Dimethoate

H302: Harmful if swallowed [Warning Acute toxicity, oral]

H312: Harmful in contact with skin [Warning Acute toxicity, dermal]

P264, P270, P280, P301+P317, P302+P352, P317, P321, P330, P362+P364, and P501 (click each P-code to see the statement)

H302 (97.3%): Harmful if swallowed [Warning Acute toxicity, oral]

H312 (97.3%): Harmful in contact with skin [Warning Acute toxicity, dermal]

Aggregated GHS information provided per 297 reports by companies from 7 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.

H301: Toxic if swallowed [Danger Acute toxicity, oral]

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H332: Harmful if inhaled [Warning Acute toxicity, inhalation]

H351: Suspected of causing cancer [Warning Carcinogenicity]

H360: May damage fertility or the unborn child [Danger 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]

H401: Toxic to aquatic life [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]

P203, P260, P261, P264, P264+P265, P270, P271, P273, P280, P301+P316, P304+P340, P305+P351+P338, P308+P316, P317, P318, P319, P321, P330, P337+P317, P391, P405, and P501 (click each P-code to see the statement)

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

P273, P391, and P501 (click each P-code to see the statement)

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

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

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

P260, P262, P264, P264+P265, P270, P280, P301+P316, P302+P352, P305+P351+P338, P308+P316, P316, P319, P321, P330, P337+P317, P361+P364, P405, and P501 (click each P-code to see the statement)

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

H331: Toxic if inhaled [Danger Acute toxicity, inhalation]

P260, P261, P262, P264, P270, P271, P272, P280, P301+P316, P302+P352, P304+P340, P316, P319, P321, P330, P333+P317, P361+P364, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

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

Remove contaminated clothes. Rinse skin with plenty of water or shower. 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!). Rest. Refer for medical attention .

Note: Dimethoate is a cholinesterase inhibitor.

Signs and Symptoms of Acute Dimethoate Exposure: Acute exposure to dimethoate 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) and chest pain may be noted. Hypertension (high blood pressure) is not uncommon. Respiratory effects may include dyspnea (shortness of breath), respiratory depression, and respiratory paralysis. Psychosis may occur.

Emergency Life-Support Procedures: Acute exposure to dimethoate 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 dimethoate.

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 dimethoate.

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. 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.

4. 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.

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

This material is an organophosphate insecticide. Procedures for organophosphorus pesticides are as follows. Dike fire control water for later disposal, do not scatter the material. Wear positive pressure breathing apparatus and protective clothing. Fight fire from maximum distance.

Small fires: dry chemical, carbon dioxide, water spray, and foam.

Large fires: water spray, fog, or foam. (EPA, 1998)

Use water spray, powder, carbon dioxide.

Dry chemicals, carbon dioxide for small fires. Water spray or foam for larger fires.

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped or safely confined. 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, carbon dioxide or dry chemical. /Organophosphorus pesticides, liquid, NOS/

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.) Use "alcohol" foam, carbon dioxide or dry chemical. /Organophosphorus pesticides, solid, NOS/

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)

Do NOT wash away into sewer. 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 protection: chemical protection suit including self-contained breathing apparatus.

Use of granular, activated carbon in the adsorption of pesticides from wastewater is presented. Dimethoate was one of the compounds studied.

Environmental considerations- land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents. /Organophosphorus pesticides, liquid and solid, NOS/

Environmental considerations- water spill: Use natural barriers or oil spill control booms to limit spill travel. Remove trapped material with suction hoses. /Organophosphorus pesticides, liquid and solid, NOS/

Environmental considerations- air spill: Apply water spray or mist to knock down vapors. /Organophosphorus pesticides, liquid and solid, NOS/

Do not contaminate water, food or feed by storage and disposal. PESTICIDE DISPOSAL: ... If these wastes cannot be disposed of by use according to label instructions, contact your State Pesticide or Environmental Control Agency, or the Hazardous Waste representative at the nearest EPA Regional Office for guidance. CONTAINER DISPOSAL: Plastc: Triple rinse (or equivalent). Then offer for recycling or reconditioning, or puncture and dispose of in a sanitary landfill, or incineration, or if allowed by state and local authorities, by vurning. If burned, stay out of smoke. /Def-Fend E-267/

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P044, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Potential candidate for rotary kiln incineration with a temperature range of 820-1600 °C with residence times for liquids and gases, seconds; solids, hours. Also, a potential candidate for fluidized bed incineration with a temperature range of 450 to 980 °C with residence times for liquids and gases, seconds; solids longer. /From table/

This compound should be susceptible to removal from wastewater by air stripping.

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

Note to Physician: For all exposures administer atropine and 2-PAM as an antidote for acetylcholinesterase inhibition.

Avoid eye, skin, clothing contact. Do not breathe dust. Use with adequate ventilation. ... Wash thoroughly after handling.

If in eyes: Hold eye open and rinse slowly and gently with water for 15-20 minutes. Remove contact lenses, if present, after the first 5 minutes, then continue rinsing eye. Call a poison control center or doctor for further treatment advice. If on skin or clothing: Take off contaminated clothing. Rinse skin immediately with plenty of water for 15-20 minutes. Call a poison control center or doctor for further treatment advice. /De-Fend E-267/

Users should: wash hands before eating, drinking, chewing gum, using tobacco, or using the toilet; remove clothing immediately if pesticide gets inside, then wash thoroughly an put on clean clothing; and remove personal protective equipment immediately after handling this product; wash the outside of gloves before removing; as soon as possible, wash thoroughly and change into clean clothing. /De-Fend E-267/

For more Preventive Measures (Complete) data for DIMETHOATE (15 total), please visit the HSDB record page.

