Oxydemeton-methyl

246.28

246.28

206-110-7

370785

2784

DTXSID8025541

Colorless liquid|Yellow oil

2930909061

106.92000

-0.74

Oxydemeton methyl is a clear amber liquid. (NTP, 1992)

1.289 g/cm³ @ Temp: 20 °C

<-20 °C

106 °C @ Press: 0.01 Torr

182.2±28.4 °C

1.519

Miscible

0-6°C

3.8×10 -3 Pa (20°C)

Oral-rat LD50: 30 mg/kg; Oral-Mouse LD50: 10 mg/kg

Thermal decomposition of toxic phosphorus oxide and sulfur oxide gas

141.78 Ų [M+H]+

...Rapidly hydrolyzed in alkaline media.

Water soluble. This material may be rapidly hydrolyzed by alkali (NTP, 1992).

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

Organophosphates such as OXYDEMETON METHYL 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.

II

6.1(a)

3018

24/25-50

23-36/37-45-61

TG1420000

T,N

The warehouse is ventilated, low temperature and dry; stored and transported separately from food materials

This compound is stable under normal laboratory conditions.

P273-P280-P301 + P310-P312

H301 + H311-H400

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

USEPA/Office of Pesticide Programs; Interim Reregistration Eligibility Decision (IRED) for Oxydemeton-methyl. EPA issues an IRED for a pesticide that is undergoing reregistration, requires a reregistration eligibility decision, and also needs a cumulative assessment under FQPA. The IRED, issued after EPA completes the individual pesticide\'s aggregate risk assessment, may include taking risk reduction measures -- for example, reducing risks to workers or eliminating uses that the registrant no longer wishes to maintain -- to gain the benefits of these changes before the final RED can be issued following the Agency\'s consideration of cumulative risks.[Available from, as of July 24, 2003: http://www.epa.gov/pesticides/reregistration/status.htm]

This chemical is flammable. (NTP, 1992)

|Danger|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P264, P270, P273, P280, P301+P310, P302+P352, P312, P321, P322, P330, P361, P363, P391, P405, and P501|H300: Fatal if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P262, P264, P270, P271, P280, P281, P284, P301+P310, P302+P350, P304+P340, P307+P311, P308+P313, P310, P314, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501

Excerpt from ERG Guide 131 [Flammable Liquids - Toxic]: As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: If you spill this chemical, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should store this material in a refrigerator. (NTP, 1992)

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves. RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use "alcohol" foam, dry chemical or carbon dioxide. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic/|If material on fire or involved in fire: Use water in flooding quantities as fog. Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) /Organophosphorus pesticides, solid, toxic/

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

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. /Organophosphorus pesticides, solid, toxic/|If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Attempt to stop leak if without undue personnel hazard. Use water spray to knock-down vapors. /Organophosphorus pesticides, liquid, toxic/|If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Use water spray to knock-down vapors. /Organophosphorus pesticides, liquid, flammable, toxic/|Personnel protection: Avoid breathing dusts, and fumes from burning material. Keep upwind. Avoid bodily contact with the material. Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. /Organophosphorus pesticides, solid, toxic/|For more Preventive Measures (Complete) data for OXYDEMETON-METHYL (8 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 OXYDEMETON-METHYL (16 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.

Oxydemeton-methyl and its oxidation product, dioxydemeton-methyl were not detected in air at 5 ambient monitoring sites and during 2 application monitoring sites collected in the Salinas Valley, Monterey County, CA, during Aug-Oct 1992(1). The detection limit for oxydemeton-methyl and its oxidation product were 2.0 and 1.5 ug/cu-m, respectively(1).

most toxic

The effects of vitamin E (alpha-tocopherol) on the rate of lipid peroxidation and lipase activity ln the discrete areas of the brain and spinal cord were studied. Administration of metasystox in two different doses 1.0 and 2.0 mg/kg body weight ip daily for 10 days have shown a dose-related depletion of total lipids cholesterol and esterified fatty acids in the rat cerebral hemisphere, cerebellum brain stem and spinal cord. The rate of lipid peroxidation and lipase activity showed dose-dependent increase in different regions of the CNS. Administration of alpha-tocopherol alone caused significant reduction of lipid peroxidation and lipase activity. When it was admistered simultaneously with metasystox, alpha-tocopherol prevented the metasystox induced increase of lipid peroxidation and lipase activity.

