Flufenoxuron

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity 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 and plant life; and conformance with environmental and public health regulations.

EC50; Species: Selenastrum capricornutum (Green Algae); Concentration: 24.6 mg/L for 96 hr; Effect: Biomass /Conditions of bioassay not specified in source examined/

LC50; Species: Oncorhynchus mykiss (Rainbow Trout); Concentration: 4.9 ug/L for 96 hr /Conditions of bioassay not specified in source examined/

LC50; Species: Colinus virginianus (Northern Bobwhite Quail) diet >5243 mg/kg /Conditions of bioassay not specified in source examined/

LD50; Species: Colinus virginianus (Northern Bobwhite Quail) >2000 mg/kg /Conditions of bioassay not specified in source examined/

For more Ecotoxicity Values (Complete) data for Flufenoxuron (9 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.3X10+4(SRC), determined from a log Kow of 6.16(2) and a regression-derived equation(3), indicates that flufenoxuron is expected to be immobile in soil(SRC). Volatilization of flufenoxuron from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.6X10-12 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Flufenoxuron is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 4.89X10-14 mm Hg at 20 °C(5). Biodegradation data in soil were not available(SRC, 2011).

TERRESTRIAL FATE: Flufenoxuron was applied at a nominal concentration of 97.5 g active ingredient/ha annually for three years via tractor-driven mist blower to experimental apple orchards in Sittingbourne, Kent U.K. Monitoring over a three-year period indicated that flufenxouron does remain in the soil at low residue concentrations(1).[(1) Gilbert JM et al; in Brighton Crop Prot. Conf. - Pests Dis. 1992

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.3X10+4(SRC), determined from a log Kow of 6.16(2) and a regression-derived equation(3), indicates that flufenoxuron 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 2.6X10-12 atm-cu m/mole(SRC), developed using a fragment constant estimation method(5). According to a classification scheme(5), an estimated BCF of 5400(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(SRC). Hydrolysis half-lives of 112 days (pH 5), 104 days (pH 7), 36.7 days (pH 9), and 2.7 days (pH 12)(6) indicate that the compound does undergo hydrolysis in the environment but the rate is affected by pH(SRC). An aqueous photodegradation half-life of 11 days in ambient water was reported(6). Biodegradation data in water were not available(SRC, 2011).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), flufenoxuron, which has a vapor pressure of 4.89X10-14 mm Hg at 20 °C(2), is expected to exist solely in the particulate phase. Particulate-phase flufenoxuron may be removed from the air by wet or dry deposition(SRC). Flufenoxuron is stable to natural sunlight(4), and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

Flufenoxuron residues were tested for but not detected in twelve tomato samples from local Greek markets; detection limit = 0.01 mg/L(1). The compound was detected in 2 of an unspecified number of Japanese agricultural samples (carrot or grapefruit) at 20.2-50.7 ng/g; detection limit = 18.8 ng/g(2).

The Koc of flufenoxuron is estimated as 1.3X10+4(SRC), using a log Kow of 6.16(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that flufenoxuron is expected to be immobile in soil.

/CASE REPORTS/ A 72-year-old woman was brought to the emergency department by ambulance. The person accompanying her brought an empty 100 mL bottle of an insecticide (Cascade), which was found at the scene. The active ingredient of the product is flufenoxuron and the other components include surfactants and solvents. A detailed composition obtained from the manufacturer was flufenoxuron, ethoxylated nonylphenol phosphate, polyoxyethylene nonylphenol, N-methyl-2-pyrrolidone, and cyclohexanone. Upon arrival at the intensive care unit (ICU), her arterial pH was 7.093, her bicarbonate level was 7.4 mEq/L, and the anion gap was 33.8 mEq/L. Her lactic acid concentration was 16.5 mmol/L. Lactic acidosis was not considered to be a consequence of circulatory shock, because there was no clinical sign of shock other than lactic acidosis, and cardiac output was never below 4.5 L/min. Her acid-base status began to improve and returned to near normal on the next day. It can be hypothesized that the toxicity of the product includes inhibition of the oxygen utilization mechanism at the cellular level. The product is composed of a number of components, similar to many other herbicide products. It is not possible to identify which of the ingredients was specifically responsible for the toxic effects in this case.

/GENOTOXICITY/ In a mammalian cell cytogenetics assay (Chromosome aberration), human lymphocyte (whole blood) cultures were exposed to WL115110 (/flufenoxuron/ 98.1% ai) in dimethyl sulfoxide (DMSO) at concentrations of 0, 78.4, 112, or 160 ug/mL for three hours with and without metabolic activation (S-9 mix). Cells were harvested 17 hours following termination of treatment both with and without S-9 mix. Cells were also harvested 41 hours following termination of treatment in another experiment at the highest concentration with S-9 mix. An additional assay was conducted by exposing cells to test material concentrations of 0, 78.4, 112, or 160 ug/mL without S9-mix for 20 hours with immediate post-treatment harvest. Yet another assay was conducted by exposing cells to test material concentrations of 0 or 160 ug/mL without S9-mix for 44 hours with immediate posttreatment harvest. Blood was obtained from a healthy male donor. The S9-fraction was obtained from Aroclor 1254 induced male Sprague-Dawley rat liver. Flufenoxuron was tested up to concentrations limited by solubility. The maximum mitotic inhibition detected was a decrease of 42% in the mitotic index following the 20-hour treatment at the highest concentration in the absence of S-9 mix. Precipitate was seen in the culture media at all concentrations tested. There were no statistically significant increases in the percentage of cells with structural aberrations including or excluding gaps or in polyploidy over the solvent control values at any test material concentration with or without S9-mix. The solvent and positive control values were appropriate, and solvent control values were within the testing laboratory's historical control ranges in all assays. There was no evidence of chromosome aberrations induced over background.

