: Acute exposure to parathion-methyl 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. Hypotension (low blood pressure) may occur although hypertension (high blood pressure) is not uncommon. Chest pain may be noted. Respiratory symptoms include dyspnea (shortness of breath), respiratory depression, and respiratory paralysis. Psychosis may occur.

Emergency Life-Support Procedures: Acute exposure to parathion-methyl 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 parathion-methyl.

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 parathion-methyl.

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 parathion-methyl 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 parathion-methyl 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.

Fight fire from maximum distance. Dike fire control water for later disposal; do not scatter the material. Wear special protective clothing.

For small fires, use dry chemical, carbon dioxide, water spray, or foam. For large fires, use water spray, fog, or foam. (EPA, 1998)

Use water spray, foam, powder, carbon dioxide.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

Fire Extinguishing Media: Dry chemical, carbon dioxide for small fires. Water spray or foam for large fires.

Excerpt from ERG Guide 131 [Flammable Liquids - Toxic]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area for at least 50 meters (150 feet) in all directions.

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: chemical protection suit including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P071, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

The reduction of methyl parathion with acid and zinc was explored to determine whether this would accelerate degradation of methyl parathion to its less toxic p-aminophenyl deriv and/or produce less toxic breakdown products. Methyl parathion disappearance was followed for 2.5 yr. The acidified powdered zinc treatment at burial proved effective in degrading methyl parathion.

The following wastewater treatment technologies have been investigated for methyl parathion: Reverse osmosis.

A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 °C and residence times of seconds for liquids and gases, and longer for solids. A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 °C and residence times of seconds for liquids and gases, and hours for solids.

For more Disposal Methods (Complete) data for METHYL PARATHION (7 total), please visit the HSDB record page.

Based on a study, contaminated denim fabrics should not be laundered in 30 °C (85 °F) temperature; Hotter temperatures are more effective to decontaminate work clothing. Although detergents could not be statistically separated, heavy duty liquid detergents appeared to excel in providing higher levels of pesticide removal in water temperatures of 49 °C and 60 °C.

Storage, preparation, dispensing (including vending machines), or eating of foods or beverages shall be prohibited in areas where methyl parathion is present. ... Smoking shall be prohibited in areas where methyl parathion is present.

All required personal protective clothing and protective equipment shall be provided by the employer and shall be laundered or cleaned daily. ... Personal protective clothing grossly contaminated with methyl parathion shall be decontaminated and laundered separately from other clothing. ... Employees occupationally exposed to methyl parathion shall be required to wash their hands and face with alkaline soap and water before eating, drinking, smoking, and using toilet facilities.

It is recommended that clothing (such as denim) contaminated with high concn of methyl parathion be disposed of by burning or burial, as the fabric remains unsafe to the wearer. Fabrics contaminated with lesser methyl parathion concn require a minimum of 3 launderings before biological activity reaches a harmless level. Procedures such as pre-washing and/or multiple washing, appear to be more effective.

For more Preventive Measures (Complete) data for METHYL PARATHION (10 total), please visit the HSDB record page.

Excerpt from ERG Guide 131 [Flammable Liquids - Toxic]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor-suppressing foam may be used to reduce vapors.

SMALL SPILL: Absorb with earth, sand or other non-combustible material and transfer to containers for later disposal. Use clean, non-sparking tools to collect absorbed material.

LARGE SPILL: Dike far ahead of liquid spill for later disposal. Water spray may reduce vapor, but may not prevent ignition in closed spaces. (ERG, 2024)

Store in an area without drain or sewer access. Keep in a well-ventilated room. Separated from food and feedstuffs.

Keep container tightly closed in a dry and well-ventilated place.

Store in original container, preferably in a locked area, away from children, feed, food. Do not heat above 55 °C. Decomposes rapidly above 100 °C, explosion may be induced.

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]

AEGL 1: Notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure (Unit: mg/m3)

AEGL 2: Irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape (Unit: mg/m3)

AEGL 3: Life-threatening health effects or death (Unit: mg/m3)

2.1 mg/m3

6.4 mg/m3

1.5 mg/m3

4.4 mg/m3

1.2 mg/m3

3.5 mg/m3

0.73 mg/m3

2.2 mg/m3

0.37 mg/m3

1.1 mg/m3

NOTE THAT VALUES ARE IN mg/m3 , NOT ppm

AEGLs Status: Interim

0.11 [mg/m3]

1.2 [mg/m3]

3.5 [mg/m3]

0.2 mg/m³

TWA 0.2 mg/m3 [skin]

none See Appendix G

See: IDLH INDEX

0.02 [mg/m3], inhalable fraction and vapor

8 hr Time Weighted Avg (TWA): 0.02 mg/cu m, inhalable fraction and vapor, 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/

0.02 mg/m

0.02 mg/m³ (inhalable fraction and vapor) [2008]

Intermediate Oral: 0.0007 mg/kg/day (L134)

Chronic Oral: 0.0003 mg/kg/day (L134)

MAC for USSR, 0.1 mg/cu m.