LD50 Rat dermal 1350 mg/kg|LD50 Rat oral 50 mg/kg|LC50 Rat inhalation 1500 mg/cu m/ 1Hr|LD50 Rat ip 20 mg/kg|For more Non-Human Toxicity Values (Complete) data for OXYDEMETON-METHYL (13 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ Symptoms of acute oral toxicity /in various birds/: ataxia, salivation, lacrimation, nutation, dyspnea, masseter tenseness, severe miosis, tenesmus, prostration or immobility in prone position, tremors, tetany, terminal wing-beat convulsions or opisthotonos. Symptoms appeared as soon as 8 min and mortalities usually occurred between 10 min and 2 hr after treatment. Remission took up to 14 days.|/BIRDS and MAMMALS/ In the bobwhite quail /reproduction/ study, statistically significant differences were noted at the 6.9 /ppm/ treatment level for the 14 day old survivor weights. The number of eggs laid per hen and the number of eggs set per hen was statistically different from the control at both the 6.9 ppm and the 17.3 ppm treatment groups. Both the number of viable embryos and live 3 wk embryos per hen was significantly different at the 17.3 ppm treatment level. In the mallard duck study, statistically significant differences were noted at the 17.3 ppm treatment level for reduced food consumption. There were no treatment related effects upon reproduction in this study.|/OTHER TERRESTRIAL SPECIES/ A bee toxicity study, to determine the toxicity of residual ODM on foliage to honey bees, provided the following information: ODM was found to have short-lived toxicity to honey bees and alkali bees exposed to foliar residues. At 0.5 lbs ai/A, 3-hr old residues were low in toxicity to both species (2-20% mortality, evaluated at 24 hours). ...When honey bee larvae were exposed to oxydemeton-methyl, the 3-4 day old larvae were the most susceptible age group (LD50 = 2.15 g/larva), while 5-6 day old larvae were the least susceptible (LD50 = 24.39 g/larva). These figures compare to an adult LD50 of 3 ug/bee.|/FIELD STUDIES/ A simulated field study with English sparrows, bobwhite quail, and New Zealand rabbits was performed in 1973 (MRID 00060638) and was found to provide supplemental information. The animals were exposed to both treated and untreated alfalfa at an application rate of 2.25 lb ai/A, applied 3 times with a 2 wk application interval. The caged animals were placed on alfalfa plots for 6 weeks; they were moved to fresh alfalfa plots weekly which had received previous applications. There was no treatment-related mortality of quail during the 42 day study. Weight losses for both treated and control birds were equivalent. The treated rabbits had no toxic symptoms or deaths, although one control rabbit died. There were high mortalities of control and treated sparrows, particularly during the last week of the study. The high death rate was attributed to stress due to being caged over an extended period of time. The data indicate that a formulated product of ODM, metasystox-r, was not significantly hazardous to caged bobwhite quail, English sparrows, and New Zealand rabbits. However, issues such as repellency were not considered. Without knowing the sizes of the cages, it is difficult to know if the animals were adequately exposed to treated food.

Oxydemeton-methyl's production may result in its release to the environment through various waste streams; its use as an insecticide(1) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 9(SRC), determined from a log Kow of -0.74(2) and a regression-derived equation(3), indicates that oxydemeton-methyl is expected to have very high mobility in soil(SRC). Volatilization of oxydemeton-methyl from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.6X10-13 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Oxydemeton-methyl is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 2.85X10-5 mm Hg(2). Percent degradation of oxydemeton-methyl after 14 days ranged from 65-99% by various soil microorganisms(5).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 9(SRC), determined from a log Kow of -0.74(2) and a regression-derived equation(3), indicates that oxydemeton-methyl is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.6X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3.1(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low. At 22 °C the half-lives for hydrolysis of oxydememton-methyl are estimated as 107, 46, and 2 days at pH 4, 7, and 9, respectively(2).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), oxydemeton-methyl, which has a vapor pressure of 2.85X10-5 mm Hg at 20 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase oxydemeton-methyl 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 3.6 hours(SRC), calculated from its rate constant of 1.1X10-10 cu cm/molecule-sec at 25 °C(SRC), that was derived using a structure estimation method(3). Particulate-phase oxydemeton-methyl may be removed from the air by wet and dry deposition(SRC).