An estimated BCF of 5400 was calculated in fish for flufenoxuron(SRC), using a log Kow of 6.16(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC), provided the compound is not metabolized by the organism(SRC).

The Henry's Law constant for flufenoxuron is estimated as 2.6X10-12 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that flufenoxuron is expected to be essentially nonvolatile from water and moist soil surfaces(2). Flufenoxuron is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 4.89X10-14 mm Hg(3).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In a 90-day oral toxicity study, WL 115110 (/flufenoxuron/ 98 % ai) was administered to four beagle dogs/sex/dose in the diet at dose levels of 0, 0.05% (500 ppm), 0.5% (5000 ppm), or 5% (50,000 ppm) (0, 38, 375 or 3750 (> 3.5 times limit dose) mg/kg/day, respectively). A mistake in the dose preparation of the 0.5% group was corrected in the second week of the study, and therefore the study was extended to 15 weeks. There were no differences between the controls and the flufenoxuron treated groups in body weights, food and water consumption, ophthalmology, and electrocardiography. There was no mortality during the study. The clinical observations were confined to pallor of the gums or sclera which occurred late in the study in the mid-and high-dose groups. In all treated males, the levels of methemoglobin were increased in a dose-related manner and were significantly higher (p<0.001) in the mid-and high-dose groups than the controls. The effect was seen in males of the 50,000 ppm group by Week 2 (p<0.05). The levels of sulfhemoglobin were also increased (p<0.05 and p<0.001) in the mid-and high-dose groups. These changes were associated with the decreases in hemoglobin, hematocrit and erythrocyte counts in the mid-and high-dose groups at Week 9, with recovery by Week 15. In addition, these changes also correlated with the increase in mean cell volume of red blood cells in the mid-dose group (at Week 9) which persisted to Week 15 in the high dose group. The effect of flufenoxuron on hematology parameters at doses > or = 0.05% was first observed at Week 9, followed by some compensatory effect and recovery in the low-and mid-dose groups. The effect persisted to Week 15 in male beagle dogs that received the mid- and high doses. Similar effects of flufenoxuron were observed in the treated females but to a lesser extent than males in the mid-and high-dose groups. In females, the presence of methemoglobinemia in the mid-and high-dose groups had no effect on red blood cells parameters. The destruction of red blood cells by flufenoxuron was compensated by increased red blood cells production and was associated with the increased incidence of yellow pigment deposition in liver Kupffer cells and in the bone marrow. Histologically, bone marrow hyperplasia was observed in the males and females at doses > or = 0.05% of flufenoxuron. Males showed increases in absolute and relative liver weight. Males in the high dose group exhibited a slight reduction in body weight gain. In contrast, no remarkable changes were found in females. There were a number of sporadic changes in clinical chemistry analyses found, such as the elevated cholesterol levels in mid-and high-dose groups of males. No remarkable changes were found in the females. The systemic toxicity LOAEL is 38 mg/kg/day (500 ppm) based on decreased hemoglobin, hematocrit levels and erythrocyte counts in males; increased absolute liver weights, bone marrow hyperplasia and methemoglobinemia in males and females. The systemic toxicity NOAEL was not established.

Reported flufenoxuron hydrolysis half-lives of 112 days (pH 5), 104 days (pH 7), 36.7 days (pH 9), and 2.7 days (pH 12) indicate that the compound does undergo hydrolysis in the environment but the rate is affected by pH(1). Flufenoxuron is stable to natural sunlight at temperatures equal to or below 190 °C(1) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC). The half-life using thin film on glass ranged from stable to >100 hours in simulated sunlight. An aqueous photodegradation half-life of 11 days in ambient water was reported(1).

Occupational exposure to flufenoxuron may occur through inhalation and dermal contact with this compound at workplaces where flufenoxuron is produced or used. Limited monitoring data indicate that the general US population may be exposed to flufenoxuron via ingestion of imported food. (SRC)

Flufenoxuron's production may result in its release to the environment through various waste streams; its use as an insecticide/acaracide will result in its direct release to the environment. If released to air, a vapor pressure of 4.89X10-14 mm Hg at 20 °C indicates flufenoxuron will exist solely in the particulate phase in the atmosphere. Particulate-phase flufenoxuron will be removed from the atmosphere by wet or dry deposition. Flufenoxuron is stable to natural sunlight, and therefore is not expected to be susceptible to direct photolysis by sunlight. If released to soil, flufenoxuron is expected to have no mobility based upon an estimated Koc of 1.3X10+4. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 2.6X10-12 atm-cu m/mole. Flufenoxuron may not volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data were not available. If released into water, flufenoxuron is expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 5400 suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism. Hydrolysis half-lives of 112 days (pH 5), 104 days (pH 7), 36.7 days (pH 9), and 2.7 days (pH 12) indicate that the compound does undergo hydrolysis in the environment but the rate is affected by pH. An aqueous photodegradation half-life of 11 days in ambient water was reported. Occupational exposure to flufenoxuron may occur through inhalation and dermal contact with this compound at workplaces where flufenoxuron is produced or used. Limited monitoring data indicate that the general US population may be exposed to flufenoxuron via ingestion of imported food. (SRC)

Insecticide/acaricide

There are currently no food/feed uses or tolerances for flufenoxuron in the U.S. BASF Corporation is supporting the use of flufenoxuron on apples, grapes and oranges grown for export to the U.S. in selected European and South American countries.