A harmful concentration of airborne particles can be reached quickly on spraying or when dispersed, especially if powdered.

The substance may cause effects on the nervous system. This may result in convulsions and respiratory depression. Cholinesterase inhibition. Exposure far above the OEL could cause death. Medical observation is indicated.

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

Tolerances are established for residues of the insecticide methyl parathion, including its metabolites and degradates, in or on the commodities in the table in this paragraph. Compliance with the tolerance levels specified in this paragraph is to be determined by measuring only methyl parathion, O,O-dimethyl O-(4-nitrophenyl) phosphorothioate, in or on the commodity.[Table#2919]

While petitions for tolerances for negligible residues are pending and until action is completed on these petitions, interim tolerances are established for residues of the listed pesticide chemicals in or on the following raw agricultural commodities:[Table#2920]

Excerpt from NIOSH Pocket Guide for Methyl parathion:

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.

Methyl parathion is a white crystalline solid which is often dissolved in a liquid solvent carrier. The commercial product is a tan liquid (xylene solution) with a pungent odor. It is slightly soluble to insoluble in water. Usually with the liquid solvent it is a combustible liquid. It is toxic by inhalation, ingestion and skin absorption. It is used as an insecticide.

White to tan, crystalline solid or powder with a pungent, garlic-like odor. [pesticide]; [NIOSH]

COLOURLESS-TO-WHITE SOLID IN VARIOUS FORMS.

White to tan, crystalline solid or powder with a pungent, garlic-like odor.

White to tan, crystalline solid or powder with a pungent, garlic-like odor. [pesticide] [Note: The commercial product in xylene is a tan liquid.]

Crystals

White crystalline solid

Crystals from cold methanol

White to tan, crystalline solid or powder [Note: The commercial product in xylene is a tan liquid]

Colorless crystals

Pungent, garlic-like odor

Odorless

246 °F at 0.13 mmHg (NTP, 1992)

154 °C at 136 Pa

99 to 100 °F (EPA, 1998)

MP: 37-38 °C

35-38 °C

commercial product, containing xylene, has flashpoint of 115F (EPA, 1998)

42 °C (Closed cup)

less than 1 mg/mL at 73 °F (NTP, 1992)

In water, 37.7 mg/L at 20 °C

Soluble in organic solvents

Readily soluble in common organic solvents, e.g. dichloromethane, toluene >200, hexane 10 to 20 (all in g/L at 20 °C). Sparingly soluble in petroleum ether and some types of mineral oil.

Readily soluble in 2-propanol. Hardly soluble in n-hexane

Solubility in water, g/100ml: 0.006

(77 °F): 0.006%

1.358 at 68 °F (EPA, 1998) - Denser than water; will sink

1.358 g/cu cm at 20 °C

1.4 g/cm³

1.358 @ 20°C

9.1 (NTP, 1992) - Heavier than air; will sink (Relative to Air)

9.7e-06 mmHg at 68 °F (EPA, 1998)

0.0000035 [mmHg]

3.5X10-6 mm Hg at 25 °C

Vapor pressure, Pa at 20 °C: 0.001

0.00001 mmHg

log Kow = 2.86

Henry's Law constant = 1.0X10-7 atm-cu m/mol at 25 °C

Hydrolyzes slowly in weak acid, rapidly in alkali

Not very stable in storage

Insoluble in water.

Nitro, Nitroso, Nitrate, and Nitrite Compounds, Organic

Sulfonates, Phosphonates, and Thiophosphonates, Organic

METHYL PARATHION is half decomposed in 8 days at 40 °C. When a sample was heated in a small test tube it decomposed in a few minutes and the residue exploded (Food Chem. 4(1):42. 1956).

Strong oxidizers, water [Note: Explosive risk when heated above 122 degrees F].

Strong oxidizers, water [Note: Explosive risk when heated above 122 °F.]

