Bifenazate

300.35

300.35

604-709-1

24Z9QW0505

DTXSID5032525

White crystals|Beige crystalline solid (technical grade)

2928000031

59.6

4.2

1.31 g/cm³ @ Temp: 25 °C

120-124 °C

Decomposes at 240 deg C

1.577

In acetonitrile = 0.0956 mg/L, ethyl acetate = 0.102 mg/L, methanol =0.0447 mg/L, toluene = 0.0247 mg/L, hexane = 0.232X10-3 mg/L at 25 deg C

0-6ºC

7.5X10-8 mm Hg at 25 deg C

LD50 in rats (mg/kg): 5000 orally, >2000 dermally (Dekeyser)

Odorless

pH = 6.78 (technical grade); pH = 4.6 (wettable powder)

Henry's Law constant = 7.9X10-9 atm-cu m/mol at 25 °C (est VP/WS)

pKa = 12.94 at 23 °C

UN 3077 9 / PGIII

3

26-36/37

Xi

P260, P264, P270, P273, P305+P351+P338, P314, P337+P313, P391, P501

H320

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

|Warning|H317: May cause an allergic skin reaction [Warning Sensitization, Skin]|P260, P261, P272, P273, P280, P302+P352, P314, P321, P333+P313, P363, P391, and P501|H317 (100%): May cause an allergic skin reaction [Warning Sensitization, Skin]|Aggregated GHS information provided by 91 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H317 (98.25%): May cause an allergic skin reaction [Warning Sensitization, Skin]|P260, P261, P264, P272, P273, P280, P302+P352, P305+P351+P338, P314, P321, P333+P313, P337+P313, P363, P391, and P501|Aggregated GHS information provided by 57 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Danger|H320: Causes eye irritation [Warning Serious eye damage/eye irritation]|P260, P264, P270, P273, P305+P351+P338, P314, P337+P313, P391, and P501

Protective clothing: Long-sleeved shirt and long pants. Shoes plus socks.

The proposed interim /Restricted Entry Interval/ (REI) is 12 hours based on bifenazate acute toxicity classification.

Slight eye and skin irritant.

IDENTIFICATION AND USE: Bifenazate is a solid. It is used as acaricide/miticide (insecticide). HUMAN EXPOSURE AND TOXICITY: There are no data available. ANIMAL STUDIES: Bifenazate causes slight eye and skin irritant to rabbits. In dogs it caused myeloid hyperplasia and a dose-related decrease in numbers of erythrocytes and increased numbers of platelets and level of serum bilirubin at concentrations of 400 and 1000 ppm. The only developmental effects noted in rats were a slightly delayed balanopreputial separation for the males treated with concentrations of 80 and 200 ppm, and vaginal perforation for the females treated with 200 ppm. It was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, and TA1537 and E. coli strain WP2 uvrA. There was no treatment-related increase in the percentage of cells with chromosomal aberrations in Chinese Hamster Ovary cells. Treatment with bifenazate did not result in an increase in the number of micronuclei in mice. ECOTOXICITY STUDIES: Bifenazate is categorized as slightly toxic to avian species on an acute oral basis (LD50=1032 mg/kg) and as moderately toxic to avian species on a subacute dietary basis (LC50=656-1862 ppm). Bifenazate is categorized as practically nontoxic to small mammals on an acute oral basis (LD50>5000 mg/kg). The available data indicate that bifenazate is categorized as highly toxic to freshwater fish (LC50=0.58-76 ppm) and aquatic invertebrates (LC50/EC50=0.50 ppm) on an acute basis.

... The ability of well-known organophosphates and carbamates to inhibit the activation of bifenazate and thus compromise its acaricidal potential was tested. Esterase activity determined in vivo after pre-exposure of mites with organophosphates and carbamates revealed-depending on the compound-varying esterase inhibition nicely correlated with the ability of the individual compound to antagonise bifenazate action on mites. The findings illustrate that organophosphates and carbamates interfere with bifenazate efficacy, most probably by inhibiting carboxylesterases responsible for the activation of the pro-drug. As a result of the strong antagonism, mixtures of bifenazate with carbamates or organophosphates should not be used under field conditions. Moreover, there exists a real threat in repeatedly applying organophosphates and bifenazate. The present study again illustrates how important mode of action information is for the proper planning of resistance management strategies.