Dimethoate is an organophosphate insecticide. Precautions for organophosphorus pesticides include the following. Keep unnecessary people away; isolate hazard area and deny entry. Stay upwind; keep out of low areas. Ventilate closed spaces before entering them. Remove and isolate contaminated clothing at the site. Do not touch spilled material; stop leak if you can do so without risk. Use water spray to reduce vapors.

Small spills: absorb with sand or other noncombustible absorbent material and place into containers for later disposal.

Small dry spills: with clean shovel place material into clean, dry container and cover; move containers from spill area.

Large spills: dike far ahead of spill for later disposal. (EPA, 1998)

Provision to contain effluent from fire extinguishing. Separated from food and feedstuffs. Keep in a well-ventilated room.

The biological activity remains practically unvaried for 2 yr under environmental conditions, provided stored in unopened and undamaged original containers, in shaded, cool, well-aired places, inaccessible to animals & unauthorized persons. Recommended temp < 25 °C/77 °F. Crystals may form in formulations stored at < 32 °F/0 °C. Stable a minimum of 1 yr at < 25-30 °C/77-86 °F. Stack containers to permit air circulation at bottom & inside of piles. Do not contaminate food, feed products.

Liquid formulations must be stored above 45 °F.

...Must be stored in its sealed original containers, in well-aired, fresh & dry storehouses or in shaded & possibly well-aired places. It is recommended that the product's temp...not exceed 25-30 °C, & keep...away from sources of heat, free flames or spark-generating equipment. Containers must be stacked in such a way as to permit free circulation of air...at bottom & inside of piles. Storage areas must be located at suitable distance from inhabited buildings, animal shelters, & food stores; moreover, they must be inaccessible to unauthorized persons, children, & domestic animals. /Dimethoate/

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]

0.60 [mg/m3]

30 [mg/m3]

170 [mg/m3]

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly.

The substance may cause effects on the nervous system at high levels. Cholinesterase inhibition. Exposure could cause death. The effects may be delayed. Medical observation is indicated.

Repeated or prolonged contact with skin may cause dermatitis. Cholinesterase inhibition. Cumulative effects are possible. See Acute Hazards/Symptoms. Animal tests show that this substance possibly causes toxic effects upon human reproduction.

Tolerances are established for total residues of the insecticide dimethoate (O,O-dimethyl S-(N-methylcarbamoylmethyl) phosphorodithioate) including its oxygen analog (O,O-dimethyl S-(N- methylcarbamoylmethyl) phosphorothioate) in or on the following food commodities: [Table#3270]

Tolerances with regional registration, as defined in §180.1(n), are established for total residues of dimethoate including its oxygen analog in or on the following food commodities: [Table#3271]

For emergency situations, wear a positive pressure, pressure-demand, full facepiece self-contained breathing apparatus (SCBA) or pressure- demand supplied air respirator with escape SCBA and a fully-encapsulating, chemical resistant suit. (EPA, 1998)

Agricultural Use Requirements. Use this product only in accordance with its labeling and with the Worker Protection Standard (WPS), 40 CFR part 170. ... Do not enter or allow worker entry into treated areas during the restricted-entry interval (REI) of 48 hours. Personal protective equipment required for early entry to treated areas that is permitted under the WPS and that involves contact with anything that has been treated, such as plants, soil, or water, is: coveralls over short-sleeved shirt and short pants, chemical-resistant gloves such as nitrile rubber or butyl rubber or neoprene or viton or barrier laminate, chemical-resistant footwear plus socks, protective eyewear, and chemical-resistant headgear for overhead exposure. /De-Fend- E-267/

/Wear/ impervious gloves, boots, body-covering ...

/Wear/ ... closed collar gowns, rubber gloves and long boots.

All applicators, including homeowners & flaggers & personnel involved with mixing, loading, & transferring operations, must wear the protective clothing & equipment enumerated. Pilots are exempt from this equipment. The protective clothing & equipment to be worn is as follows: a. Impermeable gloves (for example, rubber or plastic covered gloves). b. Rubber or synthetic rubber boots or boot covers. c. Long-sleeved shirt & long pants, made of closely woven fabric. d. Wide-brimmed hat. e. Respirators must be worn by flaggers & mixer/loaders.

For more Personal Protective Equipment (PPE) (Complete) data for DIMETHOATE (6 total), please visit the HSDB record page.

NO open flames.

PREVENT DISPERSION OF DUST! AVOID EXPOSURE OF ADOLESCENTS AND CHILDREN!

Use ventilation (not if powder).

Protective gloves. Protective clothing.

Wear safety goggles or face shield.

Do not eat, drink, or smoke during work. Wash hands before eating.

Dimethoate appears as a white crystalline solid, with a camphor-like odor, white to grayish crystals for technical product. This material is a contact and systemic organophosphate insecticide effective against a broad range of insects and mites when applied on a wide range of crops. It has not been produced in the U.S. since 1982. (EPA, 1998)

Solid; [Merck Index] Colorless when pure; [ICSC] Technical product is white to grayish; [CAMEO] White solid with an odor of mercaptans; Formulated as emulsifiable concentrate and wettable powder end-use-products; [Reference #2]

PURE: COLOURLESS CRYSTALS WITH CHARACTERISTIC ODOUR.