CDC-ATSDR Toxicological Profile

IDENTIFICATION: Methyl parathion is an organophosphorus insecticide that is relatively insoluble in water, poorly soluble in petroleum ether and mineral oils, and readily soluble in most organic solvents. Pure methyl parathion consists of white crystals; technical methyl parathion is a light tan color with a garlic-like odor. It is thermally unstable. HUMAN EXPOSURE: The production, formulation, handling, and use of methyl parathion as an insecticide are the principal potential sources of exposure of humans. Skin contact and, to a lesser degree, inhalation are the main routes of exposure to workers. The general population may be exposed to air-, water-, and food-borne residues of methyl parathion as a consequence of agricultural or forestry practices, the misuse of the agent resulting in the contamination of fields, crops, water, and air through off-target spraying. Methyl parathion is a highly toxic organophosphorus ester insecticide. Overexposure from handling during manufacture, use, and/or accidental or intentional ingestion may cause severe or fatal poisoning. Methyl parathion formulations may, or may not, be irritating to the eyes or to the skin, but are readily absorbed. Several cases of acute methyl parathion poisoning have been reported. Signs and symptoms are those characteristic of systemic poisoning by cholinesterase-inhibiting organophosphorous compounds. They include peripheral and central cholinergic nervous system manifestations appearing as rapidly as a few minutes after exposure. In case of dermal exposure, symptoms may increase in severity for more than one day and may last several days. Studies of methyl parathion suggest a decrease in blood cholinesterase activities without clinical manifestations. No cases of organophosphorous-induced, delayed peripheral neuropathy have been reported. An increase in chromosomal aberrations has been reported in cases of acute intoxications. No human data were available to evaluate the teratogenic and reproductive effects of methyl parathion. The available epidemiological studies deal with multiple exposure to pesticides and it is not possible to evaluate the effects of long-term exposure to methyl parathion. ANIMAL STUDIES: Methyl parathion poisoning causes the usual organophosphate cholinergic signs attributed to accumulation of acetylcholine at nerve endings. Methyl parathion becomes toxic when it is metabolized to methyl paraoxon. In short term toxicity studies, using various routes of administration on the rat, dog, and rabbit, inhibition of plasma, red blood cell, and brain ChE, and related cholinergic signs were observed. There is no evidence of carcinogenicity in mice and rats, following long-term exposure. In reproduction studies, at toxic dose levels (ChE inhibition), there were no consistent effects on litter size, number of litters, pup survival rates, and lactation performance. No primary teratogenic or embryotoxic effects were noted. Methyl parathion is readily absorbed via all routes of exposure (oral, dermal, inhalation) and is rapidly distributed to the tissues. The liver is the primary organ of metabolism and detoxification. The elimination of methyl parathion and metabolic products occurs primarily via the urine.

Methyl parathion is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Methyl parathion

Hematologic

2.5 x 10 ^-4 mg/kg-day

Parathion-methyl

Pesticide

Listed as Methyl parathion

Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP

Cancer Classification: Not Likely to be Carcinogenic to Humans

Classification of carcinogenicity: 1) evidence in humans: no adequate data; 2) evidence in animals: evidence suggesting lack of carcinogenicity. Overall summary evaluation of carcinogenic risk to humans is Group 3: The agent is not classifiable as to its carcinogenicity to humans. /From table/

A4; Not classifiable as a human carcinogen.

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 30: (1983) Miscellaneous Pesticides

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

TR-157: Bioassay of Methyl Parathion for Possible Carcinogenicity (CASRN 298-00-0) (1979 )

12/15/78

No Evidence

It is concluded that under the conditions of this bioassay, methyl parathion was not carcinogenic for F344 rats or B6C3F1 mice of either sex.

3, not classifiable as to its carcinogenicity to humans. (L135)

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

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

Oral (L634) ; inhalation (L634) ; dermal (L634).

Sweating. Nausea. Vomiting. Dizziness. Pupillary constriction, muscle cramp, excessive salivation. Muscle twitching. Laboured breathing. Diarrhoea. Convulsions. Unconsciousness. Symptoms may be delayed.

MAY BE ABSORBED! See Inhalation.

Blurred vision.

See Inhalation.

irritation eyes, skin; nausea, vomiting, abdominal cramps, diarrhea, salivation; headache, dizziness, lassitude (weakness, exhaustion); rhinorrhea (discharge of thin nasal mucus), chest tightness; blurred vision, miosis; cardiac irreg; muscle fasciculation; dyspnea (breathing difficulty)

Exposure to very high levels of methyl parathion may cause death, loss of consciousness, dizziness, confusion, headaches, difficult breathing, chest tightness, wheezing, vomiting, diarrhea, cramps, tremors, blurred vision, and sweating. (L634)

Developmental (effects while organs are developing), Hematological (Blood Forming), Neurological (Nervous System)

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

Chemical: METHYL PARATHION

Other Poison - Organophosphate

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

ACGIH Carcinogen - Not Classifiable.