The rate constant for the vapor-phase reaction of oxydemeton-methyl with photochemically-produced hydroxyl radicals has been estimated as 1.1X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 3.6 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). At 22 °C the half-lives for hydrolysis of oxydememton-methyl are estimated as 107, 46, and 2 days at pH 4, 7, and 9, respectively(2). At 70 °C, the half-lives for hydrolysis of oxydemeton-methyl are 34, 32, 20, 9.3, and 1.6 hours at pH 5, 6, 7, 8, and 9, respectively(3).

An estimated BCF of 3.1 was calculated for oxydemeton-methyl(SRC), using a log Kow of -0.74(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

10.00 L/kg|The Koc of oxydemeton-methyl is estimated as 9(SRC), using a log Kow of -0.74(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that oxydemeton-methyl is expected to have very high mobility in soil. One investigator estimated that oxydemeton-methyl would leach >35 cm in loam soil at 25 °C in a year(4).

The Henry's Law constant for oxydemeton-methyl is estimated as 1.6X10-13 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that oxydemeton-methyl is expected to be essentially nonvolatile from water surfaces(2). Oxydemeton-methyl is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 2.85X10-5 mm Hg(3). However, it has been estimated that between 3.5 to 6.5 kg or more of oxydemeton-methyl would volatilize from 1 ha of oxydemeton-methyl-treated loam soil at 25 °C during a year(4).

GROUND WATER: Oxydemeton-methyl was not detected in either of the California 2 wells sampled according to EPA's Pesticides in Ground Water Database, 1984-1985(1). No oxydemeton-methyl was detected in a survey of 91 farm wells in Ontario in 1984(2). Oxydemeton-methyl was used on only two of the farms. Oxydemeton-methyl was not detected, at least above 0.05 ug/l, in 206 waterworks wells in the Federal Republic of Germany in 1984(3). It was not detected (detection limit 0.5 ug/liter) in any of the 359 rural wells in Ontario with suspected contamination between 1979 and 1984(4).

In the California Department of Food and Agriculture's Priority Pesticide Program in 1989, oxydemeton-methyl was analyzed for in samples of various commodities(2). Residues were found in the following commodities (commodity, samples analyzed, samples with residues): brussel sprouts, 23, 11; cabbage, 32, 3; cauliflower, 22, 2; peppers, 12, 3; chili peppers, 4, 1; and squash (winter or unspecified), 17,1(2). All residues were within tolerance(2). No residues were found in the following commodities (commodity, samples analyzed): string beans, 16; broccoli, 11; cantaloupe, 2; sweet corn, 1; cucumber, 7; honey due, 2; lettuce, 15; summer squash, 1; zucchini, 7(2). No oxydemeton-methyl was detected in 258 vegetable samples analyzed in Ontario-grown vegetables between 1980 and 1985(1). During FDA's regulatory monitoring of domestic and imported adult food eaten by infants and children between FY 1985 and 1991 (10,000 samples), oxydemeton-methyl was only found in 9 out of 2464 samples of domestic apples, maximum residue 0.39 ppm(3). Oxydemeton-methyl was not detected in any of the 27 market baskets of infant foods and adult foods eaten by infants and children during this time period(3). Oxydemeton-methyl was not found in foods studied in the Danish National Pesticide Monitoring Program 1995-1996(4).

