Ethiofencarb (ISO)

Insecticides

Active substance -> EU Pesticides database: Not approved

Pesticides -> Carbamate Insecticides

Pesticide (Ethiofencarb) -> USDA PDB

log Kow = 2.04

2.04

2.04

2.04

1.231 (20 °C)

1.23 g/cm³

In dichloromethane, isopropanol and toluene >200, hexane 5-10 (all in g/l, 20 °C).

In water, 1.82 g/l at 20 °C

1.82 mg/mL at 20 °C

Solubility in water, g/100ml at 20 °C: 0.18 (poor)

Decomposes on distillation. ...In isopropanol/water (1:1), DT50 (37-40 °C) 330 days (pH 2), 450 hr (pH 7), 5 min (pH 11.4).

When heated to decomposition it emits very toxic fumes of /nitrogen and sulfur oxides/

33.4 °C

33.4 °C

33.4 °C

0.00000705 [mmHg]

0.94 mPa (7.1X10-6 mm Hg) at 25 °C

Vapor pressure at 20 °C: negligible

Colorless solid; mp = 33.4 deg C; [HSDB] Yellow solid; mp = 31-33 deg C; [MSDSonline]

Solid

COLOURLESS CRYSTALS.

Warning

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

P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)

High doses promoted rat liver carcinogenesis; [HSDB] Marked increase in alkaline phosphatase and histopathological changes to liver were observed in 104 week feeding study of dogs at 3000 ppm; In a two year feeding study with rats an increase in relative liver weights was observed at 1000 and 3000 ppm, but no evidence for carcinogenicity; No evidence of delayed neurotoxicity in hens; Not considered teratogenic based on studies with rats and rabbits; A dominant lethal test showed no mutagenicity; [Reference #1] See CARBAMATE INSECTICIDES.

/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. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate 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. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate 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. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate 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. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate pesticide, liquid, toxic, flammable/

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

Acute Tox. 4 (100%)

Acute toxicity - category 4

Acute toxicity (Oral) - Category 3

Acute Tox. 4 *

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.

IMO 6.1; Carbamate pesticides, solid, toxic, nos; carbamate pesticides, liquid, toxic, flammable, nos, flashpoint between 23 °C and 61 °C; carbamate pesticides, liquid, toxic, nos; carbamate pesticides, liquid, NOS

IMO 3.2; Carbamate pesticides, liquid, flammable, toxic, nos, flashpoint less than 23 °C

UN 2757; Carbamate pesticides, solid, toxic, nos; carbamate pesticides, liquid, nos

UN 2758; Carbamate pesticides, liquid, flammable, toxic, nos, flashpoint less than 23 °C

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

Carbamates produce slight to moderate skin and eye irritation, depending on the vehicle used, duration of contact, and on whether the substance is applied to the abraided or intact skin. From the available data, it cannot be excluded that some of the carbamates will have a slight to moderate sensitization potential. /Carbamate Pesticides/

Carbamates produce slight to moderate skin and eye irritation, depending on the vehicle used, duration of contact, and on whether the substance is applied to the abraided or intact skin. From the available data, it cannot be excluded that some of the carbamates will have a slight to moderate sensitization potential. /Carbamate Pesticides/

Refer immediately for medical attention.

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

Rinse with plenty of water (remove contact lenses if easily possible).

Rinse mouth. Refer immediately for medical attention.

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]

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.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Store and dispose of according to local regulations.

The protective clothing should be kept in separate places where it cannot be contaminated with toxic chemicals. It should be forbidden to keep this clothing in living quarters. Protective clothing must be washed at least once a week and each time it is contaminated with pesticides. Before washing the clothing should be soaked for several hours in a calcium carbonate solution. /Pesticides/

Smoking, eating, and drinking before washing should be absolutely prohibited when any pesticide ... is being handled or used. /Pesticides/

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

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.

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.

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. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).