FAO/WHO ADI: 0.02 mg/kg bw

IRIS Current

ATSDR Final

EC50; Species: Simocephalus serrulatus (daphnid) 1st instar; Conditions: static bioassay, 15 °C; Concentration: 0.37 ug/L for 48 hr (95% confidence limit 0.23-0.57 ug/L); Effect: immobilization. /Technical material, 80-99%/

EC50; Species: Daphnia magna (daphnid) 1st instar; Conditions: static bioassay, 21 °C; Concentration: 0.14 ug/L for 48 hr (95% confidence limit 0.09-0.20 ug/L); Effect: immobilization. /Technical material, 80-99%/

LC50; Species: Gammarus fasciatus (scud) mature; Conditions: static bioassay, 15 °C; Concentration: 3.8 ug/L for 96 hr (95% confidence limit 2.6-5.5 ug/L) /Technical material, 80-99%/

LC50; Species: Orconectes nais (crayfish) mature; Conditions: static bioassay, 15 °C, hard water; Concentration: 15 ug/L for 96 hr /Technical material, 80-99%/

For more Ecotoxicity Values (Complete) data for METHYL PARATHION (90 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ A number of studies in avian species have indicated that effects of ... methyl parathion are minimal. /Reportedly/ ... egg production in Japanese quail was inhibited and hatchability was reduced by methyl parathion at 60 ppm ...

/BIRDS and MAMMALS/ Insecticides methyl parathion 18 WP and Wofatox 50 EC, formulated as wettable powder (wp) and emulsifiable concentrate (ec), respectively, were tested for teratogenicity in Japanese quail and pheasant embryos. Each pesticide was diluted in water to 3 different concn levels and injected into the air cell in a vol of 0.05 mL/quail egg and 0.1 mL/pheasant egg. The concn were 0.05, 0.5 and 5.0% for methyl parathion 18 WP and 0.02, 0.2 and 2.0% for Wofatox 50 EC. Quail eggs were treated on day 9, and pheasant eggs on day 12, of incubation. The test methods failed to demonstrate skeletal lesions in quail and pheasant embryos with evident lordoscoliosis. High doses of Wofatox 50 EC, however, produced atrophic and, occasionally, hypoplastic changes in the cervical muscle of the embryos.

/BIRDS and MAMMALS/ Red winged blackbirds and dickcissels inhabiting wheat fields treated with 0.67 kg/ha methyl parathion and 1.35 kg/ha toxaphene showed brain cholinesterase inhibition compared with birds inhabiting untreated fields. Maximum inhibition occurred approx 5 days after insecticide application. Brain cholinesterase activities again approached normal levels 10 days after treatment. Brain cholinesterase inhibition for dickcissels and red winged blackbirds differed significantly; Maximum inhibition for the former species was 74%, and for the latter, 40%.

/BIRDS and MAMMALS/ Plasma cholinesterase (ChE) activity was monitored in hen mallards in a study of the effects of organophosphorus insecticides. At the onset of incubation (defined as cessation of egg-laying for 48 hr) birds were divided into four treatment groups: treated with 400 ppm methyl parathion in feed, pair-fed (same daily food allotment on a g/kg/d basis as consumed by the treated bird of the pair); control (unlimited food availability, no chemical in feed); or nonincubating control (birds that laid eggs but did not incubate). Both plasma and brain ChE samples were taken on day 24 of incubation. Plasma ChE levels were more variable than brain ChE among the birds. Mean of the log 10 IU/L plasma ChE levels in the egg-laying period were 2.847 - 3.266 and 2.789 - 3.172 IU/L in control and pair-fed groups, respectively; in the incubation period, 2.830 - 3.069 and 2.895 - 3.136 in control and pair-fed groups, respectively. There were no significant correlations between plasma and brain samples within treatment groups. Reduced food consumption during the incubation period did not affect plasma ChE activity (p = 0.77). Birds that abandoned their nests had significantly increased (paired t = -2.39, df = 9, ChE activity at the time of abandonment. There were significant differences (p <0.01) in plasma ChE activity between untreated birds, but within-bird variation was 2 and 11 times less than between-bird variation during egg-laying and incubation, respectively. Methyl parathion significantly reduced plasma cholinesterase activity.

For more Ecotoxicity Excerpts (Complete) data for METHYL PARATHION (45 total), please visit the HSDB record page.

1.60e+01

2.10e+02

4.50e+00

4.00e+01

7.40e-03

2.50e-04

Volatile

4.70e+01

6.20e+02

1.30e+01

The substance is very toxic to aquatic organisms. This substance may be hazardous to the environment. Special attention should be given to birds and bees. 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.