LD50 Rat oral >5000 mg/kg|LD50 Rat dermal >5000 mg/kg

/BIRDS and MAMMALS/ Bifenazate is categorized as slightly toxic to avian species on an acute oral basis (LD50=1032 mg/kg) and as moderately toxic to avian species on a subacute dietary basis (LC50=656-1862 ppm). Bifenazate is categorized as practically nontoxic to small mammals on an acute oral basis (LD50>5000 mg/kg).|/AQUATIC SPECIES/ The available data indicate that bifenazate is categorized as highly toxic to freshwater fish (LC50=0.58-76 ppm) and aquatic invertebrates (LC50/EC50=0.50 ppm) on an acute basis.|/OTHER TERRESTRIAL SPECIES/ This project assessed the potential hazards of different classical and novel acaricides against an important non-target and beneficial insect for the pollination of wild flowers and cultivated crops, the bumblebee Bombus terrestris (L). Twenty-three acaricides used commercially in the control of phytophagous mites (Acari) were tested in greenhouses and/or the open field. Side effects included acute mortality and also sublethal effects on nest reproduction. The different compounds were administered in the laboratory via three different worst-case field scenario routes of exposure: dermal contact and orally via the drinking of treated sugar water and via treated pollen. The compounds were tested at their respective maximum field recommended concentration (MFRC), and, when strong lethal effects were observed, a dose-response assay with a dilution series of the MFRC was undertaken to calculate LC(50) values. From the different acaricide classes, several chemistries caused high levels of acute toxicity in bumblebee workers, especially bifenthrin and abamectin which resulted in 100% mortality by contact. In addition, several acaricides tested were found to have a detrimental effect on drone production. For oral exposures via treated sugar water, the dose-response assay showed the LC(50) values for abamectin, bifenazate, bifenthrin and etoxazole to be 1/15 MFRC (1.17 mg AI/L), 1/10 MFRC (9.6 mg AI/L), 1/83 MFRC (0.36 mg AI/L) and 1/13 MFRC (4.4 mg AI/L) respectively, indicating that their use should be carefully evaluated. Overall, the results suggest that most of the acaricides tested are compatible with bumblebees, with the exceptions of abamectin, bifenazate, bifenthrin and etoxazole. However, the risks also depended on the type of treatment. As a result, the sugar water treatment seems to present the worst-case situation of exposure, indicating that this approach is suitable for determining the hazards of pesticides against bumblebees. Finally, it is suggested that future tier testing under more field-related conditions is required for a final decision of their risks.|/OTHER TERRESTRIAL SPECIES/ An analysis of the results indicate that bifenazate is categorized as moderately toxic to bees on an acute contact basis (LD50=7.5 ug/bee).

Bifenazate's production may result in its release to the environment through various waste streams; its use as an acaricide(1) specifically as a selective miticide/insecticide for agricultural, residential, commercial, industrial, and institutional applications(2) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values of 1,780 to 6,189(2,3), indicate that bifenazate is expected to have low to no mobility in soil(SRC). The pKa of bifenazate is 12.94(4), indicating that this compound will exist almost entirely in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of bifenazate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 7.9X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 7.5X10-8 mm Hg(4), and water solubility, 3.76 mg/L(6). Additionally, volatilization from moist soil is not expected because the compound exists as cation and cations do not volatilize. Bifenazate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure and cationic nature under environmental conditions. Utilizing the Modified Sturm test, 11.7% CO2 evolution was reached in 28 days therefore bifenazate is not considered readily biodegradable. Aerobic half-lives in water/sediment systems are reported as less than 6 hours to 7.3 hours with 18.9 to 33.7% mineralization after 100 days. These data indicate that primary biodegradation is an important fate process in soil, however rapid mineralization is not expected(7).|AQUATIC FATE: Based on a classification scheme(1), Koc values of 1,780 to 6,189(2,3), indicate that bifenazate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 7.9X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 7.5X10-8 mm Hg(5), and water solubility, 3.76 mg/L(6). Additionally, a pKa of 12.94(5) indicates bifenazate will exist almost entirely in the cation form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(7), an estimated BCF of 80(SRC), from a log Kow of 3.4(6), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Utilizing the Modified Sturm test, 11.7% CO2 evolution was reached in 28 days therefore bifenazate is not considered readily biodegradable. Aerobic half-lives in water/sediment systems are reported as less than 6 hours to 7.3 hours with 18.9 to 33.7% mineralization after 100 days. These data indicate that primary biodegradation is an important fate process in water, however rapid mineralization is not expected(8).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bifenazate, which has a vapor pressure of 7.5X10-8 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase bifenazate may be removed from the air by wet and dry deposition(SRC). Bifenazate contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). Bifenazate undergoes direct photolysis in water with half-lives of 16 to 17 hours at 25 °C(4-6) and on soil with a half-life of less than 30 minutes(4,5).