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

Occupational exposure to oxydemeton-methyl may occur through inhalation and dermal contact with this compound at workplaces where oxydemeton-methyl is produced or used. Monitoring data indicate that the general population may be exposed to oxydemeton-methyl via ingestion of food. (SRC)|In a survey of 31 Ontario greenhouse chrysanthemum producers, oxydemeton-methyl was applied an average of 12 times per year(1). The percentage of respondents that used protective clothing were (item, percent): coveralls, 100%; gloves, 100%; boots, 100%; hats, 16%; goggles, 32%; respirator, 84%). While the number of reported or suspected pesticide poisonings were low, the high frequency of pesticide use and the finding that workers tended to be long-term full-time employees indicates that there may be a potential for chronic exposure(1).|Secondary exposure of children through contact with their parents' contaminated clothing can also occur. /Organophosphorus pesticides/

4-5. 4= Very toxic: Probable oral lethal dose (human) 50-500 mg/kg, between 1 teaspoon and 1 ounce for 70 kg person (150 lb). 5= Extremely toxic. Probable oral lethal dose (human) 5-50 mg/kg, between 7 drops and 1 teaspoonful for 70 kg person (150 lb).

Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. (See all compounds classified as Insecticides.)

Following an oral dose of 5.0 mg/kg /14C-ODM/, tissue radioactivity was evaluated from 2 hr to 10 days post-dosing. ...Measurement of tissue radioactivity at 2 hours post-dosing shows that the highest concentration of radioactivity was found in the kidney (4.8 ppm); this is understandable since the urine is the predominant route of elimination. The lowest tissue level was found in the brain (1.7 ppm). Of the other tissues analyzed, concentrations ranged from 2.2 ppm in renal fat to 3.9 ppm in the lung. The remaining tissues (muscle, skin, liver, adrenal gland and testes) concentrations were between 3.0 and 3.6 ppm. After one day the levels of tissue radioactivity were 45-106 times lower that the 2 hr values. By 10 days, residual tissue radioactivity was present and ranged from a low value of 0.00035 ppm in testes to 0.085 ppm in erythrocytes.|In a metabolism study..., rats were dosed with 14C-1-ethylene-labeled ODM ( 14C-ODM) at a single dose 1 mg/kg, either iv or orally (po), a single oral dose at 20 mg/kg, or with 14 daily oral doses of unlabeled ODM at 1 mg/kg/day followed by a single oral dose of 14C-ODM at 1 mg/kg. The results of this study show that 14C-ODM was rapidly absorbed, extensively metabolized, and rapidly excreted. Over a 3-day period, most (90-108%) of the administered dose was excreted. The radioactivity was recovered almost entirely in the urine (89-105% of the administered dose), while feces and expired CO2 accounted for 0.2-2.9% and 0.1% of the administered dose, respectively. There was no indication of bioaccumulation in any tissue or organ. ...The results indicate that at 20 mg/kg a marked increase in urinary excretion of unmetabolized parent compound (59-74%) in conjunction with a marked decline in the urinary excretion of metabolites compared to the corresponding values for males and female rats receiving 1 mg/kg (excretion of unmetabolized parent: 34-55%).|Whole body autoradiography was performed on rats dosed /with 14C-ODM/ iv at 1.0 mg/kg or orally at 10 mg/kg. Following the iv dosing the radioactivity was rapidly distributed throughout the body at 5 min post-dosing. The highest concentrations of radioactivity were found in the kidney, bladder, and accessory genital gland. Lower concentrations were found in the brain, spinal cord, and testes. The concentration in fatty tissues and boney structures were at the limit of detection. Autoradiographs taken 8 hours after the oral dose were found to be essentially the same as with iv administration.|In a dermal absorption study..., radiolabeled ODM (14C-ODM), at a single dose level of 2 mg/kg, was administered dermally or by iv injection to 3 Sprague-Dawley rats/sex/group/time period. Animals were sacrificed 2, 4, 8, 12, 24, 48 and 72 hours or until the radioactivity in urine dropped to 2 times background. For the dermally treated animals, a 12 sq cm area of the application site was removed, washed and counted. For each time period, radioactivity was counted in urine, plasma, the skin, skin solvent wash samples. ...Total recoveries for iv route of administration were 67% for males and 81% for females. For the dermal route of exposure total recoveries were 33% for males and 41% for females. Recoveries of ODM were low, probably due to metabolism and failing to include residual total body counts. Dermal absorption was calculated to be 50.4% for males and 51.8% for females. The dermal absorption rates, as calculated by regression analysis based on mg equivalents of 14C-ODM over time, were 0.15 g/sq cm/hr for males and 0.17 g/sq cm/hr for females.