Methyl parathion's production and use as an insecticide will result in its direct release to the environment. In the USA, end-use products will not be sold after August 31, 2013 and cannot legally be used after December 31, 2013. If released to air, a vapor pressure of 3.5X10-6 mm Hg at 25 °C indicates methyl parathion will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase methyl parathion 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 0.3 days. Particulate-phase methyl parathion will be removed from the atmosphere by wet and dry deposition. Methyl parathion absorbs at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, methyl parathion is expected to have low to moderate mobility based upon Koc values ranging from 366 to 1,516. Volatilization from moist soil surfaces is not expected to be an important fate process based upon methyl parathion's measured Henry's Law constant of 8.4X10-8 atm-cu m/mole. Methyl parathion is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Utilizing loam soils maintained at 10 and 33 kPa soil-water tension, 14C-methyl parathion was approximately 50% mineralized in 28 days, indicating that biodegradation is an important environmental fate process in soil. Hydrolysis is expected to be an important process in moist soils since methyl parathion hydrolyzes in natural waters. If released into water, some adsorption of methyl parathion to suspended solids and sediment in the water column is expected based upon the Koc values. Utilizing a river die-away test using water and sediment cores, methyl parathion exhibited half-lives of 77 to 154 hrs, indicating that biodegradation is an important environmental fate process in water. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. BCFs of 8.3 and 959 suggest bioconcentration in aquatic organisms is low to high, provided the compound is not metabolized by the organism. An elimination half-life of 7.0 hours was calculated for methyl parathion in guppies. Hydrolysis is expected to be an important environmental fate process since this compound exhibits half-lives from 6.5 to 13 days at 40 °C in natural waters; pH values were less than 8. Occupational exposure to methyl parathion may occur through inhalation of spray mists and dermal contact with this insecticide during or after its application or at workplaces where it is formulated. The general population may be exposed to methyl parathion via ingestion of contaminated food and drinking water, inhalation of ambient air, or dermal contact with this insecticide. However, occupational exposure and general population exposure in the US should be low or non-existent since methyl parathion is no longer legally used(Dec, 2013). (SRC)

Methyl parathion's production and use as an insecticide(1,2) is expected to result in its direct release to the environment(SRC). The US EPA has canceled the sale and distribution of methyl parathion as of December 31, 2012. In the USA, end-use products will not be sold after August 31, 2013 and cannot legally be used after December 31, 2013(1).

Production, transport and application of the insecticide. 1.0 lb/1000 lb of production as air emissions. 7.4 lb/1000 lb of production are potentially emitted from lagoons by evaporation. Approximately 40 million lb/year released due to use as broad spectrum insecticide.

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values ranging from 366 to 1,516(2,3) indicate that methyl parathion is expected to have moderate to low mobility in soil(SRC). Volatilization of methyl parathion from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 1.0X10-7 atm-cu m/mole(4). Methyl parathion is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.5X10-6 mm Hg at 25 °C(5). Hydrolysis is expected to be an important process in moist soils(SRC), since methyl parathion hydrolyzes in natural water with half-lives ranging from 6.5 to 13 days at 40 °C and pH values less than 8(6). Utilizing loam soils maintained at 10 and 33 kPa soil-water tension, 14C-methyl parathion was approximately 50% mineralized in 28 days(7), indicating that biodegradation is an important environmental fate process in soil(SRC).

TERRESTRIAL FATE: Simulated spillage of emulsifiable concentrate and microencapsulated formulations of methyl parathion on soil were studied. Persistence of residues from both formulations spilled as concentration and as simulated drum rinses were followed for up to 45 mo. Spillage of encapsulated formulation resulted in the formation of a solid cake-like deposit on the soil surface. At 45 mo, soil residues had decreased by 64% for emulsifiable concentrate spills, and 68% for the soil beneath the cake. Residue in the cake itself only decr by 31%. Soil residue levels from simulated drum rinses were essentially innocuous by 45 mo for the emulsifiable concentrate and by 1 yr for the microencapsulated material.

TERRESTRIAL FATE: 73 acres of alfalfa in Vernal, Utah, were sprayed with an emulsifiable concentrate (EC) containing 6 lb/gal ethyl parathion and 3 lb/gal methyl parathion. The material was applied at 4.15X10-2 gal/acre. Wind conditions were negligible. Samples were taken from the sprayed plot (sites A and B) and from an adjoining non-target pasture (site C). Immediately after treatment, methyl parathion residues averaged 40% of ethyl parathion levels at the 3 sampling stations. Foliar residues of the parent cmpd dissipated rapidly with time. At Site A, the residues dropped below 1.25 mg/kg within 28 hr for methyl parathion. First-order half-life of methyl parathion was 12 hr.

