Sulfosulfuron

LC50; Species: Colinus virginianus (Northern Bobwhite Quail, age 10 days) diet >5310 ppm for 8 days

LC50; Species: Anas platyrhynchos (Mallard Duck, age 10 days) diet >5320 ppm for 8 days

LD50; Species: Colinus virginianus (Northern Bobwhite Quail, age 35 weeks) oral via capsule >2250 mg/kg

LD50; Species: Anas platyrhynchos (Mallard Duck, age 25 weeks) oral via capsule >2250 mg/kg

For more Ecotoxicity Values (Complete) data for Sulfosulfuron (17 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 33(SRC), determined from a structure estimation method(2), indicates that sulfosulfuron is expected to have very high mobility in soil(SRC). Sulfonylurea herbicides, such as sulfosulfuron, are more mobile in alkaline soils and in soils with lower organic matter content(3). The pKa of sulfosulfuron is 3.51(4), indicating that this compound will partially exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of sulfosulfuron from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.5X10-13 atm-cu m/mole(SRC), derived from its vapor pressure, 6.61X10-10 mm Hg(5), and water solubility, 1627 mg/L(6). Sulfosulfuron is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(5). Biodegradation data were not available(SRC, 2011).

TERRESTRIAL FATE: Using a simulated model wheat-crop ecosystem, sulfosulfuron applied at 25 and 50 g ai/ha dissipated with first-order rate constants resulting in half-lives of 3.50, 3.92, and 3.15 days in soil, plant, and water, respectively, for the 25 g/ai ha concentration. At a dosage of 50 g ai/ha, half-lives of 3.72, 4.02, and 3.28 days in soil, plant, and water, respectively, were observed. Under natural field conditions, half-lives of 3.00 and 2.94 days in soil and plant, respectively, were observed at the 25 g ai/ha dosage; 3.17 and 3.07 days in soil and plant, respectively, for the 50 g ai/ha dosage(1).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 33(SRC), determined from a structure estimation method(2), indicates that sulfosulfuron is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.5X10-13 atm-cu m/mole(SRC), derived from its vapor pressure, 6.61X10-10 mm Hg(4), and water solubility, 1627 mg/L(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from a log Kow of -0.77(5) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2011). Hydrolysis half-lives of 9.3, 40.6, 13.9 and 35.0 days at pH values of 4.0, 7.0, 9.2, and 6.8 (distilled water), respectively, were measured(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), sulfosulfuron, which has a vapor pressure of 6.61X10-10 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase sulfosulfuron may be removed from the air by wet or dry deposition(SRC). Sulfosulfuron exhibited a half-life of 9.1 days irradiated as an acetonitrile solution(4), suggesting that it may be susceptible to direct photolysis by sunlight(SRC).

/AQUATIC SPECIES/ ... Data presented here demonstrate that exposure to initial sulfosulfuron concentrations of 3.33 ug/L for up to 21 days was tolerated by /Glyceria maxima (Hartm) Holmb, Lagarosiphon major (Ridl) Moss and Myriophyllum spicatum L/ ... and that adverse effects were observed only when plants were exposed to initial concentrations of 3.33 and 10 ug/L for 70 days. As the occurrence of such high initial concentrations for long periods is unlikely in the aquatic environment, sulfosulfuron is not expected to have adverse effects on the growth of these species. ...

Using a structure estimation method based on molecular connectivity indices(1), the Koc of sulfosulfuron can be estimated to be 33(SRC). According to a classification scheme(2), this estimated Koc value suggests that sulfosulfuron is expected to have very high mobility in soil. Sulfonylurea herbicides, such as sulfosulfuron, are more mobile in alkaline soils and in soils with lower organic matter content(3). The pKa of sulfosulfuron is 3.51(4), indicating that this compound will partially exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

/GENOTOXICITY/ In an in vitro cytogenetic assay, cultured human lymphocytes, obtained from a single donor, were exposed to Sulfosulfuron in initial (3-hr exposure with and without S9 to Sulfosulfuron, followed by 17-hr incubation and then 2-hr exposure to colcemid) and confirmatory (-S9: 19.5- and 43.4-hr exposures to Sulfosulfuron, followed by colcemid; +S9: same as initial) assays. The S9 homogenate was derived from Aroclor 1254-induced rat livers and the test material was delivered to the test system as a solution in DMSO. The highest dose level evaluated (with and without S9) in all assays and harvest times was 1000 ug/mL. A precipitate was observed at this dose level. In addition, reductions (from 14.9 to 66.7%) were seen in mitotic indices at this dose level with and without S9. However, there were no indications of any increased incidence of cells with chromosomal aberrations and/or numbers of polyploid cells. The positive controls induced the expected high yields of metaphase spreads with chromosomal aberrations. Based on the these considerations, it is concluded that Sulfosulfuron did not induce a clastogenic response in human lymphocytes under the conditions of this assay either in the presence or absence of S9 at doses up to and including those associated with cytotoxicity and/or test material precipitation.

