SPECTRUM

Chemical Fact Sheet

Chemical Abstract Number (CAS #) 944229
CASRN 944-22-9
SynonymsDYPHONATE
Difonatol,Ethylphosphonodithioic acid o-ethyl s-phenyl ester
Molecular FormulaC10H15OP2

Link to the National Library of Medicine's Hazardous Substances
Database for more details on this compound.

UseDYFONATE IS SOIL INSECTICIDE USEFUL IN CONTROLLING SOIL INSECTS SUCH AS CORN ROOTWORMS (DIABROTICA SPECIES), WIREWORMS (ELATERIDAE), GARDEN SYMPHYLAN (SCUTIGERELLA IMMACULATA), ROOT MAGGOTS (HYLEMYA SPECIES), CRICKETS (GRYLLIDAE) & OTHERS. [R5] Control of soil insects in cereals, maize, sorghum, vegetables, ornamentals, fruit (including citrus and bananas), vines, olives, potatoes, sugar beet, sugar cane, groundnuts, tobacco, and turf. [R6] Soil fumigant [R7] Controls corn borers and rootworms, cutworms, symphylans (garden centipedes), wireworms, other soil, foliar pests. [R2]
Apparent ColorLIGHT YELLOW LIQUID; Colorless
OdorAromatic; Pungent mercaptan
Boiling Point 130 DEG C @ 0.1 MM HG
Melting PointN/A
Molecular Weight 246.32
MiscDENSITY:1.16 @ 25 deg C/25 deg C SOLUBILITY: MISCIBLE WITH ACETONE, ETHANOL, KEROSENE, 4-METHYLPENTAN-2-ONE, XYLENE; SOLUBILITY IN WATER: 13 PPM @ 22 DEG C SHIPPING: UN 2783; Organophosphorus pesticides, solid, toxic, NOS UN 3018; Organophosphorus pesticides, liquid, toxic, NOS UN 2784; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint 23 deg C or more UN 3017; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint less than 23 deg C IMO 6.1; Organophosphorus pesticides, solid, toxic, NOS; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint 23 deg C or more; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint less than 23 deg C; Organophosphorus pesticides, liquid, toxic, NOS REACTION OF THIOPHENOL & O-ETHYL ETHYL PHOSPHONOCHLORIDOTHIOATE YIELDS THE INSECTICIDE FONOFOS (O-ETHYL S-PHENYL ETHYL PHOSPHONODITHIOATE) [R1] FORM: GRANULES; EMULSIFIABLE CONCENTRATE [R2] Dyfonate 4EC (emulsifiable concentrate 480 g ai/l); Dyfonate 2G, Dyfonate 10G, Dyfonate 15G, Dyfonate 20G, granules (20, 200, 150 or 200 g/kg). Mixtures include: Doubledown, granules (fonofos + disulfoton); Dyfonate Tillam 1-4E, emulsifiable concentrate (120 g fonofos + 480 g pebulate/l); Dyfonate thiram 5-10G, granules (50 g fonofos + 100 g thiram/kg). [R3] The chiral forms have been isolated. Optical rotations of the chiral forms are reversed on solution in carbon tetrachloride, cyclohexane, methanol. The (R)-isomer is more toxic to insects and mice and a more potent inhibitor of cholinesterase than the (S)-isomer. [R4, 429] GENERALLY ... SAFE TO PLANTS EXCEPT WHEN PLACED DIRECTLY IN CONTACT WITH THE SEEDS OF SMALL SEEDED CROPS. DIRECT EXPOSURE TO WILDLIFE SHOULD BE AVOIDED. [R5] A combined granule with disulfoton is used in Brassicas to extend the activity to control aphids ... . [R4, 429] Soil insecticide with contact and stomach action. [R6] An insecticide suitable at 1.0-1.5 kg ai/ha. [R4, 429] INDEX OF REFRACTION: 1.5883 @ 30 DEG C/D; Intense mass spectral peaks: 109 m/z (100%), 137 m/z (60%), 246 m/z (46%), 110 m/z (23%) 28 mPa at 25 deg C Henry's Law constant= 5.4X10-6 atm-cu m/mole (est). 1. INSURE THAT A CLEAR AIRWAY EXISTS BY ASPIRATION OF SECRETIONS IF NECESSARY. ADMIN OXYGEN BY MECHANICALLY ASSISTED PULMONARY VENTILATION IF RESPIRATION IS DEPRESSED. IMPROVE TISSUE OXYGENATION AS MUCH AS POSSIBLE BEFORE ADMIN ATROPINE TO MINIMIZE RISK OF VENTRICULAR FIBRILLATION. IN SEVERE POISONINGS, IT MAY BE NECESSARY TO SUPPORT PULMONARY VENTILATION MECHANICALLY FOR SEVERAL DAYS. 2. ADMIN ATROPINE SULFATE IV, OR IM IF IV INJECTION IS NOT POSSIBLE. ... IN MODERATELY SEVERE POISONING: ADULT DOSAGE AND CHILDREN OVER 12 YR: 0.4-2.0 MG REPEATED EVERY 15 MIN UNTIL ATROPINIZATION IS ACHIEVED. MAINTAIN ATROPINIZATION WITH REPEATED DOSAGE OF 0.02-0.05 MG/KG BODY WEIGHT. /ORGANOPHOSPHATE PESTICIDES/ [R20] 2. SEVERELY POISONED INDIVIDUALS MAY EXHIBIT REMARKABLE TOLERANCE TO ATROPINE; TWO OR MORE TIMES THE DOSAGES SUGGESTED ABOVE MAY BE NEEDED. THE DOSE OF ATROPINE MAY BE INCREASED AND THE DOSING INTERVAL DECREASED AS NEEDED TO CONTROL SYMPTOMS. CONTINUOUS INTRAVENOUS INFUSION OF ATROPINE MAY BE NECESSARY WHEN ATROPINE REQUIREMENTS