LD50 Mallard ducks oral 140-275 mg/kg

LD50 Japanese quail oral 155 mg/kg

LC50 Golden orfe 61.8 mg/L/96 hr /Conditions of bioassay not specified/

LC50 Rainbow trout 12.8 mg/L/96 hr /Conditions of bioassay not specified/

LC50 Daphnia 0.22 mg/L/48 hr /Conditions of bioassay not specified/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 230(SRC), determined from a structure estimation method(2), indicates that ethiofencarb is expected to have moderate mobility in soil(SRC). Volatilization of ethiofencarb from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 1.2X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 7.1X10-6 mm Hg (3) and water solubility, 1820 mg/l(4). Ethiofencarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). Five weeks after application of a 10% 14C-carbonyl-labeled ethiofencarb granular formulation to soil under greenhouse conditions, the metabolites (sulfoxide and sulfone) were found in the soil, and the parent compound was no longer detectable(5). Radiochemical determination of the degradation rate showed that ethiofencarb had a half-life of about 2 weeks under greenhouse condtions(5). Similar rates of degradation were determined under field conditions(5). In a study of the photolysis of sulfur containing pesticides on soil surfaces, the percent loss of ethiofencarb from three agricultural sandy loam soils with 0.53, 2.2, and 6.3% organic matter, were 74, 70, and 30%, respectively, after 8 hours of sunlight exposure(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 230(SRC), determined from a structure estimation method(2), indicates that ethiofencarb is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon a Henry's Law constant of 1.2X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 7.1X10-6 mm Hg(4), and water solubility, 1820 mg/l(5). According to a classification scheme(6), an estimated BCF of 7.4(SRC), from its log Kow of 2.04(4) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). At pH 6 and 50 °C, the half-life of ethiofencarb was 3.2X10+4 seconds (8 hours) and was not degraded at pH 6 and 20 °C(8). At pH 9, 20 and 50 °C, the half-lives of ethiofencarb were 1.1X10+6 seconds (300 hours) and 1.1X10+3 seconds (3.0 hours), respectively(8). At pH 2, ethiofencarb was not degraded at any of the studied temperatures(8). At pH 12 and 20 and 50 °C degradation was instantaneous(8). The half-life for hydrolysis of ethiofencarb in water (65.6 mg/l Ca2+, 10.7 mg/l Mg2+, pH 6.8) was 8 days; CO2 was evolved by hydrolysis of the carbamate group(9). The half-lives of ethiofencarb by photodegradation in water were 51.7, 9.9, and 1.3 hours with humic acid potassium salt concentrations of 0, 10, and 100 mg/l, respectively; solutions were irradiated for 8 hours in a standardized irradiation test using a mercury high pressure lamp with a filter tube of borosilicate glass(10).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ethiofencarb, which has a vapor pressure of 7.1X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase ethiofencarb 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 16 hours(SRC), calculated from its rate constant of 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase ethiofencarb may be removed from the air by wet and dry deposition(SRC). While ethiofencarb was found to photodegrade in aqueous and nonaqueous solution(4,5) and on soil(6), do data were found regarding the direct photolysis of ethiofencarb by sunlight in air(SRC).

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

Inhalation (L793) ; oral (L793); dermal (L793)

...Milk collected from the /Holstein/ cow 6 hr after treatment /with a single oral dose (0.5 mg/kg) of ring (14C) croneton/ contained 128 ppb 14C residues; 60% of this was as the free carbamate metabolites, croneton sulfoxide and sulfone. ...

Ethiofencarb is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. 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.

/BIRDS and MAMMALS/ As a rule, birds are not very sensitive to carbamates while bees are extremely sensitive. /Carbamate pesticides/

/PLANTS/ Phytotoxic to anthurium and begonias.

Dizziness. Nausea. Muscle twitching. Sweating. Pupillary constriction, muscle cramp, excessive salivation. Vomiting. Diarrhoea. Laboured breathing. Cough. Blurred vision.

See Inhalation.