The rate constant for the vapor-phase reaction of bifenazate with photochemically-produced hydroxyl radicals has been estimated as 8.0X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1.6 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). However, this is not expected to be an important fate process because this compound is not expected to exist in the vapor-phase in the ambient atmosphere. Bifenazate has reported hydrolysis half-lives of 6.34 to 9.10 days at pH 4, 2.68 to 5.4 days at pH 5, 7.7 hours to 0.8 days at pH 7, and 0.45 hours to 0.08 days at pH 9 (25 °C)(1-3). Degradation products from hydrolysis include diazenecarboxylic acid, 2-[4-methoxy(1,1'-biphenyl)-3-yl], 1-methylethyl ester (D3598), [1,1'-Biphenyl]-3,4-diol (D9472), and 4-methoxybiphenyl (D1989)(4). Bifenazate contains chromophores that absorb at wavelengths >290 nm(5) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). Bifenazate undergoes direct photolysis in water with half-lives of 16 to 17 hours at 25 °C(1,4) and on soil with a half-life of less than 30 minutes(2,3). A major degradation product from photodegradation in water is 4-Methoxy-(1,1'-biphenyl)-3-ol(D9963)(4).

An estimated BCF of 80 was calculated in fish for bifenazate(SRC), using a log Kow of 3.4(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC).

In column leaching experiments, bifenazate was reported to be immobile in silt and clay loams, and have low mobility in sandy loams(1). The Koc of bifenazate has been reported to range from 3,011 to 6,189 in soils(1). Bifenazate has a reported log Koc value of 3.25 (Koc = 1,780) from an adsorption/desorption screening test(2). According to a classification scheme(3), these Koc values suggest that bifenazate is expected to have low to no mobility in soil. The pKa of bifenazate is 12.94(4), indicating that this compound will exist almost entirely in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

The Henry's Law constant for bifenazate is estimated as 7.9X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 7.5X10-8 mm Hg(1), and water solubility, 3.76 mg/L(2). This Henry's Law constant indicates that bifenazate is expected to be essentially nonvolatile from water surfaces(3). Bifenazate is not expected to volatilize from dry soil surfaces(SRC) based upon its a vapor pressure(1).

SURFACE WATER: Water quality data compiled from the Retrieval (STORET) Data Warehouse report 2002 monitoring data from the Arizona Department of Environmental Quality indicating that bifenazate was not detected in surface water samples collected from July 2002 to Aug 2002 (limit of quantitation = 0.03 to 0.06 ug/L)(1).

Residues of bifenazate were detected at concentrations ranging from 0.25 to 5.49 ppm in commercial hop samples taken from Idaho, Oregon, and Washington in 2006 and 2007(1). In an FDA total diet study analyzing foods in 4 market basket studies from the fiscal year 2012, bifenazate was detected in 11 of 159 food items considered to be infant and toddler foods at a range of 0.0001 to 0.003 ppm and in 24 of 912 food items other than infant and toddler foods at a range of 0.0001 to 0.556 ppm(2). In an FDA total diet study analyzing foods in 4 market basket studies from the fiscal year 2013, bifenazate was detected in 25 of 1,070 food items at a range of 0.0004 to 0.024 ppm(3).

Occupational exposure to bifenazate may occur through inhalation of dust or aerosols and dermal contact with this compound at workplaces where bifenazate is produced or used. Limited monitoring data indicate that the general population may be exposed to bifenazate via ingestion of food containing residues of bifenazate(SRC). Use data indicate that the greatest potential for dermal and inhalation exposure to bifenazate is expected for members of the general population who have frequent contact with products containing bifenazate, and are frequently in areas where this chemical has been applied (ie. greenhouses/shadehouses, nurseries, golf courses, parks, athletic fields, rights-of-way). The greatest potential for dermal and inhalation exposure to bifenazate is expected for acaricide applicators(1,2).