In a metabolism study..., rats were dosed with 14C-1-ethylene-labeled ODM ( 14C-ODM) at a single at dose 1 mg/kg, either iv or orally (po), a single oral dose at 20 mg/kg, or with 14 daily oral doses of unlabeled ODM at 1 mg/kg/day followed by a single oral dose of 14C-ODM at 1 mg/kg. ...The identification of major urinary and fecal metabolites were determined for each treatment group. Analysis of the urinary radioactivity revealed that most of administered 14C-ODM was not metabolized. The respective % for males and females of unmetabolized ODM were 43% and 47% for the 1 mg/kg, iv group; 38% and 47% for the 1 mg/kg, po group; 34% and 55% for the repeat, 1 mg/kg/day, po group; and 59% and 74% for the 20 mg/kg, po group. Two major metabolites and three minor ones were also identified. One major metabolite was identified as 2- (ethylsulfinyl)-1-(methylsulfinyl) ethane, and accounted for 18-21% of the administered dose at 1 mg/kg, iv; 24-25%, at 1 mg/kg, po; 15%, at 15 x 1 mg/kg/day, po; and 5-6%, at 20 mg/kg, po. The second major metabolite was identified as 2-(ethylsulfonyl)-1-(methylsulfinyl) ethane; this metabolite accounted for 11-19% of the administered dose at 1 mg/kg, iv; 16-20%, at 1 mg/kg, po; 12-23%, at 15 x 1 mg/kg/day, po; and 6-19%, at 20 mg/kg, po. One minor metabolite (as a % of the administered dose for both males and females) was identified as ODM sulfone and was present at 1.7-3.4% of the total administered dose at 1 mg/kg, iv; 1.6%, at 1 mg/kg, po; 2.4-2.6%, at 15 x 1 mg/kg/day, po; and 2.6-3.9%, at 20 mg/kg, po. Two other minor metabolites were identified as desmethyl ODM and desmethyl ODM sulfone and were detected only in the 20 mg/kg, po, group at 2.6-3.1% and 1.0-3.1%, respectively. Primary fecal metabolites included unmetabolized ODM (0.2%), ODM sulfide (0.8%) and ODM sulfone (0.2%). The differences in the metabolic profiles suggests that the biotransformation may be saturated at high doses. The results indicate that at 20 mg/kg a marked increase in urinary excretion of unmetabolized parent compound (59-74%) in conjunction with a marked decline in the urinary excretion of metabolites compared to the corresponding values for males and female rats receiving 1 mg/kg (excretion of unmetabolized parent: 34-55%).|Demeton S-methyl sulfoxide is degraded by Pseudomonas putida 1453 by cleavage of thioester bond to form 2-(ethylsulfinyl)ethanethiol, 2-(ethylsulfonyl)ethanethiol and bis(2-(ethylsulfinyl)ethyl)disulfide. Nocardia sp dsm 43252 converts it into bis(2-(ethylsulfonyl)ethyl)disulfide, bis(2-(ethylsulfinyl)ethyl)sulfide, and bis(2-(ethylsulfonyl)ethyl)sulfide. o,o-Dimethylthiophosphoric acid was detected.|Metabolism occurs principally by oxidation, hydrolysis by esterases, and by transfer of portions of the molecule to glutathione. Oxidation of organophosphorus insecticides may result in more or less toxic products. The glutathione transferase reactions produce products, that are, in most cases, of low toxicity. Hydrolytic and transferase reactions affect both thioates and their oxons. /Organophosphorus Pesticides/

In a dermal absorption study..., radiolabeled /oxydemeton-methyl/ (ODM) (14C-ODM), at a single dose level of 2 mg/kg, was administered dermally or by iv injection to 3 Sprague-Dawley rats/sex/group/time period. ...The plasma half-life of ODM was 2 hr in both males and females following iv administration, and 3 hr in males and 4 hr in females following dermal exposure. For iv administration, the urine half-live was 5-14 hr in males and 2-20 hr females; and for the dermal exposure, 5-10 hr in males and 4-9 hr in females.|Following an oral dose of 5.0 mg/kg /14C-ODM/, tissue radioactivity was evaluated from 2 hr to 10 days post-dosing. The tissue levels of radioactivity paralleled that of the blood. Peak radioactivity in the blood occurred at 1 hr with elimination half-lives of 1.5 hours for the interval of 2-6 hours followed by a longer half-life of approximately 5 days for the interval of 6-24 hours. ...