A white crystalline solid, with a camphor-like odor, white to grayish crystals for technical product.

White crystalline solid

Colorless crystals (Tech., white solid pellets)

CAMPHOR-LIKE ODOR

Mercaptan odor

243 °F at 0.1 mmHg (NTP, 1992)

107 °C at 0.05 mm Hg

at 0.01kPa: 117 °C

243 °F at 0.1 mmHg

125 °F 113 to 117 °F for technical product. (EPA, 1998)

52-52.5 °C

51-52 °C

124 °F (EPA, 1998)

107 °C (closed cup)

107 °C c.c.

1 to 10 mg/mL at 75 °F (NTP, 1992)

Readily soluble in most organic solvents, e.g. alcohols, ketones, benzene, toluene, chloroform, dichloromethane >300 g/kg at 20 °C; carbon tetrachloride, saturated hydrocarbons, n-octanol >50 g/kg at 20 °C

More than 5000 mg/L water at 20 plus or minus 1.5 °C

In water, 2.5X10+4 m/L at 25 °C

SOL IN CYCLOHEXANONE; LOW SOLUBILITY IN XYLENE, HEXANE

Solubility in water, g/100ml at 21 °C: 2.5

1.277 at 149 °F (EPA, 1998) - Denser than water; will sink

1.277 at 65 °C

1.3 g/cm³

1.277 at 149 °F

1.277 @ 65°C

8.5e-06 mmHg at 77 °F (EPA, 1998)

0.00000825 [mmHg]

1.875X10-5 mm Hg at 25 °C

Vapor pressure, Pa at 25 °C: 0.001

8.5x10-6 mmHg

log Kow = 0.78

The biological activity remains practically unvaried for 2 yr under environmental conditions, provided stored in unopened and undamaged original containers, in shaded, cool, well-aired places. ... Crystals may form in formulations stored at < 32 °F/0 °C. Stable a minimum of 1 yr at < 25-30 °C/77-86 °F.

Stability increases at pH values between 4 to 7

... 50% loss occurs in 12 days at pH 9 ...

Dimethoate is thermally unstable and decomposes on heating after first being converted to the more toxic dithio-isomer. It is hydrolyzed more rapidly in alkaline medium: 50% hydrolysis @ 70 °C @ pH 9 in 0.8 hr and 21 hr @ pH 2.

...Stable in aqueous solutions at pH 2-7, but hydrolyzes in alkaline media.

It is stable in aqueous solution but is hydrolyzed by aqueous alkali.

Amides and Imides

Esters, Sulfate Esters, Phosphate Esters, Thiophosphate Esters, and Borate Esters

DIMETHOATE is incompatible with alkaline preparations. It is slightly corrosive to iron. It is incompatible with sulfur based formulations. (NTP, 1992). Organophosphates 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.

Dimethoate may decompose violently at temperatures >60 °C due to catalytic effects. However, it is not considered to be an explosive.

Dimethoate 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.

Dimethoate

2 x 10 ^-4 mg/kg-day

Pesticide

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: Group C Possible Human Carcinogen

TR-004: Bioassay of Dimethoate for Possible Carcinogenicity (CASRN 60-51-5) (1977 )

No Evidence

Tremors and hyperexcitability, both indications of dimethoate toxicity, were observed in the treated animals. However, it is considered that the low-dose group of rats and both dose groups of mice survived long enough to permit an evaluation of carcinogenicity. Pathologic evaluation revealed no statistically significant increase in tumors associated with dimethoate treatment in either species of animal, and it is concluded that there was no carcinogenic effect under the conditions of the experiment.

Spraying and application of nonarsenical insecticides entail exposures that are probably carcinogenic to humans (Group 2A). (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, through the skin and by ingestion.

Oral (L1188) ; inhalation (L1188) ; dermal (L1188)

Pupillary constriction, muscle cramp, excessive salivation. Sweating. Nausea. Dizziness. Laboured breathing. Weakness.

MAY BE ABSORBED! Further see Inhalation.

Redness. Pain.

Abdominal cramps. Convulsions. Diarrhoea. Unconsciousness. Vomiting. Further see Inhalation.

The first symptoms include bloody or runny nose, coughing, chest discomfort, difficult or short breath, and wheezing due to constriction or excess fluid in the bronchial tubes. Skin contact may cause localized sweating and involuntary muscle contractions. Eye contact will cause pain, bleeding, tears, pupil constriction, and blurred vision. Other symptoms following any way of exposure may include pallor, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred vision, constriction or dilation of the eye pupils, tears, salivation, sweating, and confusion. Severe poisoning will affect the central nervous system, producing incoordination, slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle contractions, twitching, tremors of the tongue or eyelids, and eventually paralysis of the body extremities and the respiratory muscles. In severe cases there may also be involuntary defecation or urination, psychosis, irregular heart beats, unconsciousness, convulsions and coma. Death may be caused by respiratory failure or cardiac arrest. (L1188)

Chemical: DIMETHOATE

Other Poison - Organophosphate

FAO/WHO ADI: 0.01 mg/kg

HEAST Current

Children

General Population

Human Health Benchmarks for Pesticides - 2021 Update

LC50 = 1,680 mg/m3

LD50: 60 to 387 mg/kg (Oral, Rat)

LD50: 60 mg/kg (Oral, Mouse)

LD50: 400 mg/kg (Oral, Dog)

LD50: 200 mg/kg (Oral, Hamster)

LD50: 300 mg/kg (Oral, Rabbit)

LD50: 350 mg/kg (Oral, Guinea pig)

LD50: 100 mg/kg (Oral, Cat)

LD50: 1000 mg/kg (Dermal, Rabbit)

LD50: 353 mg/kg (Dermal, Rat)

LC50: 1.2 mg/l (Rat)

On the basis of a number of cases, the oral lethal dose for human beings was estimated to be of the order of 50-500 mg/kg bw ... .