See Inhalation.

As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)

The substance is very toxic to aquatic organisms. This substance may be hazardous to the environment. Special attention should be given to birds. This substance does enter the environment under normal use. Great care, however, should be taken to avoid any additional release, for example through inappropriate disposal.

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

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

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

Carbamates are effective insecticides by virtue of their ability to inhibit acetylcholinesterase (AChE) in the nervous system. They also inhibit other esterases. The carbamylation of the enzyme is unstable, and the regeneration of AChE is relatively rapid compared with that from a phosphorylated enzyme. Thus, carbamate pesticides are less dangerous with regard to human exposure than organophosphorus pesticides. The ratio between the dose required to produce death and the dose required to produce minimum symptoms of poisoning is substantially larger for carbamate compounds than for organophosphorus compounds. /Carbamate Pesticides/

The main metabolites are ethiofencarb sulfoxide and sulfone, ethiofencarb phenol and the corresponding sulfoxide and sulfone.

The first step in the metabolism of carbamates is hydrolysis to carbamic acid, which decomposes to carbon dioxide (CO2) and the corresponding amine. The mechanism of hydrolysis is different for N -methyl and N -dimethyl derivatives. The N -methyl carbamates pass through an isocyanate intermediate, whereas in the hydrolysis of N - dimethylcarbamates, an addition product with a hydroxyl ion is formed yielding the alcohol and N -dimethyl substituted acid. The rate of hydrolysis by esterases is faster in mammals than in plants and insects. Apart from hydrolysis, oxidation also takes place including: hydroxylation of the aromatic ring, O -dealkylation, N -methyl hydroxylation, N -dealkylation, oxidation of aliphatic side chains, and sulfoxidation to the corresponding sulfone. Oxidation is associated with the mixed-function oxidase (MFO) enzymes. Conjugation leads to the formation of O - and N -glucuronides, sulfates, and mercapturic acid derivatives in mammals. Glycosides and phosphates are conjugation products more common in plants. /Carbamate Pesticides/

The fate of Croneton, 2-ethylthiomethylphenyl N-methylcarbamate, was determined in rats following single oral or dietary exposure to the 14C-carbonyl- and 14C-ring-labeled insecticide. Greater than 95% of the (14C)Croneton equivalents was excreted in the urine or as a combination of 14CO2 (47%) and urinary products (41%) 72 hr after a single oral dose. The feces contained 27% of the dose. A similar excretion pattern was observed during a 7-day feeding period. The principal urinary metabolites were Croneton sulfoxide (23-28% of the dose), phenol sulfoxide (20-23%), phenol sulfone (9-25%), and Croneton sulfone (3-11%) after a single oral dose and similar in the long term study. The carbamates were excreted primarily as free metabolites while the phenolic constituents were eliminated as acid labile conjugates.

The comparative ester hydrolysis and selective toxicity of carbamate insecticides were studied in 4 mammalian species. Hydrolysis rates of carbaryl and ethiofencarb (Croneton) were examined in the rat, mouse, guinea pig and gerbil. Respiratory 14CO2 resulting from the hydrolysis of orally administered (carbonyl-14C)carbamates (0.2 mg/kg) was taken as measure of in vivo hydrolytic capabilities. Ester hydrolysis was greater for ethiofencarb in all species tested, although the relative order of hydrolysis among species was the same with both compounds. After 24 hr, gerbils had hydrolyzed 91% of the ethiofencarb an 65% of the carbaryl. Guinea pigs hydrolyzed somewhat less of the compounds, 65 and 85%, but more than rats and mice, 40 and 25%.

About 75% of the radiocarbon in the eggs /from White Leghorn hens given one to 14 oral doses of croneton/ occurred as free phenol sulfoxide and sulfone, 10% occurred as free croneton sulfoxide and croneton sulfone, 5% occurred as water-soluble metabolites, and 5% occurred as unextracted residues. The remaining 5% was accounted for by unknown metabolites in the organo-extractable fraction.

The carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (L793)

In animals, 14C-ethiofencarb is rapidly excreted.

When administered as a single oral dose to rats, 41% of the carbonyl-labelled compound was eliminated in the urine and 7% in the feces (within 72 hr), while 47% was eliminated as 14CO2. When similarly administered but in ring-labelled form, 96% was eliminated in the urine and 2% in the feces within 72 hr. The compound, therefore, undergoes hydrolysis, producing a phenol and a carbamic acid derivative which breaks down further to CO2.

Maintenance of rats on a diet containing 6.6 ppm of ethiofencarb gave ...total excretion (urine plus feces) decreasing to 1% of one day's intake by the third day after return of the animals to the normal diet. The major metabolites identified were the sulfoxide and sulfone of ethiofencarb and the sulfoxide and sulfone of the phenol; the latter two compounds were excreted mainly as conjugates, and the parent compound was detected in the urine only in trace amounts. Tissue residues detected after either a single oral dose of 0.5 mg/kg bw or administration of 6.6 ppm in the diet for one week were below 1 mg/kg, and these declined more rapidly after administration of the ring-labelled than the carbonyl-labelled compound. This suggests that the carbonyl-labelled residues were incorporated into normal tissues components, as would be expected.

Bile-duct-cannulated rats were orally administered 14C-ethiofencarb. Biliary radioactive carbon measurements made two days after administration revealed the following percentage of the dose 20.2%. /Most/ of the dose was eliminated in the urine, while the feces did not exceed an elimination rate of 3%. Enterohepatic circulation of metabolites is suggested by these findings.

A lactating Holstein cow and a male Yorkshire pig treated with a single oral dose (0.5 mg/kg) of ring (14C) croneton excreted 97.8% and 90.0% of the dose, respectively, in the urine after 24 hr. None of the swine tissues examined 24 hr after treatment contained detectable residues, and of the bovine tissues, only the kidney, liver, and skin contained detectable activity (0.016, 0.017, and 0.05 ppm 14C-croneton equivalents, respectively). Milk collected from the cow 6 hr after treatment contained 128 ppb 14C residues; 60% of this was as the free carbamate metabolites, croneton sulfoxide and sulfone. White Leghorn hens given ring 14C-croneton as a single oral dose (0.5 mg/kg) or in twice-daily doses (0.5 mg/kg) over 7 consecutive days showed patterns of metabolism and excretion similar to those observed in the pig and cow. Birds sacrificed 4 hr after the last dose contained from 0.019 ppm 14C-croneton equivalents in the fat to 0.324 ppm in the kidney. By 24 hr, only the liver and kidney (0.044 and 0.022 ppm, respectively) contained residues in excess of 0.01 ppm, and within 4 days the residues in these organs were 0.01 ppm or less. Residues in eggs laid by these hens were 0.03 to 0.04 ppm 14C-croneton equivalents 2 days after treatment; egg residues reached a maximum of 0.06 to 0.07 ppm 7 days after treatment and declined rapidly following the termination of treatment. About 75% of the radiocarbon in the eggs occurred as free phenol sulfoxide and sulfone, 10% occurred as free croneton sulfoxide and croneton sulfone, 5% occurred as water-soluble metabolites, and 5% occurred as unextracted residues. The remaining 5% was accounted for by unknown metabolites in the organo-extractable fraction.

Formerly used as an insecticide for control of aphids on fruit crops, ornamentals, and vegetables; [HSDB]

Not currently registered as a pesticide for use in the US; [HSDB]

Farming (Pesticides) [Category: Industry]

For ethiofencarb (USEPA/OPP Pesticide Code: 112101) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

Insecticide. For specific control of aphids by contact and stomach action with systemic properties on fruit crops, ornamentals, and vegetables.

Ethiofencarb is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.

Emulsifiable concentrate, granules.

Tradenames: 'Croneton' (Bayer); ...'Arylmate' (Bayer).