Organophosphorus insecticides exert their acute effects in both insects and mammals by inhibiting acetylcholinesterase (AChE) in the nervous system with subsequent accumulation of toxic levels of acetylcholine (ACh), which is a neurotransmitter. In many cases, the organophosphorylated enzyme is fairly stable, so that recovery from intoxication may be slow. /Organophosphorus Pesticides/

SYMPTOMS: This compound is a cholinesterase inhibitor. Symptoms from exposure to this compound include anorexia; nausea; vomiting; diarrhea; excessive salivation; pupillary constriction; bronchoconstriction; muscle twitching; convulsions; coma; respiratory failure; pulmonary edema; perspiration; dyspnea; and cyanosis. The effects are cumulative. ACUTE/CHRONIC HAZARDS: This compound may be absorbed readily through the skin. Acute exposure is evidenced by rapid onset of blurred vision and constricted pupils. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: CHOLINESTERASE INHIBITORS ARE EXTREMELY TOXIC AND FAST-ACTING POISONS. IMMEDIATELY call a hospital of poison control center and transport the victim to a hospital. Atropine is an antidote for cholinesterase inhibitors but should only be administered by properly trained personnel. In the absence of this option and if the victim is conscious and not convulsing, it may be worth considering the risk of inducing vomiting, even though the induction of vomiting is not usually recommended outside of a physician's care. Ipecac syrup or salt water may be used to induce vomiting in such an emergency. If the victim is convulsing or unconscious, do not give anything by mouth, assure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Airway protection. Ensure that a clear airway exists. Intubate the patients and aspirate the secretions with a large-bore suction device if necessary. Administer oxygen by mechanically assisted pulmonary ventilation if respiration is depressed. Improve tissue oxygenation as much as possible before administering atropine, so as to minimize the risk of ventricular fibrillation. In severe poisonings, it may be necessary to support pulmonary ventilation mechanically for several days. /Organophosphate pesticides/|Atropine sulfate. Administer atropine sulfate intravenously, or intramuscularly if intravenous injection is not possible. Remember that atropine can be administered through an endotracheal tube if initial IV access if difficult to obtain. Depending on the severity of poisoning, doses of atropine ranging from very low to...high... . The objective of atropine antidotal therapy is to antagonize the effects of excessive concentrations of acetylcholine at end-organs having muscarinic receptors. Atropine does not reactivate the cholinesterase enzyme or accelerate disposition of organophosphate. Recrudescence of poisoning may occur if tissue concentrations of organophosphate remain high when the effect of atropine wears off. Atropine is effective against muscarinic manifestations, but it is ineffective against nicotinic actions, specifically muscle weakness and twitching, and respiratory depression. Despite the limitations, atropine is often a life-saving agent in organophosphate poisonings. Favorable response to a test dose of atropine can help differentiate poisoning by anticholinesterase agents from other conditions. However, lack of response, with no evidence of atropinization (atropine refractoriness) is typical of more severe poisonings. The adjunctive use of nebulized atropine has been reported to improve respiratory distress, decrease bronchial secretions, and increase oxygenation. ...Do not administer atropine or pralidoxime prophylactically to workers exposed to organophosphate pesticides. Prophylactic dosage with either atropine or pralidoxime may mask early signs and symptoms of organophosphate poisoning and thus allow the worker to continue exposure and possibly progress to more severe poisoning. Atropine itself may enhance the health hazards of the agricultural work setting: impaired heat loss due to reduced sweating and impaired ability to operate mechanical equipment due to blurred vision. This can be caused by mydriasis, one of the effects of atropine. /Organophosphate pesticides/|Glycopyrolate has been studied as an alternative to atropine and found to have similar outcomes using continuous infusion. Ampules of... glycopyrolate were added to... saline and this infusion was titrated to the desired effects of dry mucous membranes and heart rate above 60 beats/min. During this study, atropine was used as a bolus for a heart rate less than 60 beats/min. The other apparent advantage to this regimen was a decreased number of respiratory infections. This may represent an alternative when there is a concern for respiratory infection due to excessive and difficult to control secretions, and in the presence of altered level of consciousness where the distinction between atropine toxicity or relapse of organophosphate poisoning is unclear. /Organophosphate pesticides/|Pralidoxime. Before administration of pralidoxime, draw a blood sample (heparinized) for cholinesterase analysis (since pralidoxime tends to reverse the cholinesterase depression). Administration pralidoxime (Protopam, 2-PAM), a cholinesterase reactivator, in cases of severe poisoning by organophosphate pesticides in which respiratory depression, muscle weakness, and/or twitching are severe. When administered early (usually less than 48 hours after poisoning) pralidoxime relieves the nicotinic as well as the muscarinic effects of poisoning. Pralidoxime works by reactivating the cholinesterase and also by slowing the "aging" process of phosphorylated cholinesterase to a non-reactivatable form. ... Dosage of pralidoxime may be repeated in 1-2 hours, then at 10-12 hour intervals if needed. In very severe poisonings, dosage rates may be doubled. Repeated doses of pralidoxime are usually required. In cases that involve continuing absorption of organophosphate (as after ingestion of large amounts), or continuing transfer of highly lipophilic organophosphate from fat into blood, it may be necessary to continue administration of pralidoxime for several days beyond the 48 hour post-exposure interval usually cited as the limit of its effectiveness. ... Blood pressure should be monitored during administration because of the occasional occurrence of hypertensive crisis. Administration should be slowed or stopped if blood pressure rises to hazardous levels. Be prepared to assist pulmonary ventilation mechanically if respiration is depressed during or after pralidoxime administration. If intravenous injection is not possible, pralidoxime may be given by deep intramuscular injection. /Organophosphate pesticides/|For more Antidote and Emergency Treatment (Complete) data for OXYDEMETON-METHYL (18 total), please visit the HSDB record page.