LD50 Rat female oral 240-336 mg/kg technical material /From table/

LD50 Mouse subcutaneous 60 mg/kg technical material /From table/

LD50 Hamster male sc 60 mg/kg technical material /From table/

LD50 Rabbit oral 300 mg/kg technical material /From table/

For more Non-Human Toxicity Values (Complete) data for DIMETHOATE (20 total), please visit the HSDB record page.

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

The effects of various classes of insecticides were studied on N-demethylation of dimethylnitrosamine (DMN) by mouse liver enzymes. Organochlorine insecticides increased the activities of dimethylnitrosamine demethylases I and II. Dimethoate, an organophosphorus cmpd, was the only insecticide tested to inhibit the N-demethylation of dimethylnitrosamine, with more pronounced effect on dimethylnitrosamine demethylase I.

Organophosphates are usually found in the environment with other pesticides and with pollutants of industrial origin can cause combined exposure involving unknown interactions between the agents. In this study, female Wistar rats were given 1/25 LD50 of dimethoate by gavage, combined with the same LD50 fractions of propoxur and cypermethrin or with arsenic (6.66 mg/kg). The doses were given from day 5 to 15 of pregnancy, or that plus for the 4 weeks of lactation, or that plus 8 weeks for the male offspring after weaning. Control rats received distilled water. Electrophysiological recording was done when the male offspring reached 12 weeks of age. Spontaneous activity and evoked potentials from the somatosensory, visual and auditory cortex; and conduction velocity and absolute and relative refractory periods of the tail nerve were measured. The general trend was a shift of the spontaneous cortical activity to higher frequencies and increase in the evoked potential latency. The results showed that combined exposure to several environmental toxicants could be more harmful than the effects of each substance alone ...

Carbon disulfide pretreatment potentiated the anticholinesterase action of parathion and EPN, but suppressed that of dimethoate and diazinon. Carbon disulfide had no significant effect or a slightly suppressive effect on the other compounds. Some of these effects were contrasted with the repeated alteration of the toxicity following phenobarbital pretreatment.

Antidote for acute dimethoate poisoning: 1. Adults: After cyanosis is overcome, use atropine sulfate, 2-4 mg iv. Repeat doses at 5- to 10-min intervals until signs of atropinization appear. Maintain for 24 hr or longer if necessary. 2. Children: Atropine sulfate in proportion to body weight: approx 0.05 mg/kg. 3. Support atropine treatment with 2-PAM (pralidoxime chloride) ... Adult dose: 1 g, slowly, intravenously; Infants: 0.25 g, slowly intravenously ... contraindicated are morphine, aminophylline, theophylline, phenothiazine tranquilizers, and barbiturates. /from table/

Data on the effects of oxime reactivators in dimethoate poisoning are contradictory, some indicating that they may have a negative effect on cholinesterase inhibition ... It is therefore suggested, that if oxime reactivators are indicated, these should be used with caution and under close supervision.

Hemoperfusion may be effective in the early stages of dimethoate poisoning ...

LC50 Lepomis macrochirus (Bluegill, weight 0.3 g) 6.0 mg/L/96 hr; temp 24 °C. Static bioassay without aeration, pH 7.2-7.5, water hardness 40-50 mg/L as calcium carbonate and alkalinity of 30-35 mg/L. /Technical, 97.4%/

LC50 Lepomis macrochirus (Bluegill) 28.0 mg/L/24 hr /Conditions of bioassay not given/

LD50 Agelaius phoeniceus (Red-winged blackbird) oral 5.4 mg/kg /from table/

LD50 Starlings oral 31.6 mg/kg

For more Ecotoxicity Values (Complete) data for DIMETHOATE (49 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ Dimethoate is particularly toxic in avian species; however, it is 20 fold more toxic in pheasants because the oxygen analog is formed and accumulates which leads to a slower degradation to non-toxic products.

/BIRDS and MAMMALS/ The embryotoxicity of dimethoate (aqueous emulsion) applied externally to mallard (Anas platyrhynchos) eggs was investigated. Abnormalities were observed in bill, brain, joint, and growth in survivors (day 18). Gastroschisis was also noted.

/BIRDS and MAMMALS/ The 30 day estimated minimum lethal dose for mallards of both sexes is 6.0 mg/kg/day. ... The 30 day estimated minimum lethal dose for 20 to 25 week old pheasants of both sexes appears to fit between 4.00 and 10.00 mg/kg/day. ... Acetylcholinesterase measurements were made on the brains of ... /the animals that died/ and survivors of the pheasant 30 day sMLD test. When compared with their estimated minimum lethal dose controls, survivors which were sacrificed on the day following final treatment showed 71.7% inhibition. When compared with their controls, mortalities showed 88.0% inhibition.