ARE MASSIVE. REVERSAL OF MUSCARINIC SYMPTOMS AND SIGNS, NOT AN ARBITRARY DOSE LIMIT, IS THE DESIRED END-POINT. PRESERVATIVE-FREE ATROPINE PRODUCETS SHOULD BE USED WHENEVER POSSIBLE. NOTE: PERSONS NOT POISONED OR ONLY SLIGHTLY POISONED BY ORGANOPHOSPHATES MAY DEVELOP SIGNS OF ATROPINE TOXICITY FROM SUCH LARGE DOSES. FEVER, MUSCLE FIBRILLATIONS, AND DELIRIUM ARE THE MAIN SIGNS OF ATROPINE TOXICITY. IF THESE APPEAR WHILE THE PATIENT IS FULLY ATROPINIZED, ATROPINE ADMINISTRATION SHOULD BE DISCONTINUED, AT LEAST TEMPORARILY, WHILE THE SEVERITY OF POISONING IS REEVALUATED. /ORGANOPHOSPHATE PESTICIDES/ [R21] 3. DRAW BLOOD SAMPLE (HEPARINIZED) FOR CHOLINESTERASE ANALYSIS BEFORE ADMINISTRATION OF PRALIDOXIME, WHICH TENDS TO REVERSE THE CHOLINESTERASE DEPRESSION. 4. ADMIN PRALIDOXIME (PROTOPAM, 2-PAM) IN CASES OF SEVERE POISONING...IN WHICH RESP DEPRESSION, MUSCLE WEAKNESS & TWITCHINGS ARE SEVERE. ... ADULT DOSAGE AND CHILDREN OVER 12): GIVE 1.0-2.0 G IV @ NO MORE THAN 0.2 G/MIN. CHILD'S DOSE (UNDER 12 YR): GIVE 20-50 MG/KG (DEPENDING ON SEVERITY) IV, INJECTING NO MORE THAN HALF TOTAL DOSE/MIN. DOSAGE...MAY BE REPEATED IN 1-2 HR, THEN @ 10-12 HR INTERVAL IF NEEDED. IN VERY SEVERE POISONINGS, DOSAGE...MAY BE DOUBLED. /ORGANOPHOSPHATE PESTICIDES/ [R21] 4. BE PREPD TO ASSIST PULMONARY VENTILATION MECHANICALLY IF RESP ... DEPRESSED ... . 5. IN PATIENTS WHO HAVE BEEN POISONED BY ORGANOPHOSPHATE CONTAMINATION OF SKIN, CLOTHING, HAIR, AND/OR EYES, DECONTAMINATION MUST PROCEED CONCURRENTLY WITH WHATEVER RESUSCITATIVE AND ANTIDOTAL MEASURES ARE NECESSARY TO PRESERVE LIFE. ... 6. IF ... INGESTED IN QUANTITY PROBABLY SUFFICIENT TO CAUSE POISONING, THE STOMACH AND INTESTINE MUST BE EMPTIED. A. EMPTY THE STOMACH BY INTUBATION, ASPIRATION, AND LAVAGE, USING SLURRY OF ACTIVATED CHARCOAL IN ISOTONIC SALINE. RIGOROUS PRECAUTIONS MUST BE TAKEN TO PROTECT THE AIRWAY FROM ASPIRATION OF REGURGITATED. IF VICTIM IS UNCONSCIOUS OR OBTUNDED, INSERT A CUFFED ENDOTRACHEAL TUBE PRIOR TO GASTRIC INTUBATION. KEEP VICTIM'S HEAD BELOW LEVEL OF STOMACH DURING GASTRIC INTUBATION AND LAVAGE ... . KEEP VICTIM'S HEAD TURNED TO THE LEFT. /ORGANOPHOSPHATE PESTICIDES/ [R22] 6B. AFTER ASPIRATION OF STOMACH CONTENTS AND LAVAGE, INSTILL ACTIVATED CHARCOAL ... TOGETHER WITH A CATHARTIC IN THE CHARCOAL SLURRY. ADULTS AND CHILDREN OVER 12 YR: 50-100 G IN 300-800 ML WATER. CHILDREN UNDER 12: 1.0-1.5 G/KG BODY WT TO A MAXIMUM OF 50 G PER DOSE. ALTERNATIVE CATHARTICS THAT MAY BE USED INSTEAD ARE SODIUM OR MAGNESIUM SULFATE OR CITRATE: DOSAGE OF SODIUM OR MAGNESIUM SULFATE: ADULTS AND CHILDREN OVER 12 YR: 20-30 G. CHILDREN UNDER 12 YR: 250 MG/KG BODY WEIGHT. DOSAGE OF MAGNESIUM CITRATE SOLUTION: ADULTS AND CHLIDREN: 4 ML/KG BODY WEIGHT OF PROPRIETARY SOLUTION, UP TO A MAXIMUM OF 300 ML. C. IF GASTRIC ASPIRATION AND LAVAGE IS NOT PERFORMED DUE TO DELAY IN TREATMENT, AND IF PATIENT IS FULLY ALERT, ADMINISTER DOSES OF CHARCOAL AND CATHARTIC ORALLY. WHEN SORBITOL IS GIVEN ORALLY, IT SHOULD BE DILUTED WITH AN EQUAL VOLUME OF WATER TO YIELD A 35% SOLUTION. D. SAVE A SAMPLE OF EMESIS OR INITIAL GASTRIC WASHINGS FOR CHEMICAL ANALYSIS. E. IN SOME CASES OF ORGANOPHOSPHATE INGESTION THERE MAY BE BENEFIT FROM REPEATED ADMINISTRATION OF ACTIVATED CHARCOAL, EITHER BY INGESTION OR STOMACH TUBE ... . /ORGANOPHOSPHATE PESTICIDES/ [R23] 7. OBSERVE PATIENT CLOSELY FOR AT LEAST 72 HOURS (LONGER IN CASES OF ORGANOCHOSPHATE INGESTION) TO INSURE THAT SYMPTOMS (SWEATING, VISUAL DISTURBANCES, VOMITING, DIARRHEA, CHEST AND ABDOMINAL DISTRESS, AND SOMETIMES PULMONARY EDEMA) DO NOT RECUR AS ATROPINIZATION IS WITHDRAWN. IN VERY SEVERE POISONINGS BY INGESTED ORGANOPHOSPHATES, PARTICULARLY THE MORE LIPOPHILIC AND SLOWLY HYDROLYZED COMPOUNDS, METABOLIC DISPOSITION OF TOXICANT MAY REQUIRE AS MANY AS 5-14 DAYS. /ORGANOPHOSPHATE PESTICIDES/ [R24] 8. PARTICULARLY IN POISONINGS BY LARGE INGESTED DOSES OF ORGANOPHOSPHATE, MONITOR PULMONARY VENTILATION CAREFULLY, EVEN AFTER RECOVERY FROM MUSCARINIC SYMPTOMATOLOGY, TO FORESTALL RESPIRATORY FAILURE. 9. IN SEVERELY POISONED PATIENTS, MONITOR CARDIAC STATUS BY CONTINUOUS ECG RECORDING. /ORGANOPHOSPHATE PESTICIDES/ [R25] 10. FUROSEMIDE MAY BE CONSIDERED FOR RELIEF OF PULMONARY EDEMA IF RALES PERSIST IN THE LUNGS EVEN AFTER FULL ATROPINIZATION. ... 