Sprague-Dawley Crl:CD/BR rats of both sexes were dosed with either 10 or 1,000 mg/kg of [(14)C] ... /bifenazate/ ... (radiochemical purity: >98%, specific activity: 34.4 mCi/mmol, label on the aromatic ring, /bifenazate/... (unlabeled ... purity: 99.6%) by oral gavage. In the Distribution, Metabolism and Excretion study, 5 animals/sex/group were dosed and urine and feces were collected for 7 days. In the Biliary study, 3 animals/sex/group with cannulated bile ducts were dosed and urine, feces and bile were collected for 72 hrs. The Pilot Pharmacokinetic and Pharmacokinetic studies were performed in which 3 animals/sex/group and 5 animals/sex/group, respectively, were dosed. In the pilot study, urine and feces were collected for 4 days and blood samples were collected via a jugular cannula for 72 hrs. In the main study, urine and blood were collected for 4 days from the animals in the 10 mg/kg treatment group. In the 1,000 mg/kg group, urine, feces and blood were collected for 7 days. In the Tissue Distribution study, 9 animals/sex/group were dosed. In the 10 mg/kg group, 3 animals/sex/time point were serially euthanized at 6, 24 and 48 hrs after dosing. In the 1,000 mg/kg group, 3 animals/sex/time point were euthanized at 18, 42 and 72 hrs post-dose. Urine and feces were collected at designated intervals. Tissue samples from Distribution, Metabolism and Excretion study and the Tissue Distribution study were processed for the presence of radiolabel. Radiolabeled materials were isolated from the urine and feces derived from the Distribution, Metabolism and Excretion and the Biliary studies and structurally analyzed for a metabolic profile. The predominant route of excretion for both doses was via the feces. For the 10 mg/kg group, 66% of the administered dose (AD) was recovered in the feces with 75-82% of that total excreted in the first 24 hrs. Radiolabel recovered in the urine and cage wash constituted 27-29% of the AD after 7 days. For the 1,000 mg/kg treatment group, the % of AD recovered in the feces up to 7 days post-dose was 82% with 46-57% of that total recovered in the first 24 hrs. The % of AD isolated in the urine and cage wash was 10-15%. The Biliary study demonstrated that the bile was a significant pathway for excretion by the 10 mg/kg treatment group with 69-74% of the administered dose recovered in the bile up to 72 hrs after dosing. In contrast, for the high dose group, 21-26% of the dose was isolated in the bile by 72 hrs. Recovery in the feces of the 10 mg/kg group was limited to 7-8% of the AD as compared to 56-64% of the AD for the 1,000 mg/kg group. A significant fraction of the AD for the high dose group was not being absorbed. The following pharmacokinetic parameters were derived: tmax, 5 and 6 hrs and 18- 24 hrs for males and females of the 10 mg/kg and 1,000 mg/kg groups, respectively, Cmax, 6.4 and 5.6 ug equiv./g and 119 and 71 ug equiv./g for the males and females in the 10 mg/kg and 1,000 mg/kg groups, respectively, and t1/2, 11.5 and 13.3 hrs and 12 and 15.6 hrs for males and females in the low and high dose groups, respectively. In the Tissue Distribution study, among the 10 mg/kg animals, maximal residue levels were noted at 6 hrs with none of the radiolabel being sequestered in any of the tissues. In the 1,000 mg/kg group, maximal residue levels were noted in a majority of the tissues at 18 hrs post-dose for the males and 42 hrs post-dose for the females. For some of the organs, appreciable levels of radiolabel were still evident at 7 days (e.g., spleen, red blood cell, liver, and kidney). Analysis of the radiolabeled moieties recovered in the feces revealed a number of modifications of the parent cmpd. Hydrazine oxidation, demethylation, ring hydroxylation, separation into biphenyl and hydrazinecarboxylic acid moieties and conjugation with glucuronic acid or sulfate. For the 10 mg/kg group, identified moieties extracted from the feces constituted 39% of the AD. The predominant compounds were ... /bifenazate/ glucuronide (6.3-8.9% of AD), ... /bifenazate/ (4.8-7.2% of AD) and ... biphenyl, 4-hydroxy (5.5-7.1% of AD). In contrast, for the 1,000 mg/kg group, the parent cmpd which was recovered in the feces constituted 48-61% of the AD. /Bifenazate/... glucuronide constituted 4.7-5.6% of the AD ... Overall, the test material was well absorbed at the low dose, metabolized and conjugated before being excreted in the bile. At the high dose level, a much lower % of the dose was absorbed.