/BIRDS and MAMMALS/ Bobwhite quail (Colinus virginianus) reproduction rate /was tested for/ 196 days. At each of the two dose levels 15 male and 30 female birds were held in 15 separate cages. The animals were given commercial diet with Dimethoate incorporated for 13 weeks during the pre-egg-production period and during 15 weeks of egg production. Weight, shell thickness, embryonic mortalities, hatchability and body weight gain of chicks until 14 days after hatching was monitored. In the high dose group (30 mg/kg diet), compound related toxic effects were observed with regards to feed consumption, body weight gain (males), reduced egg production, shell thickness and body weight of chicks at hatching. As a result of the lower egg production and fertility rate of the eggs, the absolute number of offspring (hatched chicks) was roughly one-third lower in the high dose group as compared to the control and the low dose group. Post mortem examination of adults and F1 chicks revealed no compound related findings. No compound related toxic effects were observed in the low dose group (NOEL=6 mg/kg diet). /96.75% pure/

For more Ecotoxicity Excerpts (Complete) data for DIMETHOATE (26 total), please visit the HSDB record page.

1.40e+02

1.80e+03

4.40e+01

5.00e+00

9.90e-03

2.20e-03

Volatile

4.20e+02

5.40e+03

1.30e+02

The substance is toxic to aquatic organisms. This substance may be hazardous to the environment. Special attention should be given to bees and birds. Avoid release to the environment in circumstances different to normal use.

Dimethoate's production may result in its release to the environment through various waste streams; its use as a contact and systemic insecticide will result in its direct release to the environment. If released to air, a vapor pressure of 1.87X10-5 mm Hg at 25 °C indicates dimethoate will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase dimethoate 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 hours. Particulate-phase dimethoate will be removed from the atmosphere by wet or dry deposition. Due to a lack of absorbance of wavelengths of light above 290 nm, dimethoate is not expected to be susceptible to direct photolysis by sunlight. If released to soil, dimethoate is expected to have very high mobility based upon Koc values of 5.2-50. Volatilization of dimethoate from moist soil surfaces is not expected to be an important fate process given an estimated Henry's Law constant of 2.4X10-10 atm-cu m/mole. Microbially-mediated oxidative and hydrolytic degradation is the major degradation pathway in aerobic soil with a half-life of 2.2 days reported. Soil half-lives of 7 and 11 days were reported. However, a half-life of 122 days has also been measured in soil. If released into water, dimethoate is not expected to adsorb to suspended solids and sediment based upon the Koc values. Dimethoate may be subject to biodegradation in natural waters based on a half-life of 8 weeks for degradation in raw river water. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. BCFs of 1.1-2.4 and 2.7-6 suggest bioconcentration in aquatic organisms is low. Dimethoate hydrolyzes very slowly in sterile buffered solutions at pHs 5 and 7 with half-lives of 156 and 68 days respectively, but hydrolyzes rapidly to desmethyl dimethoate and dimethylthiophosphoric acid with a half-life of 4.4 days at pH 9. Occupational exposure to dimethoate may occur through inhalation and dermal contact with this compound at workplaces where dimethoate is produced or used. Monitoring and use data indicate that the general population may be exposed to dimethoate via inhalation of ambient air, ingestion of food and contaminated drinking water, and dermal contact with this compound and other products containing dimethoate. (SRC)

Dimethoate's production may result in its release to the environment through various waste streams; its use as a acaracide and insecticide(1) will result in its direct release to the environment(SRC).

FORMOTHION & DIMETHOATE SHOULD BE CONSIDERED TOGETHER SINCE THEIR SIGNIFICANT RESIDUES APPEAR TO BE IDENTICAL @ HARVEST; THAT IS, EFFECT OF APPLYING DIMETHOATE & FORMOTHION WILL BE ADDITIVE.

TERRESTRIAL FATE: Based on a classification scheme(1), experimental Koc values which range from 5.2 to 50(2-6), indicate that dimethoate is expected to have very high mobility in soil(SRC). Volatilization of dimethoate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.4X10-10 atm-cu m/mole(SRC) derived from its vapor pressure, 1.87X10-6 mm Hg(15), and water solubility, 23,300 mg/L(15). Dimethoate soil half-life values of 2.2 days(16), 7 days(7-9), 11 days(10) and as much as 122 days(11) have been reported. After 6 days, average dimethoate losses due to evaporation from uncovered soil columns were 40.4, 32.3, 23.0, and 24.9% in sand, sandy clay loam, loam, and clay loam, respectively; dimethoate losses were directly proportional to water losses(12); this study indicates that dimethoate may be removed from terrestrial surfaces via evaporation(SRC). Dimethoate will be susceptible to hydrolysis in moist alkaline soils based on a reported base catalyzed rate constant of 756 1/m-hr at pH 9 which corresponds to a half-life of 3.7 days in water(13). Biodegradation may be an important fate process in soil(SRC) with 77% degradation reported in clay loam soil in 2 wks compared to 18 and 20% degradation in the same soil that had been autoclaved or irradiated(14).