11. THE FOLLOWING DRUGS ARE PROBABLY CONTRAINDICATED IN NEARLY ALL ORGANOPHOSPHATE POISONING CASES: MORPHINE, THEOPHYLLINE, PHENOTHIAZINES, AND RESERPINE. ADRENERGIC AMINES SHOULD BE GIVEN ONLY IF THERE IS A SPECIFIC INDICATION, SUCH AS MARKED HYPOTENSION. /ORGANOPHOSPHATE PESTICIDES/ [R26] SYMPTOMATOLOGY: 1. NAUSEA ... VOMITING, ABDOMINAL CRAMPS, DIARRHEA, EXCESSIVE SALIVATION ... 2. HEADACHE, GIDDINESS, VERTIGO & WEAKNESS. 3. RHINORRHEA & SENSATION OF TIGHTNESS IN CHEST ARE COMMON IN INHALATION EXPOSURE. 4. BLURRING OR DIMNESS OF VISION, MIOSIS ... TEARING, CILIARY MUSCLE SPASM, LOSS OF ACCOMMODATION & OCULAR PAIN ... MYDRIASIS ... SOMETIMES SEEN ... PROBABLY DUE TO SYMPATHO-ADRENAL DISCHARGE. 5. LOSS OF MUSCLE COORDINATION, SLURRING OF SPEECH, FASCICULATIONS & TWITCHING OF MUSCLES (PARTICULARLY OF TONGUE & EYELIDS), & GENERALIZED PROFOUND WEAKNESS. 6. MENTAL CONFUSION, DISORIENTATION & DROWSINESS. /PARATHION/ [R27] SYMPTOMATOLOGY: 7. DIFFICULTY IN BREATHING, EXCESSIVE SECRETION OF SALIVA & OF RESP TRACT MUCUS, ORONASAL FROTHING, CYANOSIS, PULMONARY RALES & RHONCHI & HYPERTENSION, (PRESUMABLY DUE TO ASPHYXIA). 8. RANDOM JERKY MOVEMENTS, INCONTINENCE, CONVULSIONS, & COMA. 9. DEATH PRIMARILY DUE TO RESP ARREST ARISING FROM FAILURE OF RESP CENTER, PARALYSIS OF RESP MUSCLES, INTENSE BRONCHOCONSTRICTION OR ALL THREE. /PARATHION/ [R27] Accidental and Intentional Poisoning. A 19 year old woman developed nausea, vomiting, salivation, and sweating soon after breakfast, and she was taken to a local hospital. She suffered cardiorespiratory arrest. Following successful resuscitation she was transferred to a medical center, where she arrived unconscious and without spontaneous respiration; she had muscle fasciculations, blood pressure of 64/0 mm Hg, a pulse rate of 46, pinpoint pupils, and profuse salivary and bronchial secretions. She was maintained on a respirator. In addition to predictable findings, she showed temperature spiking to 40 deg C and an increase in serum amylase, which decreased rapidly to normal on the 4th hospital day and then peaked again between days 9 and 18. On the 9th day, abdominal distension was noted, and an epigastric mass was palpated. On the 12th day a 10 cm pancreatic pseudocyst was drained externally. The postoperative course was stormy, but the patient was discharged 2 mon later and was still well when last reported 15 mon later. During her illness, she received no specific treatment because it was not until the 10th day in the medical center that investigation by the medical examiner revealed the true cause of illness as an organic phosphorus compound, specifically fonofos, a formulation of which had been used as flour in making pancake batter the night before the cakes were cooked for breakfast. ... Three other members of the family were poisoned by the pancakes, and one of them died. A fifth family member who may have mixed the batter but did not eat pancakes remained well. [R28] GRANULARS ... ARE MUCH LESS HAZARDOUS /TO ANIMALS/ THAN EMULSIONS. [R2] AVG ACUTE ORAL LD50 OF TECHNICAL FONOFOS IN MALE RATS IS 13.2 MG/KG ... IN FEMALE RATS IS 3 MG/KG, INDICATING SEX-RELATED DIFFERENCE IN ACUTE LETHALITY. ... TECHNICAL FONOFOS ... INSTILLED INTO EYE OF ALBINO RABBITS CAUSED DEATH, USUALLY DURING 1ST 24 HR ... BUT LOCAL EYE IRRITATION ... NEGLIGIBLE. ... FONOFOS INCORPORATED INTO DIET OF ... MALE & FEMALE CHARLES RIVER ... RATS FOR 105 WK PRODUCED NO-EFFECT LEVEL OF 10 PPM. ... DID NOT SHOW ... CARCINOGENIC EFFECTS. [R11] ACUTE DYFONATE ADMIN PRODUCED MILD HEN BRAIN NEUROTOXIC ESTERASE (NTE) INHIBITION (19%, P <0.05) BUT THERE WAS NO TREATMENT-RELATED NEUROPATHY IN HENS RECEIVING CHRONIC ORAL DYFONATE, INDICATING THAT CHRONIC TREATMENT DID NOT PRODUCE DELAYED NEUROTOXICITY. [R29] In acute oral toxicity of mallards, the signs of intoxication /are/: hyperexcitability, wide stance, reluctance to leave the swimming pond, ataxia, goose-stepping ataxia, falling, sitting, tremors, spasms, using wings to aid pedestrian locomotion, wing-drop, immobility, & terminal wing beat convulsions. Signs appeared as soon as 25 min and mortalities