Sprague-Dawley Crl:CD/BR rats of both sexes were dosed with either 10 or 1,000 mg/kg of [(14)C] ... /bifenazate/ ( ... radiochemical purity: >98%, specific activity: 34.4 mCi/mmol, label on the aromatic ring, ... /bifenazate/ (unlabeled ... purity: 99.6%) by oral gavage. ... Analysis of the radiolabeled moieties recovered in the feces revealed a number of modifications of the parent cmpd. Hydrazine oxidation, demethylation, ring hydroxylation, separation into biphenyl and hydrazinecarboxylic acid moieties and conjugation with glucuronic acid or sulfate. For the 10 mg/kg group, identified moieties extracted from the feces constituted 39% of the administered dose (AD). The predominant compounds were ... /bifenazate/ glucuronide (6.3-8.9% of AD), ... /bifenazate/ (4.8-7.2% of AD) and ... biphenyl, 4-hydroxy (5.5-7.1% of AD). In contrast, for the 1,000 mg/kg group, the parent cmpd which was recovered in the feces constituted 48-61% of the AD. ... /Bifenazate/ glucuronide constituted 4.7-5.6% of the AD. The primary moieties recovered in the urine were conjugates of ... p, p-biphenol or sulfates of ... /p, p'-biphenol/ and ... /biohenyl, 4-hydroxy/. The total of these cmpds constituted 19-21% of the administered dose for the 10 mg/kg group and 6-7% of the administered dose for the 1,000 mg/kg group. Major metabolites identified in the bile were ... /biphenyl, 4-hydroxy/ (17-20% of AD in the 10 mg/kg group and 2.1-2.5% of the AD in the 1,000 mg/kg group), ... biphenyl, 4-hydroxy, 4-methoxy (17-19% of the AD in the 10 mg/kg and 2.8% of the AD in the 1,000 mg/kg group) and ... /bifenazate/ glucuronide (9-12% of the AD in the 10 mg/kg and 9-13% of the AD in the 1,000 mg/kg group).

Sprague-Dawley Crl:CD/BR rats of both sexes were dosed with either 10 or 1,000 mg/kg of [(14)C] ... /bifenazate/ ... (radiochemical purity: >98%, specific activity: 34.4 mCi/mmol, label on the aromatic ring, /bifenazate/ ... (unlabeled ... purity: 99.6%) by oral gavage. ... The following pharmacokinetic parameters were derived: tmax, 5 and 6 hrs and 18-24 hrs for males and females of the 10 mg/kg and 1,000 mg/kg groups, respectively, Cmax, 6.4 and 5.6 ug equiv./g and 119 and 71 ug equiv./g for the males and females in the 10 mg/kg and 1,000 mg/kg groups, respectively, and t1/2, 11.5 and 13.3 hrs and 12 and 15.6 hrs for males and females in the low and high dose groups, respectively.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

bifenazate

Bifenazate Technical (Macdermid Agricultural Solutions, Inc): Active ingredient: Bifenazate 96.7%.|Floramite (Macdermid Agricultural Solutions, Inc): Active ingredient: Bifenazate 50.0%.|Acramite-50WS (Macdermid Agricultural Solutions, Inc): Active ingredient: Bifenazate 50.0%.|Floramite SC (Macdermid Agricultural Solutions, Inc): Active ingredient: Bifenazate 22.6%.|For more Formulations/Preparations (Complete) data for Bifenazate (14 total), please visit the HSDB record page.

The WHO Recommended Classification of Pesticides by Hazard identifies Bifenazate as unlikely to present an acute hazard in normal use; Main Use: acaricide.

An analytical method was developed for the determination of eleven agrochemicals [abamectin (as B1a), bifenazate, bifenthrin, carfentrazone-ethyl, cymoxanil, hexythiazox, imidacloprid, mefenoxam, pymetrozine, quinoxyfen, and trifloxystrobin] in dried hops. The method utilized polymeric and NH2 solid phase extraction (SPE) column cleanups and liquid chromatography with mass spectrometry (LC-MS/MS). Method validation and concurrent recoveries from untreated dried hops ranged from 71 to 126% for all compounds over three levels of fortification (0.10, 1.0, and 10.0 ppm). Commercially grown hop samples collected from several field sites had detectable residues of bifenazate, bifenthrin, hexythiazox, and quinoxyfen. The control sample used was free of contamination below the 0.050 ppm level for all agrochemicals of interest. The limit of quantitation and limit of detection for all compounds were 0.10 and 0.050 ppm, respectively.|The "modified excised leaf disc method" is based on leaf discs that fit tightly the bottom halves of 50-mm petri dishes. The bottom half of each petri dish is covered with wet cotton wool to prolong leaf freshness. The side wall of each bottom half has a small hole to allow the petiole of the leaf disc to protrude outside the petri dish. The top half of each petri dish has a 28-mm (diameter) window. For phytophagous mites the window is covered with a 40-um mesh Pecap polyester screen. Using this method it was possible to estimate the LC50 value of bifenazate to be 0.00413 g (AI)/L and the LC50 value of spirodiclofen to be 0.40050 g (AI)/L to the twospotted spider mite, Tetranychus urticae Koch (Acari: Tetranychidae). The method reduces losses due to escapees and allows observations to be made as long as 9 d after treatment.

Agrochemicals -> Acaricides|Acaricides, Insecticides|Environmental transformation -> Pesticides (parent, predecessor)

Bifenazat has known environmental transformation products that include diazinecarboxylic acid, 2-(4-methoxy-(1,1-biphenyl)-3-yl),1-methylethyl ester.