AQUATIC FATE: Based on a classification scheme(1), experimental Koc values which range range from 5.2 to 50(2-6), indicate that dimethoate is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(7) based upon an estimated Henry's Law constant of 2.4X10-11 atm-cu m/mole(SRC) derived from its vapor pressure, 1.87X10-6 mm Hg(8), and water solubility, 23,300 mg/L(8). According to a classification scheme(9), BCFs of 1.1-2.4 and 2.7-6(10), suggests bioconcentration in aquatic organisms is low(SRC). Dimethoate hydrolyzes very slowly in sterile buffered solutions at pHs 5 and 7 with half-lives of 156 and 68 days respectively, but hydrolyzes rapidly to desmethyl dimethoate and dimethylthiophosphoric acid with a half-life of 4.4 days at pH 9(11). Photolysis and volatilization from water do not appear to be important removal process of dimethoate from water(SRC). Half-lives of 171, 173 and 219 days were given for river water, filtered river water and sea water, respectively, at 6 °C, and 43, 29 and 36 days, respectively, at 22 °C(12), suggesting that biodegradation may be a slow environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dimethoate, which has a vapor pressure of 1.87X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase dimethoate 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 hrs(SRC), calculated from its rate constant of 7.9X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase dimethoate may be removed from air via dry deposition(SRC), and one monitoring study(4) indicates that dimethoate is removed from the atmosphere via wet deposition. Products of oxidation and hydrolysis accounted for 1.5 and 11%, respectively, of the dimethoate deposited on an untreated glass surface left in a greenhouse for 7 days(5). Therefore, some oxidation and hydrolysis may account for the removal of dimethoate from air(SRC). Based on a lack of absorbance of wavelengths of light above 290 nm(6), dimethoate is not expected to be susceptible to direct photolysis by sunlight(SRC).

When applied to plants, dimethoate was ... decomposed ... on surface ... by hydrolysis & oxidation. On the plant surface, dimethoate underwent non-enzymatic oxidation to the oxygen analog & hydrolysis to water sol deriv identified as dimethyl phosphoric & O,O-dimethyl phosphorothioic acids, desmethyl dimethoate ...

AEROBIC: The concn of dimethoate left (initial concn 10 ppb) after various times in raw water from Little Miami river at pH 7.3-8.0 was 10 ppb after 1 hr, 10 ppb after 1 wk, 8.5 ppb after 2 wks, 7.5 ppb after 4wks, and 5.0 ppb after 8 wks(1). Biodegradation may play a minor role in the disappearance of dimethoate in the river water; no experiments were conducted with sterilized river water(1). Half-lives of 171, 173 and 219 days were given for river water, filtered river water and sea water, respectively at 6 °C, and 43, 29 and 36 days at 22 °C(2). Percent degradation in chehalis clay loam soil in 2 wk, non-sterile, 77%, autoclaved, 18%, irradiated, 20%(3). Half-lives in soil in June-July averaged 11 days, and less than 2% of applied dimethoate residue detected after 10 months(3). Dimethoate half-lives in soil from Zhejiang Province, China were given as 5.1 and 7.1 days in 1989 and 1990, respectively(4). Dimethoate was given a half-life of 7 days(5-7) and 11 days(8) in an unspecified field soil sample. In laboratory experiments at 20-30 °C half-lives for degradation were 28.9 and 36.7 days(3). However, dimethoate degraded faster when incubated for 30 days in samples of autoclaved sand, sandy clay loam, loam, and clay soils than in similarly treated nonsterile soils(9). Biodegradation appears to depend on the soil type and the microorganisms present in the soil(9). A half-life of 122 days has been observed in soil(10) which also suggests that biodegradation of dimethoate can be slow. In moist soils, dimethoate is readily oxidized to dimethoxon(11), but the role of microbial degradation on the removal of dimethoate from the environment is uncertain(12). Recovery of dimethoate incubated with enrichment cultures using raw sewage: 0 days, 54 ppm; 0.5 days, 54 ppm; 1 day, 52.5 ppm; 6 days, 22.4 ppm; 9 days, 13.5 ppm; 12 days, not detected(13). Using an initial concn of 100 mg/L dimethoate, 0-17 %Theoretical BOD was observed after a 4 week period in a biodegradation screening test using 30 mg/L sludge(14). Dimethoate has been reported to have an aerobic half-life of 2.2 days(15).

ANAEROBIC: Dimethoate has been reported to have an anaerobic half-life of 22 days with the major degradate being desmethyl dimethoate(1). A half-life of 44 days has also been reported(2).

The rate constant for the vapor-phase reaction of dimethoate with photochemically-produced hydroxyl radicals has been estimated as 7.9X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Hydrolysis half-lives at 70 °F were measured to be 22 hr in River Thames water at pH 8.0, 18 hr in River Irving water at pH 7.5, and 12 hr in ethanol/pH 6.0 buffer solution; it was roughly estimated that hydrolysis rates would be several hundred times slower at environmentally important temperatures(2). Dimethoate has a hydrolysis half-life of 62 days(4). Reported hydrolysis half-lives at 70 °F were 0.8 hr at pH 9 and 21 hr at pH 2(3). A hydrolysis a half-life of 120 days at pH 7 has also been reported(5). Based on respective neutral (pH 7) and base catalyzed (pH 9) hydrolysis rate constants at 25 °C of 1.7X10-4/hr and 756 1/m-hr, respective hydrolysis half-lives of 118 and 3.7 days can be estimated for dimethoate in water(6). Hydrolysis half-lives for dimethoate at 25 °C are reported as 230, 220 and 4.4 days at pHs of 5, 7 and 9, respectively(7). Dimethoate hydrolyzes very slowly in sterile buffered solutions at pHs 5 and 7 with half-lives of 156 and 68 days respectively, but hydrolyzes rapidly to desmethyl dimethoate and dimethylthiophosphoric acid with a half-life of 4.4 days at pH 9(10). Based on a lack of absorbance of wavelengths of light above 290 nm(8), dimethoate will not be expected to undergo direct photolysis under sunlit conditions. Products of oxidation and hydrolysis accounted for 1.5 and 11%, respectively, of the dimethoate deposited on an untreated glass surface left in a greenhouse for 7 days(9).