AQUATIC FATE: Based on a classification scheme(1), Koc values ranging from 366 to 1,516(2,3) indicate that methyl parathion is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon a Henry's Law constant of 1.0X10-7 atm-cu m/mole(5). According to a classification scheme(6), a BCF range of 8.3 to 959(7,8) suggests bioconcentration in aquatic organisms is low to moderate(SRC). However, methyl parathion is rapidly metabolized in some aquatic organisms(9). Aqueous photolysis half-lives range from 8 to 38 days(10). Hydrolysis is expected to be an important environmental fate process since this compound exhibits half-lives from 6.5 to 13 days at 40 °C in natural waters; pH values were less than 8(11). The half-life of methyl parathion in untreated estuarine sediment water studies was 1.2 days (95% confidence limit 0.60-2.0 days). The half-life of methyl parathion in untreated estuarine sediment water studies was 1.2 days (95% confidence limit 0.60-2.0 days)(12). Utilizing a river die-away test using water and sediment cores, methyl parathion had half-lives of 77 to 154 hrs, while in a sterile control the half-life was 367 hrs(13), indicating that biodegradation is an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), methyl parathion, which has a vapor pressure of 3.5X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase methyl parathion 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 0.3 days(SRC), calculated from its rate constant of 5.9X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase methyl parathion may be removed from the air by wet and dry deposition(SRC). Methyl parathion absorbs light at wavelengths between 290 and 410 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Methyl parathion is degraded in soil, water and sediment(1,2). Products include aminomethylparathion, p-nitrophenol and O-methyl-O'-p-nitrophenylthiophosphoric acid(1). Biodegradation may be fairly rapid especially when microorganisms are acclimated to methyl parathion(2). Comparison of degradation rates in sterile versus nonsterile estuarine systems indicated that biodegradation was the primary route of methyl parathion degradation(3). In a die-away test using water and sediment cores from three sites (Escambia River, FL), methyl parathion had half-lives of 77 to 154 hrs, while in a sterile control the half-life was 367 hrs(4). In strongly reducing anaerobic sediments, the degradation rate was found to be about two orders of magnitude faster than in the same sediments which had been heat-sterilized(5). Biodegradation is significantly faster in sediment containing water than in water alone(4,5). 14C-Methyl parathion was degraded rapidly to carbon dioxide in Cecil sandy loam and Webster silty clay loam maintained at 10 and 33 kPa soil-water tension; >40% mineralization was observed in 14 days, leveling off to approximately 50% by day 28(6). After 32 days incubation in static sediment/water microcosms, 24% of the (14)C-methyl parathion had been mineralized to (14)CO2; degradation products included aminomethyl parathion, 4-aminophenol, and 4-nitrophenol(7).

At a concentration of 200 ug/L, methyl parathion degraded rapidly in a non-sterile sediment slurry; half-life of 2.3 days(1). Half-lives in nonsterile water, sterile water, and sterile sediment were >30 days, indicating an abiotic process, probably hydrolysis(1). Ring-labeled methyl parathion added to shake flasks containing Pensacola Bay area sediment/water slurries exhibited half-lives ranging from 0.9 to 30 days(2). Rates in nonsterile water, sterile sediment and sterile water were similar, suggesting abiotic loss processes, possibly hydrolysis(2). Degradation was more rapid under flooded conditions than under non-flooded conditions in soils(3,4). In five flooded (non-flooded) Indian soils, methyl parathion half-lives were 4.17 (2.33), 5.50 (8.56), 5.44 (274.56), 3.58 (11.32), and 17.68 (22.43) days in Alluvial, Sukinda, Kari, Pokkali, and Canning soils, respectively(6). Hydrolysis was implicated under non-flooded and to a minor extent in flooded conditions(3,4); degradation under flooded conditions proceeded essentially by nitro group reduction(3,4). In aquatic environments, aufwuchs bacteria were capable of transforming methyl parathion(5).

Three outdoor ponds were treated with methyl parathion applied beneath the water surface at a concentration of 100 ug/L. The rate of loss of methyl parathion from pond water isolated in an aquarium was similar to the predicted rate. However, the rate of loss from outdoor ponds, or from aquaria containing plants and sediment, was greater than predicted. Methyl parathion was not detected in sediment even though predicted concentration far exceeded the limit of detection. It is suggested that the rate of biodegradation in shallow bodies of water may be determined predominantly by bacteria attached to sediments and plants, rather than by planktonic bacteria.

The rate constant for the vapor-phase reaction of methyl parathion with photochemically-produced hydroxyl radicals has been estimated as 5.9X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 0.3 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). A hydrolysis half-life of 72 days was determined at pH 7 and 25 °C(2). Half-lives of 12 days, 11 days, and 4.9 days were measured at pH values of 3.0, 7.0, and 9.0, respectively, at 40 °C(1). Hydrolysis half-lives in natural waters ranged from 6.5 to 13 days at 40 °C and pH values less than 8(3). Identified products are p-nitrophenol and O-methyl-O'-p-nitrophenylthiophosphoric acid(3). Aqueous photolysis half-lives of 712 hours and 812 hours have been reported(4). Photolysis in water containing algae was up to 390 times faster than in distilled water(4). Methyl parathion absorbs light at wavelengths between 290 and 410 nm(5) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