usually occurred between 1 and 3 hr after treatment. Remission took up to 4 days. [R30] A three generation reproduction study conducted in rats at dietary levels of 10 ppm and 31.6 ppm indicated that there were no adverse effects noted at either level on overall reproductive performance among the parental animals, or on the numbers, well being or integrity of the offspring. [R11] LD50 RAT MALE ORAL 24.5 MG/KG /(+ OR -)DYPHONATE/ [R4, 429] LD50 RAT FEMALE ORAL 10.8 MG/KG /(+ OR -)DYPHONATE/ [R4, 429] LD50 GUINEA PIG PERCUTANEOUS 278 MG/KG [R4, 429] LD50 RABBIT PERCUTANEOUS 159 MG/KG [R4, 429] LD50 Rat oral 8-17.5 mg/kg [R6] LC50 Rat inhalation 1.9 mg/l air/1 hr [R6] LD50 Salmo gairdneri (Rainbow trout) 0.020 mg/l/96 hr @ 13 deg C (95% confidence limit 0.016-0.025mg/l), wt 1.7 g. 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. [R31] LD50 Lepomis macrolophus (Bluegill) 0.007 mg/l/96 hr @ 24 deg C (95% confidence limit 0.005-0.009 mg/l), wt 1.0 g. 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. [R31] LD50 Anas platyrhynchos (Mallard) oral 16.9 mg/kg (95% confidence limit 13.4-21.3 mg/l), males 3-4 mo of age [R30] Work ... must not be carried out by young persons under 18 yr, expectant or nursing mothers, or persons for whom work with toxic chemicals is contraindicated on account of their state of health; the same applies to alcoholics. Contraindications for work with organophosphorus pesticides are organic diseases of the CNS, mental disorders & epilepsy, pronounced endocrine & vegetative disorders, pulmonary tuberculosis, bronchial asthma, chronic respiratory diseases, cardiovascular diseases and circulatory disorders, gastrointestinal diseases (peptic ulcer), gastroenterocolitis, diseases of the liver & kidneys, eye diseases (chronic conjunctivitis and keratitis). /Organophosphorus pesticides/ [R32] WHEN (14)C ETHOXY LABELED DYFONATE WAS ADMINISTERED /TO RATS/, 95% OF LABEL WAS FOUND IN URINE; 5% IN FECES; AND ... 0.5% IN EXHALED AIR. WITH (35)S LABEL, 63% OF DOSE WAS RECOVERED IN URINE; 32% IN FECES; 2% IN TISSUES; AND 0.1% IN EXHALED AIR. [R33] /AFTER ORAL ADMIN IN OIL TO RATS/ ... POLAR PRODUCTS ... EXCRETED IN URINE & FECES. [R34] WHEN PLANTS WERE GROWN IN NITROGEN DEFICIENT NUTRIENT SOLN, CONCN OF DYFOXON /METABOLITE/ IN GREENS WERE REDUCED DUE TO DEFICIENCIES OF ALL ELEMENTS (POTASSIUM, CALCIUM, & MAGNESIUM) EXCEPT NITROGEN. [R35] Organophosphates are efficiently absorbed by inhalation, injestion, and skin penetration. /Organophosphate pesticides/ [R36] After a single oral or ip dose of fonofos labeled in the ring position, 98% of the radioactivity was excreted in the urine and feces within 96 hours. Conditioning with unlabeled fonofos did not change the excretion pattern. Excretion of radioactivity from the (14)C-ethoxy moiety was essentially complete in 4 days, with about 91% in the urine, 7.4% in the feces, and 0.35% in the expired air. Radioactivity in the bile was an important source of activity in the feces. Tissue residues were very small and had virtually disappeared by the 16th day. [R28] Rapidly absorbed through the skin. [R6] METABOLISM OF DYFONATE IN RATS WAS STUDIED ... /WITH (35)S LABEL/. ... DIETHYL PHOSPHATE & THIOPHOSPHATE, METHYLPHENYLTHIOETHER, & THIOLATE ANALOG OF DYFONATE WERE OBSERVED. [R33] DYFONATE IN OIL WAS ADMIN ORALLY TO ALBINO RATS. RAPID METAB ... PRODUCED ... DYFONATE OXON, O-ETHYL O-METHYL ETHYLPHOSPHONATE, METHYLPHENYL SULFOXIDE & SULFONE, O-ETHYL ETHYLPHOSPHONOTHIOIC ACID, O-ETHYL ETHYLPHOSPHONIC ACID & 3-HYDROXY- & 4-HYDROXY-PHENYL SULFONES /AND/ OTHER UNIDENTIFIED MATERIALS ... . [R34] DYFONATE WAS INCUBATED WITH MICROSOMES ... FROM RAT LIVERS. ... THE OXON, EOP /O-ETHYL ETHYLPHOSPHONIC ACID/, ETP /O-ETHYL ETHYLPHOSPHONOTHIOIC ACID/ & THIOPHENOL /WERE IDENTIFIED/ AS MAJOR MICROSOME METABOLITES. FORMATION OF ETP & THE OXON REQUIRED PRESENCE OF NADPH2. [R34] Potato plants were grown in soil treated with dyfonate. In addition to unchangeddyfonate, seven metabolites were identified: oxon, EOP /o-ethyl ethylphosphonic acid/, EOP-CH3 /o-ethyl o-methyl ethylphosphonate/, ETP-CH3 /o-ethyl ethylphosphonothioate/, & some unknowns. The water-sol metabolites incl EOP, ETP, MPSO2 /methylphenyl sulfoxide/ & several unknowns of which 49% gave rise to EOP when subjected to acid hydrolysis. Two unknown materials were cleaved by beta-glucosidase or glusulase but less by beta-glucuronnidase. This suggested that the 2 metabolites existed in the plant largely as glycoside & sulfate conjugates ... . [R34] When labeled fonofos was incubated with mouse liver mixed-function oxidase, steroselective metabolism occurred. ... Some racemizatin also occurred. Diphenyl disulfide and diphenyl disulfide oxide were also observed. In the presence of mouse and rat serum, fonofos was stable; however, the oxon glowly gave rise to diphenyl disulfide. [R37, 313] When phenyl (35)S fonofos was administered to mice, the (S)p isomer was eliminated, primarily in urine, more rapidly than the (R)p isomer. In addition to unchanged fonofos, other identified (35)Slabeled metabolites included: fonofos oxon, diphenyl disulfide, diphenyl disulfide oxide, methyl phenyl sulfoxide and sulfone, and 3-OH- and 4-OH-phenyl methyl sulfones. When phenyl (35)S-fonofos oxon was used, (35)S-labeled metabolites included methyl phenyl sulfoxide, methyl phenyl sulfone, and 3-OH- and 4-OH-phenyl methyl sulfones. [R37, 313] After topical application of phenyl (35)S fonofos to houseflies, unchanged fonofos was the main compound in the external wash. In addition some oxon, methyl phenyl sulfoxide, and methyl phenyl sulfone were also observed. Internally, in addition to unchanged fonofos, metabolites identified included diphenyl disulfide, methyl phenyl sulfoxide and sulfone, and 3-OH- and 4-OH-phenyl methyl sulfones. [R37, 313] (14)C Ring and (14)C ethoxy-labeled fonofos was incubated with the soil fungus Rhizopus japonicus. Four metabolites were identified by GLC and MS: fonofos oxon; O-ethyl ethylphosphonic acid; thiophenol; and methyl phenylsulfone. Other compounds were found in the mixture but their origin was not clear: O-ethyl S-phenyl methylphosphonodithioate and its oxon analog; O-ethyl S-phenyl butylphosphonodithioate; and bis(phenylsulfide). [R37, 313] In pea plants, dyfonate was converted in part to its oxon analog. [R37, 314] Soil fungi degraded dyfonate primarily to dyfoxon, O-ethyl ethylphosphonothioic acid, O-ethyl ethylphosphonic acid, methyl phenyl sulfoxide, and methyl phenyl sulfone. In soil, the fungus R. arrhizus metabolized dyfonate to the oxon and water-soluble unidentified metabolites. [R37, 314] In the presence of rat liver microsomal enzymes, fonofos is metabolized to the oxon and also by a different reaction, to O-ethyl-ethylphosphonothiotic acid and thiophenol. The oxon, in turn, is hydrolyzed to O-ethylphosphoric acid and thiophenol. Similar metabolites were formed by the intact rat, except that the oxon was not found due to rapid hydrolysis. The other metabolites were much less toxic than the parent compound. [R28] Organophosphates poison insects and mammals primarily by phosphorylation of the acetylcholinesterase enzyme at nerve endings. ... At sufficient dosage, loss of enzyme function allows accumulation of acetylcholine (the impulse- transmitter substance) at cholinergic neuroeffector junctions (muscarinic effects, and at skeletal myoneural junctions and in autonomic ganglia (micotinic effects). Organophosphates also impair nerve impulse transmission in the brain ... . /Organophosphate pesticides/ [R36] CHOLINESTERASE INHIBITOR. [R38] INTC: ... PRONAMIDE HAS LITTLE OR NO EFFECT ON DEGRADATION OF ... DYFONATE ... IN PLANTS. [R39] WHEN APPLIED PRE-SEEDING TO SWEET CORN (ZEA MAYS L CV GOLDEN JUBILEE), COMBINATIONS OF ERADICANE & FONOFOS CAUSED UP TO 29% MALFORMATION OF EARS. [R40] Dyphonate may be released in the environment during production and during its use as an insecticide. If released to soil, the loss of dyphonate will occur primarily due to biodegradation. Loss of dyphonate from soil due to volatilization and hydrolysis may not be important. With the exception of sandy soils, dyphonate is expected to have a low mobility in most soils. The half-life of dyphonate in soil is about 40 days. The major pathway for the loss of dyphonate from water may be adsorption to suspended solids and sediment. Minor loss may occur