/HUMAN EXPOSURE STUDIES/ ...A 41 yr old woman, who was 5 months pregnant, ...attempted to commit suicide by ingesting half a bottle (12 g) of oxydemeton methyl. She was admitted to the hospital, and conscious, about 3 and 1/2 hr later. Oxydemeton methyl was found in the gastric aspirate, blood, and urine. She experienced miosis, respiratory distress due to abundant bronchial secretions, hyperreflexia, muscular fasciculations, and diarrhea and went into a coma about 12 hr after admission. Her blood cholinesterase level was 10% of the normal level. The patient was released from the hospital to psychiatric care after 14 days and the last 4 months of pregnancy were uneventful. A neurological exam, which was normal, was given to the baby as a part of a general physical exam immediately after she was born and again on the 8th day.|/HUMAN EXPOSURE STUDIES/ Plasma and erythrocyte ChE activities were evaluated in 15 human volunteers administered ODM (97.5%) either acutely or repeated daily doses for up to 120 days. Prior to the start of the study, all subjects were given physical, hematological and urological exams. Plasma and erythrocyte ChE activities were determined prior to dosing to establish the mean activity and standard deviation for each subject; these values were used as the control values. ODM was administered orally using either undiluted in gelatin capsules or diluted with 25 mL of corn oil. In a pilot study, a single subject was treated at 0.4 mg/kg/day for 5 days; this subject formed the basis for the dose levels used in the study. For acute toxicity, 7 subjects were treated with ODM, each received a dose of 0.0125, 0.025, 0.05, 0.25, 0.5, 1.0, or 1.5 mg/kg. For these subjects, ChE activities were measured at 0.5, 1, 2, 4, 8, or 24 hr, with additional measurements at 48 and 60 hr for subjects treated at 1.0 and 1.5 mg/kg. For the subchronic portion of the study, ChE activities were evaluated in 4 subjects treated at 0.05 mg/kg/day for 25-30 days and 2 subjects treated for 60 days. A single subject was treated for 120 days at 0.1 mg/kg/day. In the pilot study, a single subject was dosed at 0.4 mg/kg/day for 5 days. At 24 hr post dosing, plasma and erythrocyte ChE activities were inhibited by 50% and 35%, respectively. Findings of the acute toxicity study showed that the NOEL was 0.5 mg/kg for both plasma and erythrocyte ChE. At 1.0 mg/kg plasma ChE was inhibited by about 18% and erythrocyte ChE by about 14%. For the subacute study, volunteers treated at 0.05 mg/kg/day for 30-60 days, did not result in inhibition of either plasma or erythrocyte ChE. Treatment at 0.1 mg/kg/day for 120 days, resulted in a progressive inhibition of ChE activities. Plasma ChE was inhibited by 40% within the first 2 wk of exposure; erythrocyte ChE was also progressively inhibited, reaching a plateau of 50% by day 60 of the 120 day exposure. No cholinergic signs were noted in any of the subjects at anytime. Based on the results of this study (inhibition of plasma ChE by 18% and erythrocyte ChE by 14%), the acute LOEL was established at 1.0 mg/kg. The NOEL was established at 0.5 mg/kg. The LOEL for subacute toxicity was established at 0.1 mg/kg/day, based on one subject showing 40% inhibition of plasma ChE at two weeks and 50% inhibition of erythrocyte ChE at 60 days. The subacute NOEL was established at 0.05 mg/kg/day, based on no effects in 6 subjects at this dose.|/HUMAN EXPOSURE STUDIES/ Electroencephalographic (EEG) changes were measured in a group of nine farmers after 30 min crop spraying using the organophosphate pesticide, oxydemeton methyl. Analysis of blood samples and an estimation of skin contamination indicated that exposure was low; cholinesterase activity remained unchanged. For EEG measurements in the closed eye condition, the spectral power of the beta2-band of a higher exposed group (4 farmers) was significantly elevated in comparison to a lower exposed group (7 farmers). Even low exposure to organophosphates may result in characteristic changes in the human EEG without a decrease in cholinesterase activity.|/SIGNS AND SYMPTOMS/ Signs and symptoms of acute intoxication by organophosphorus insecticides include muscarinic, nicotinic, and central nervous system (CNS) manifestations. Symptoms may develop rapidly, or there may be a delay of several hours after exposure before they become evident. The delay tends to be longer in the case of more lipophilic compounds, which also require metabolic activation. Symptoms may increase in severity for more than one day and may last for several days. In severe cases, respiratory failure is a dominant effect. /Organophosphorus pesticides/|For more Human Toxicity Excerpts (Complete) data for OXYDEMETON-METHYL (6 total), please visit the HSDB record page.