In fly ash suspensions, hydrolysis was extensive ranging from 61.7 to 62.5% of the initial amount after 12 hours; this was attributed to the high pH (11.89) of the suspension(1). Hydrolysis of methyl parathion in sandy clay loam soil suspensions and clay soil suspensions ranged between 2.5 to 2.8% and 2.5 to 2.7%, respectively, of the initial amount after 12 hours(1). Addition of fly ash to the soil suspensions resulted in increased hydrolysis(1). In an alluvial soil, soil flooding hastened the degradation of (14)C-methyl parathion; mineralization to (14)CO2 was negligible, hydrolysis was attributed as the major degradation pathway(2). Methyl parathion residues declined to approx 50% within 168 hours post-application in water 7 to 9 m deep(3). Hydrolysis rate constants of 0.0680/day, 0.0584/day, 0.0592/day, and 0.0540/day were observed in buffered Milli-Q water, water from Orestimba Creek, water from Del Puerto Creek, and Eucalyptus Ave Drain water (a small agricultural drain), respectively, at pH 8.0 and 40 °C(4); all samples collected in the San Joaquin Valley, CA. These rate constants correspond to hydrolysis half-lives of 10, 12, 12, and 13 days at 40 °C(SRC). Hydrolysis half-lives of 96 days and 146 days were observed in pH 8.0 phosphate-buffered Milli-Q water at 32 and 24 °C, respectively(SRC); these half-lives were calculated from rate constants of 0.00723/day and 0.00475/day, respectively(4). Half-lives of 237 and 46 days were observed when methyl parathion was incubated in pH 6.1 ultrapure water in darkness at 6 °C and 22 °C, respectively(5). Half-lives of 95 (173) and 23 (18) days were observed when methyl parathion was incubated in pH 7.3 river water (filtered river water) in darkness at 6 °C and 22 °C, respectively; the half-life decreased to 11 days when methyl parathion was incubated in pH 7.3 river water in sunlight(5). Half-lives of 233 and 30 days were observed when methyl parathion was incubated in pH 8.1 seawater in darkness at 6 and 22 °C, respectively; a half-life of 34 days was observed when methyl parathion was incubated in seawater in sunlight(5). Degradation of methyl parathion in natural water (pH 9.0) and tap water (pH 7.5) was rapid with half-lives of 11.1 and 13.4 hours, respectively; chemical degradation was thought to play a primary role with biological degradation having a secondary role(6).

Analysis of oxidation and hydrolysis data on methyl parathion at various pH values(1).[Table#2918]

Twenty gram samples of three Indian soils, a laterite (Sukinda) soil (pH 6.9, organic matter 0.62%, total nitrogen 0.04%), an acid sulfate (Pokkali) soil (pH 5.4, organic matter 5.51%, total nitrogen 0.21%) and a laterite (Pattambi) soil (pH 6.0, organic matter 1.04%, total nitrogen 0.063%) were air dried and flooded with sterile distilled water. After 10 days, an aqueous soln of methyl parathion (MP) was added for a final concn of 50 ug active ingredient/g soil. Periodically after 25 and 35 °C incubation, residues of methyl parathion were separated and analyzed. In other expts, Sukinda soil was flooded for 30 days before addition of methyl parathion, or soil samples were amended with rice straw powder to accelerate reduction of the soil prior to the addition of methyl parathion 10 days later. Methyl parathion disappeared more rapidly at 35 °C than at 25 °C in all soils under flooded conditions. In Pokkali and Pattambi soils at 35 °C, methyl parathion reached undetectable levels (< 100 ug/20 g soil) in 12 days. In Sukinda soil, hydrolysis was the only pathway of methyl parathion degradation at both temp and after both 10 and 30 days preflooding before methyl parathion treatment. In the other 2 soils, degradation proceeded by both nitro group reduction and hydrolysis at both temp; both nitro group reduction was more pronounced than hydrolysis. No hydrolysis occurred in soil preflooded for 10 days and then sterilized by autoclaving. In nonsterilized Sukinda soil, methyl parathion declined from 715 + or - 12 ug/20 g soil to 137 + or - 12 ug/20 g soil and p-nitrophenol was recovered only in traces. Addition of rice straw distinctly increased the degradation rate of methyl parathion at both temp. Addition of rice straw to flooded Sukinda soil triggered nitro group reduction; the redox potential of rice straw amended Sukinda soil 10 days after flooding dropped to -187 mV at 25 °C and -205 mV at 35 °C (vs -100 mV after 10 days flooding, and -145 mV after 30 days preflooding).

The potential of zero valent iron (ZVI) for remediation of contaminated groundwater from an abandoned chemical disposal site was examined through batch and column experiments. The key contaminants were organophosphate pesticides but the chemical analysis also comprised additional 22 compounds including synthesis intermediates and degradation products of organophosphates. The ZVI treatment showed that all the contaminants were degraded with the exception of two diesters (phosphorothioates). The most rapid reduction was found for methyl parathion, ethyl parathion and malathion, which had first-order degradation rate constants on the order of 10X-3/min. In the study, acute toxicity towards freshwater crustaceans (Daphnia magna) was included to evaluate the overall efficiency of ZVI treatment of the complex mixture. The acute toxicity tests with D. magna showed that the untreated groundwater was highly toxic. Thus, 50% of the daphnids were unable to swim upon 24 h exposure to groundwater diluted 770 times. ZVI facilitated degradation resulted in a complete toxicity removal for the first four pore volumes, where after a three times dilution caused 50% inhibition of the mobility of the daphnids. The rapid degradation of the highly toxic organophosphates combined with the significant decrease in the ecotoxicological potential shows a promising potential for site remediation of organophosphates with ZVI technologies.