as a result of biodegradation and photolysis. Some bioconcentration of dyphonate may occur in aquatic organisms. Reaction of dyphonate with photochemically produced hydroxyl radicals may be one of the most important loss processes in the atmosphere. The half-life of dyphonate due to this reaction has been estimated to be 1.4 hrs. Partial removal of dyphonate will also occur as a result of dry and wet deposition. The food intake of dyphonate for US population is estimated as 0.0001 ug/kg body wt/day or less. The applicators of the insecticide and farm workers are the most likely people for exposure to dyphonate by inhalation and dermal routes. (SRC) Dyphonate is not known to occur naturally. (SRC) Since dyphonate is commercially produced and used as a insecticide(1), it may be released to the environment during production and will enter the environment during the use(SRC). [R41] TERRESTRIAL FATE: HALF-LIFE OF DYFONATE IN SOIL UNDER BROAD RANGE OF CONDITIONS IS 30-45 DAYS WHICH AVOIDS ANY LONG-TERM ENVIRONMENTAL PROBLEMS. ... DYFONATE SHOWS VERY LITTLE LEACHING OR MOVEMENT IN SOIL ... . [R5] TERRESTRIAL FATE: DYFONATE WAS INCORPORATED INTO SOIL @ RATE OF 5.6 & 11.2 KG/HA AS GRANULES OR EC ... 4 MO AFTER APPLICATION, 33-35% OF GRANULAR ... & 38-41% OF EC APPLICATION (BOTH 5.6 KG/HA) REMAINED IN SOIL. NO DYFOXON /METABOLITE/ DETECTED IN SOIL. [R35] Under Quebec, Canada, weather conditions (May-August), somewhate more than half of the fonofos applied to soil disappeared in about 4 months. In other studies under subtropical conditions, only 36% of fonofos applied to soil was recovered after 6 weeks. The rate of degradation increased with subsequent applications. [R37, 313] TERRESTRIAL FATE: Biodegradation will be the major process by which dyphonate will be lost from most soils(1). Photolysis on silica gel plates indicate that some loss of dyphonate from soil surface may occur as a result of photolysis by sunlight(2). Based on hydrolysis in water, hydrolysis of dyphonate in soil may not be important(3,SRC). Both laboratory and field studies indicate that the leaching potential of dyphonate from soil is low except in the case of sandy soil(4-6). Only a small percent (1 to 6 percent) of dyphonate may be lost as a result of runoff from applied fields(7). Volatilization is not expected to be important for the dissipation of dyphonate from soil(8). [R42] TERRESTRIAL FATE: Depending on the nature of soil and climatic conditions, the field half-life of dyphonate in soil ranged from 18-82 days(1-3); an average half-life of 40 days has been suggested(4). [R43] AQUATIC FATE: The major process for the loss of dyphonate from natural water will be adsorption to suspended solids and sediment(1). Some loss (approximately 5-10% of total) of dyphonate may occur due to volatilization(1-2). Based on the observed biodegradation in soil(3) and photolysis of aqueous suspensions(4), some loss of dyphonate in water may occur via both processes(SRC). The hydrolysis of dyphonate in most natural waters will not be important(5). The estimated overall half-life of dyphonate in water is approximately 2 days(1). The measured log BCF value of less than 2(6) indicates that bioconcentration of dyphonate in aquatic organisms will not be important in aquatic organisms that can metabolize dyphonate(7). [R44] ATMOSPHERIC FATE: A vapor pressure of 2.3X10-4 mm Hg at 25 deg C(1) indicates that dyphonate may be present partially in the vapor phase and partially in the particulate form in air(2,SRC). Based on an estimation method(3), gas phase dyphonate will be removed from the atmosphere with a half-life of 1.4 hrs due to reaction with photochemically produced hydroxyl radicals(SRC). Partial removal of particulate dyphonate from the air may occur by dry deposition(SRC). Both vapor and particle phase dyphonate will be partly removed from the atmosphere by wet deposition. It has been detected in fog and rain water(4-6). [R45] Two fungal species isolated from soil readily degraded dyphonate(1). Metabolites isolated were dyphonate-oxon, ethylethoxyphosphonothioic acid, ethylethoxyphosphonic acid, methyl phenyl sulfoxide and methyl phenyl sulfone(1). Biodegradation was