demeton-methyl

About 30% as an insecticide or acaricide on cotton; about 30% as an insecticide or acaricide on deciduous fruits and nuts; and about 30% as an insecticide or acaricide on vegetables; and about 10% as an insecticide or acaricide on other field crops (1974)

Metasystox R: Soluble liquid (500 g active ingredient/L)|Croneton MR: Liquid (50 g methyl oxydemeton + 250 g ethiofencarb/L)|Emulsifiable concentrate (250 g active ingredient/L)

The WHO Recommended Classification of Pesticides by Hazard identifies Oxydemeton-methyl (technical grade) as Class IB: highly hazardous; Main Use: insecticide.|Introduced by Bayer AG...as code numbers Bayer 21097, R 2170, trade mark metasystox-r; oxydemeton-methyl is a systemic and contact insecticide suitable for control of sap-feeding insects and mites, with range of action similar to that of demeton-s-methyl of which it is metabolic product.|Patents: protected by West German patent 947,368; US patent 2,963,505; Canadian patent 534,370.

Extraction from crops and solvent partitioning. Cleanup followed by oxidation to the sulfone with detection by alkali flame gas chromatography.|Gas chromatographic method is described for analysis of residues of metasystox-R and its sulfone metabolites in plant and animal tissues and soil.|Product analysis by hplc ... by oxidation to phosphoric acid which is measured by standard colorimetric methods ... by reduction of the sulfoxide group by titanium(III) sulfate and titration of the excess. ... Residues determined, after oxidation to the corresponding sulfone (demeton-S-methylsulphon), by glc with FID.|AOAC Method 991.05, Oxydemeton Methyl in Pesticide Formulations; Liquid Chromatographic Method

Agrochemicals -> Acaricides, Insecticides|Insecticides|INSECTICIDES