A BCF of 8.3 was determined for (14)C-methyl parathion in Oreochromis niloticus (Nile talapia) fingerlings(1). A BCF (calculated on an extractable lipid weight basis) of 959 was determined for methyl parathion in guppies (Poecilia reticulata)(2). According to a classification scheme(3), these BCF values suggest bioconcentration in aquatic organisms is low to high. However, methyl parathion does not bioconcentrate but rather is rapidly metabolized(4). An elimination rate constant of 2.38/day was measured(2), corresponding to a half-life of 7.0 hours(SRC). Methyl parathion was hydrolyzed by several shrimp and crayfish species(5).

Koc values of 366 to 423 were reported for methyl parathion(1). Average Koc values of 1,374 and 1,516 were measured for methyl parathion on 19 soil and sediment materials after 2 and 24 hours equilibration, respectively, using a batch equilibration technique; organic matter was the most important factor affecting adsorption of methyl parathion(2). According to a classification scheme(3), these Koc values suggest that methyl parathion is expected to have moderate to low mobility in soil.

Moderate adsorption of the parent compound and metabolites to soil and sediment was observed(1-6). Adsorption does not appear to be correlated with % organic content in soil(2). Clay content of soil is important(4). Adsorbs interlaminarly to clay(3,4). Typical soil-water distribution constants range from 3 to 147(1-6), with median values around 50(SRC). Kom (organic matter-normalized partition coefficient) values of 102.0, 95.9, 88.2, and 82.0 were observed in sandy clay loam soil, sandy clay loam soil with 0.1% fly ash, sandy clay loam soil with 0.2% fly ash, and sandy clay loam soil with 0.5% fly ash, respectively(7). Kom values of 636.2, 619.5, 587.8, and 554.2 were observed in clay soil, clay soil with 0.1% fly ash, clay soil with 0.2% fly ash, and clay soil with 0.5% fly ash, respectively(7). A Kd value of 6.2 was determined for homoionic K-montmorillonite(8). An average log Koc of 3.85 was reported in various sediments(9). Sorption of methyl parathion on laboratory-modified humic acids ranged from 4.2 to 7.8 g/kg; sorption on an untreated humic acid was 6.5 g/kg(10). The addition of humic acid to topsoil had no systematic effect on increasing methyl parathion's sorption(10). Kom values of 423.07, 541.55, 366.60, 121.29 were determined in four rice soils(11). Methyl parathion was assigned a pesticide leaching potential of 9; a pesticide leaching potential of 0 indicates no leaching potential, while a pesticide leaching potential of 100 indicates maximum leaching potential(12).

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P071, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

The reduction of methyl parathion with acid and zinc was explored to determine whether this would accelerate degradation of methyl parathion to its less toxic p-aminophenyl deriv and/or produce less toxic breakdown products. Methyl parathion disappearance was followed for 2.5 yr. The acidified powdered zinc treatment at burial proved effective in degrading methyl parathion.

The following wastewater treatment technologies have been investigated for methyl parathion: Reverse osmosis.

A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 °C and residence times of seconds for liquids and gases, and longer for solids. A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 °C and residence times of seconds for liquids and gases, and hours for solids.

For more Disposal Methods (Complete) data for METHYL PARATHION (7 total), please visit the HSDB record page.

/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 METHYL PARATHION (16 total), please visit the HSDB record page.

2783 152(solid)

3018 152(liquid)

UN 2783; Organophosphorus pesticides, solid, toxic

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

UN 3017; Organophosphorus pesticides, liquid, toxic, flammable, flash point not less than 23 °C

UN 3018; Organophosphorus pesticides, liquid, toxic

49 214 42; Methyl parathion, liquid Poison B, combustible, environmentally hazardous substance

49 214 43; Methyl parathion mixture, dry Poison B, environmentally hazardous substance

49 214 44; Methyl parathion mixture, liquid (containing 25% or less methyl parathion) Poison B, environmentally hazardous substance

49 214 47; Methyl parathion mixture, liquid (containing over 25% methyl parathion) Poison B, environmentally hazardous substance

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.

Poison Flammable Liquid

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

Symbol: T+, N; R: 5-10-24-26/28-48/22-50/53; S: (1/2)-28-36/37-45-60-61

UN Hazard Class: 6.1; UN Pack Group: II