the major process for the loss of dyphonate in soil(2). Biodegradation of dyphonate is faster in dyphonate-treated soil than untreated soil(3-4). The major metabolite of biodegradation of dyphonate in dyphonate-treated soil is carbon dioxide with dyphonate-oxon, methyl phenyl sulfone and other unidentified polar products as minor metabolites(5). [R46] The rate of mineralization was higher in soil which had been previously treated with dyphonate(1). In a soil with a history of dyphonate use, 20.8% of applied dyphonate mineralized to carbon dioxide during 1 week of incubation(1). Dyphonate persisted longer in manure-applied soil, possibly due to greater soil binding of the insecticide making it less available for microbial degradation(2). [R47] The hydrolysis half-lives of dyphonate in water at 25 deg C and pH 5, 6, 7 and 8 were 50, 41, 22 and 6.9 weeks, respectively(1). The hydrolysis half-life in the presence of cupric ion in solution at pH 5 was less than 1 day(2). Therefore, in the absence of catalytic acceleration, hydrolysis may not be important in neutral and acidic solution. When dyphonate deposited on silica gel chromatoplates was exposed to sunlight, some photodegradation of dyphonate was observed(3). In the presence of anthraquinone, the photodegradation by sunlight was complete in 1 hr(3,5). Other compounds that significantly photosensitized dyphonate were anthracene, rotenone and chloroplasts(3-4). Since rotenone and chloroplasts occur naturally in some plants(4), photolysis of dyphonate may be enhanced on surface of leaves(SRC). [R48] Based on an estimation method(5), the rate constant for the reaction of dyphonate with hydroxyl radicals in air is 8.88X10-11 cu cm/molecule-sec(SRC). This corresponds to a half-life of 1.4 hr based on a 12 hr average OH concentration of 1.5X10+6 radicals/cu cm(4) in the atmosphere. [R49] Based on regression equations(1), log BCF values of 2.11 and 2.76 are estimated assuming a water solubility of 16 mg/l at 25 deg C(2) and a log Kow value of 3.94(3), respectively(SRC). In a model ecosystem study, log BCF for dyphonate in mosquito fish (Gambusia affinis) was less than 2(4). The difference between experimentally measured and estimated bioconcentration of dyphonate in aquatic organisms may be due to metabolism of dyphonate(SRC) and it has been concluded(5) that bioconcentration is not important. [R50] The adsorption of dyfonate on humic acid, saturated with various cations, was studied. Adsorption was affected by the cation. Data suggested physical adsorption and the Freundlich constants, K and 1/n, decreased and increased, respectively, with increase in temperature. [R37, 314] Experimental and estimated log Koc values for dyphonate in soil vary widely and range from 1.83 to 3.71(1-4). One of the suggested log Koc value is 2.94(4). This log Koc value indicates that dyphonate would have a low mobility in soil(5). Conversely, it would be strongly sorbed to soil and sediment in water. Laboratory and field leaching studies indicate that dyphonate has low to very low mobility in silt loam, sandy loam and organic soil, but is relatively mobile in quartz sand(6-8). The adsorption of dyphonate increases with decreasing temperature and increase in organic content, particularly humic acid and associated cation content of soil(9). A certain fraction of both dyphonate and its oxon metabolite form bound residues in soil and the latter fraction increases with time(10). [R51] Based on an estimated Henry's Law constant for dyphonate of 5.4X10-6 atm-cu m/mole(1), the volatilization half-life of dyphonate from a 1 m deep model river flowing at a current speed of 1 m/sec and a wind speed of 5 m/sec would be 7 days(2,SRC). Experimentally, the volatilization half-life of dyphonate from water containing soil was determined to be 5 days(3). Similar rates of volatilization of dyphonate from water were also observed by others(4). The rate of volatilization of dyphonate from soil is much slower and less than 1% of dyphonate volatilized from soil at 30 deg C(3). [R52] GROUNDWATER: In a nationwide survey of pesticide, dyphonate was detected in groundwater of 2 states at a max and median concn of 0.9 and 0.1 