After a 6 week period in a flow through system at 25 °C, BCF ranges of 1.1-2.4 and 2.7-6 were determined in carp (Cyprinus carpio) using initial concns of 1 and 0.1 mg/L dimethoate, respectively(1). According to a classification scheme(3), these BCFs suggest the potential for bioconcentration in aquatic organisms is low(SRC). Bioconcentration of dimethoate in Mytillus galloprovincialis after 92 hours exposure at concentrations of 3.2, 5.6, 10, 32 and 56 ug/L was 1.0, 1.1, 1.4, 2.0 and 3.1 ug/g, respectively(3). Bioconcentration of dimethoate in Venus gallina after 92 hours exposure at concentrations of 5.6, 10 and 32 ug/L was 2.2, 2.3 and 3.1 ug/g, respectively(3).

The Koc values for dimethoate were measured to be 18 and 36 in a clay loam soil and clay soil, respectively(1). In other studies, the Koc was measured to be 5.2(2), 50(3) and 17(4) in unspecified soils. The Pesticide Properties Database lists the experimental Koc value for dimethoate as 20(5). According to a suggested classification scheme(6), these Koc values suggest that dimethoate will have very high mobility in soil. Average dimethoate losses due to leaching of various soil columns with the equivalent of 2.5 cm of rain ranged from 39.6% (clay) to 78.6% (sand)(7). In four soils containing less than 1% organic content, the soil TLC Rf values ranged from 0.89 to 0.97(8). The soil TLC Rf values in two other soils (0.35-1.05% OC) was 0.40-0.50 and was not affected by pH or salt concentration changes(9). Of 7 values sited in literature the mean Kd is 0.45(10). Kds were given for soil A (2.4 % clay, 0.8% silt, 96.4% sand, 2.1% organic material, pH 5.3) and soil B (13.4 % clay, 10.8% silt, 75% sand, 1.5% organic material, pH 6.4) as 0.08 and 0.05, respectively(11).

No dimethoate migration was observed below 3 inches in field sandy loam soil treated at a rate of 1 lb/acre dimethoate up to three times and analyzed for dimethoate up to 14 days after application(1). It has been reported that the downward movement of dimethoate in the field depends somewhat on the soil type; it increases with increasing soil moisture content(2). It was estimated that dimethoate could move approximately 2.5 cm in 1 month in soil containing 42.9% moisture; movement thereafter will probably decrease over time(3).

Soil sorption constants based on the organic carbon content of 15 pesticides were measured using 2 soils (clay loam and high clay) at 0.01, 0.1 and 1.0 ppm pesticide. The soil sorption coefficients ((ug pesticide/g soil)/(ug pesticide/g water)) for dimethoate were 0.8 + or - 0.3 in clay loam and 0.5 + or - 0.1 in high clay soil. The soil sorption constants were 18 and 36 respectively, with a mean of 27. Significant correlations were found between organic carbon content and water solubility, octanol/water partition coefficient, retention time in reversed phase high pressure liquid chromatography and molecular wt.

The Henry's Law constant for dimethoate is estimated as 2.4X10-10 atm-cu m/mole(SRC) derived from its vapor pressure, 1.87X10-6 mm Hg(1), and water solubility, 23,300 mg/L(1). This Henry's Law constant indicates that diemthoate is expected to be essentially nonvolatile from water surfaces(2). After 6 days, average dimethoate losses due to evaporation from uncovered soil columns were 40.4, 32.3, 23.0, and 24.9% in sand, sandy clay loam, loam, and clay loam, respectively; dimethoate losses were directly proportional to water losses(3). Dimethoate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1). The vaporization index for dimethoate was estimated to be 0.2-3 kg/ha/yr, or more(4).

GROUNDWATER: According to the U.S. EPA's Pesticides in Groundwater Database, dimethoate was detected at a concn range of 0.38-10 ug/L in 12 of 2,844 wells from 9 different states monitored between 1984-1991(1). Dimethoate was qualitatively identified in 24 groundwater samples from wells in California between May 1979-April 1984(2). Dimethoate was not detected in 150 ground water samples from Imathia, Northern Greece from May 1996-April 1997(3). Dimethoate was not detected (detection limit 0.02 ug/L) in 94 well water samples from 12 Midwest states in the summer of 1992(4). Dimethoate was not found in 80 samples taken from 25 rivers and lakes in Greece collected from Mar - Dec 1996(5). Dimethoate has been identified in ground water samples from GDR (former, German Democratic Republic), France and the Netherlands at concentrations of 0.4, 0.07 and 0.06 ug/L, respectively, number of total samples and locations not reported(6). Dimethoate was not detected in 35, 32, 53, or 184 Danish ground water samples taken from Lille Baek, Hojvads Rende, Odder Baek or Bolbro Baek catchment basins, respectively, from 1993-1996(7). Dimethoate was found in 17% of 281 samples taken Oct 1995-Mar 1997 from the Northern Patagonic region in Argentina with a mean concn of 0.268 ug/L and maximum concn of 10.9 ug/L(8). Dimethoate was found in 1 of 128 ground water samples taken from 6/1987-6/1992 at a concn of 70 ng/L from France(9). A surface and ground water survey taken from 1981-91 from Lyonnaise des Eaux-Dumez, France reported 4 of 705 samples at conc above 100 ng/L(9). 1 Of 102 wells contained dimethoate taken from farm wells of Kings county, Nova Scotia, Canada from the 3 month summer of 1989(10).

DRINKING WATER: Dimethoate was not detected in water from 54 wells in California, in an area where it was used for at least 15 years(1). Dimethoate was not detected in 82 samples from 80 stations in New York State, 1964-66, including wells, groundwater, and surface water(2).