ug/l, respectively(1). The presence of dyphonate was due to agricultural use of the insecticide(1). The typical concn of dyphonate in positive samples from groundwater in IA was 0.1 ug/l(2-3). Dyphonate was detected in 0.07 percent groundwater in NB at a median concn of 0.05 ug/l(4). Dyphonate was qualitatively detected in groundwater primarily used for municipal drinking water from a selected but unspecified location in CA(5). [R53] DRINKING WATER: Dyphonate was detected in 4.3 percent of groundwater used for public water supplies in IA at a max concn of 0.9 ug/l, but it was not detected in any finished drinking water(1-2). [R54] RAIN WATER: Dyphonate was infrequently detected in rainwater from IA, IN and OH in the concn range less than 0.1 to 0.5 ug/l(1-2). FOG WATER: Dyphonate was detected in fog water from agricultural use areas near Monterey, CA in the concn range 0.018 to 0.030 ug/l(3). [R55] (1) Great Lakes Water Quality Board; 1987 Report on Great Lakes Water Quality, Appendix B. Vol. II. Detroit, MI: International Joint Commission (1989) SURFACE WATER: Dyphonate was detected in 4 Michigan rivers in the concn range 0.001-0.097 ug/l(1). The median concn of dyphonate in water from tailwater pits of irrigated corn and sorghum fields in KS ranged 0.2-0.4 ug/l(1). A maximum concn of 5.9 ug/l was detected in the water of one pit(2). The max concn of dyphonate in unfiltered water from agricultural drainage networks in the Lake Erie basin was in the range 0.96 to 11.86 ug/l(2). Dyphonate was detected in 0.4 percent tile-line effluents from agricultural lands in IA at a max concn of 0.78 ug/l(3). It was detected at max concn of greater than 1,000 ug/l in puddles in loading and rinse areas of a farm-chemical supply in IA(3). [R57] Dyphonate was detected in the concn range not detected (detection limit 0.01 mg/kg) to 1.10 mg/kg in 28 farms in 6 vegetable growing area in Southwestern Ontario in 1976(1). The median concn of dyphonate in sediment of tailwater pits from irrigated corn and sorghum fields in KS ranged 4.0-48.4 ug/kg(2). A maximum concn of 771 ug/kg was detected in the sediment of one pit(2). Dyphonate was detected at max concn of greater than 1000 ug/kg in soils in loading and rinse areas of a farm chemical supply in IA(3). [R58] FOOD: At a detection limit of 0.1 mg/kg, dyphonate has been detected at low frequency both in raw agricultural commodities and in adult total diet samples(1-4). [R59] 4 MO AFTER /SOIL/ APPLICATION ... POTATOES, BEETS, & RUTABAGAS HAD LITTLE OR NO DETECTABLE RESIDUE @ EITHER /5.6 OR 11.2 KG/HA/ APPLICATION RATE. WHEAT HAD 0.01-0.07 PPM DYFONATE BUT LITTLE OR NONE IN MATURE PLANT OR GRAIN. CARROTS ... @ THE LOWER RATE HAD 0.35 & 0.04 PPM DYFONATE & DYFOXON, RESPECTIVELY. [R35] The applicators and workers in farmlands are the most likely group for exposure to dyphonate(SRC). Judging from the formulations used for field application, the most probable routes of exposure to dyphonate among this group would be inhalation and dermal contact(1,SRC). [R60] The estimated total dietary intake of dyphonate in three groups of US population in 1989 were as follows: 6-11 months, less than 0.0001 ug/kg body wt/day; 14-16 yr old male: 0.0001 ug/kg body wt/day; 60-65 yr old female, less than 0.0001 ug/kg body wt/day(2). The corresponding values for 1990 were as follows: 6-11 months, 0.0001 ug/kg body wt/day; 14-16 yr old male: 0.0001 ug/kg body wt/day; 60-65 yr old female, less than 0.0001 ug/kg body wt/day(1,3). [R61] Manufacture, formulation and application /of dyphonate/. [R62] Dyphonate was detected in the cotton coveralls actually worn by a Midwestern farmer(1). This strongly suggests that both farm workers and pesticide applicators are likely to be exposed to this insecticide(SRC). [R63] PRODUCT ANALYSIS IS BY GLC, RESIDUES IN CROPS AND SOIL ARE DETERMINED BY GLC. [R4, 430] EPA Method 622.1. GC with alkali flame detector for the determination of thiophosphate pesticides including dyphonate in industrial and municipal wastewater. Under the prescribed conditions for dyphonate, the method has a detection limit of 0.70 ug/l as defined by EPA. [R69]

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