SURFACE WATER: Dimethoate was detected at a concn range of 9.7-368.4 ng/L in river water from 4 rivers in Southern Italy(1). In 1985, dimethoate was detected in surface waters in the UK at a maximum concn of 0.94 ug/L(2). Dimethoate was not detected in 120 surface water samples from Imathia, Northern Greece from May 1996-April 1997(3). Dimethoate was detected in 19 of 20 samples with a concn range of 11-2980 ng/L in samples taken from the River Elbe at Zollenspieker, Germany in 1992-1993(4). Dimethoate was detected in 17 of 20 samples with a concn range of 15-3210 ng/L in samples taken from the River Elbe at Seemannshoft, Germany in 1992-1993(4). Dimethoate has been identified in the Rhine river surface water following an accident in Wiesbaden, Germany resulting in concns of 0.22 ug/L(5). Dimethoate was found at 3 of 4 sites sampled from Apr-Aug 1996 from the Shinana River in Japan at concn of 26-200 ng/L(6). River water sample concns were reported as 9.84-22.86 ng/L from the Wuchuan river in China(7). Dimethoate concns in main rivers in Thailand were 0.03-0.24, 0.06, and 0.06 ug/L in 1985, 1987, and 1988 respectively(8). Of 83 samples taken from Feb-Dec 1993 in Spain, 1 sample had dimethoate at 0.01 ug/L, and of 14 samples taken May-June 1995 from Catalonia river basin two samples had dimethoate at a concn range of 0.01-0.16 ug/L(9). Dimethoate concns of <1.0, 101, <1.0, 51 and <1.0 ng/L were detected in Salt Slough, Orestimba Creek, Dry Creek, San Joaquin river at Patterson and Mokwlumme river at Woodbridge, respectively in CA in 1992(10). Dimethoate was detected at a maximum concn of 46 ng/L from the Sacramento-San Joaquin delta water(11). 1 of 25 samples taken from Apr 1993- Apr 1994 from the South Platte river basin, CO were positive for dimethoate(12). Dimethoate was found in 17.8% of the river water samples taken from Syr-Darya river basin, Ukraine from 1988-1990(13). A surface and ground water survey taken from 1981-91 from Lyonnaise des Eaux-Dumez, France reported 4 of 705 samples at concns above 100 ng/L(14). Dimethoate concns in Venezuelan Andean Highlands in Mar 1990 were 4.5, 1.2, 10.8, 15.5, 14.3, 13.1, 2.9, 5.4 and <0.3 ug/L at La Playa, La Cascada, Bailadores, Potresito, Aguas calientes, Las Tapias, Zarzales, Rio Arriba and Veriguaca, respectively(15). Dimethoate concns in Venezuelan Andean Highlands in Aug 1990 were 3.4, 14.3, 16.5, 3.8, 11.4, 10.4, 3.7, 12.4 and <0.3 ug/L at La Playa, La Cascada, Bailadores, Potresito, Aguas calientes, Las Tapias, Zarzales, Rio Arriba and Veriguaca, respectively(15). Dimethoate was detected at 0.270, 0.340, 0.170, 0.311 and 0.282 ug/L from the Rosetta esturarie in Egypt in the summer of 1995, autumn of 1995, summer of 1996, autumn of 1996 and summer of 1997, respectively(16). Dimethoate was not detected in the Rosetta estuary in the winter of 1995-6, spring of 1996, the winter of 1996-7, or the spring of 1997(16). Dimethoate was detected in drain water at 0.6 ug/L 41 days after application of 1.56 kg/5.2 ha and 15 mm of rain at ADAS Rosemaund, Herefordshire, UK(17). Dimethoate was detected in stream water at 3.0 ug/L 27 days after application of 4.80 kg/16.0 ha and 10.5 mm of rain at ADAS Rosemaund, Herefordshire, UK(17).

RAIN/SNOW: Dimethoate was detected at an average concn of 0.19 ug/L and a maximum concn of 0.23 ug/L in precipitation samples from Iowa during November 1987- September 1990(1). Dimethoate was not detected in rain water samples from 7 sites in Northern Greece(2). Dimethoate was not detected in 520 precipitation samples taken from Jun-Sep 1992 and May-Sep 1993 in Norway(3). Dimethoate was not detected (0.1 ng/L) from May-Jul 1997 in South Holland, Netherlands(4).

Do not contaminate water, food or feed by storage and disposal. PESTICIDE DISPOSAL: ... If these wastes cannot be disposed of by use according to label instructions, contact your State Pesticide or Environmental Control Agency, or the Hazardous Waste representative at the nearest EPA Regional Office for guidance. CONTAINER DISPOSAL: Plastc: Triple rinse (or equivalent). Then offer for recycling or reconditioning, or puncture and dispose of in a sanitary landfill, or incineration, or if allowed by state and local authorities, by vurning. If burned, stay out of smoke. /Def-Fend E-267/

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P044, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Potential candidate for rotary kiln incineration with a temperature range of 820-1600 °C with residence times for liquids and gases, seconds; solids, hours. Also, a potential candidate for fluidized bed incineration with a temperature range of 450 to 980 °C with residence times for liquids and gases, seconds; solids longer. /From table/

This compound should be susceptible to removal from wastewater by air stripping.

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

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: Xn; R: 21/22; S: (2)-36/37

UN Hazard Class: 6.1; UN Pack Group: III