An estimated BCF of 3 was calculated in fish for sulfosulfuron(SRC), using an estimated log Kow of -0.77(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC). However, bioaccumulation studies of sulfosulfuron residues in catfish (Genus species not specified) exposed to 9 and 18 mg/L over 56 days showed the presence of high amounts of the herbicide (0.009 to 0.496 ug/g) and its metabolite aminopyrimidine in homogenized fish samples(4).

The Henry's Law constant for sulfosulfuron is estimated as 2.3X10-11 atm-cu m/mole at pH 5(SRC) derived from its vapor pressure, 6.61X10-10 mm Hg(1), and water solubility, 18 mg/L(2). This Henry's Law constant indicates that sulfosulfuron is expected to be essentially nonvolatile from water and moist soil surfaces(3). Sulfosulfuron is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In a subchronic toxicity study, Sulfosulfuron (98.4% a.i.) was administered to 50 beagle dogs (5 Males/5 Females/dose) by gelatin capsule at dose levels of (0, 30, 100, 300 and 1,000 mg/kg/day) for 90 days. Controls received empty gelatin capsules. Sulfosulfuron's toxic effects were expressed primarily in the urinary tract and appeared to be secondary to formation of urinary calculi at 300 and 1000 mg/kg/day. Abnormal crystals (unidentified) were observed in the urine at day 45 at 300 and 1,000 mg/kg/day (males, 1 and 2, respectively; females, 3 and 2, respectively) and in females at study termination (3 at 300 mg/kg/day and 4 at 1,000 mg/kg/day). Hemorrhage, ulceration, inflammation, and/or mucosal epithelial hyperplasia in the urinary bladder were observed in one female in the 1000 mg/kg/day dose group and one in the 300 mg/kg/day dose group. Two males at 1000 mg/kg/day also showed treatment-related effects. One high dose male was sacrificed due to advanced urolithiasis and associated complications throughout the urinary tract, which included glomerulonephritis, degeneration of renal tubular epithelium, suppurative inflammation of the renal pelvis, arteritis/periarteritis, congestion, tubular protein accumulation and fibrin deposition in the capsular/pericapsular areas. Hemorrhage, erosions and ulcerations with acute inflammation, and degeneration of the tunica muscularis were also observed in the urinary bladder. Inflammation, edema and hemorrhage of periureteral tissue were associated with ureter damage. Inflammation and epithelial necrosis occurred in the urethra. Hemorrhage, acute inflammation and vasculitis/perivasculitis were noted in the prostate gland; the relationship of these lesions to treatment was unclear. The investigators concluded that necrosis of thymic lymphocytes in this male was probably due to release of adrenal cortical hormones subsequent to stress. A second male dog had bladder lesions of acute inflammation, erosions/ulcerations and edema. There were no differences in clinical signs, body weight/weight gain, food consumption, ophthalmologic results or hematology and clinical chemistry parameters related to administration of the Sulfosulfuron. The systemic toxicity LOEL is 300 mg/kg/day, based on lesions in the urinary bladder in females occurring subsequent to urinary crystal ormation/urolithiasis and on abnormal urinary crystals in males and females. The NOEL for systemic toxicity is 100 mg/kg/day.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a combined carcinogenicity/chronic toxicity study, Sulfosulfuron (MON 37500 tech., 98.4% a.i.) was administered to 60 Sprague-Dawley rats/sex/dose in the diet at dose levels of 0, 50, 500, 5,000 ppm and to 60 females at 20,000 ppm for 22 months. Surviving males at 20,000 ppm were sacrificed on day 259 due to excessive mortality (individual animal data only were provided for these males). Ten rats/sex/dose were sacrificed at 12 months. Average daily intake of test material was 0, 2.4, 24.4 or 244.2 mg/kg/day (males up to 5,000 ppm; 1,178.3 mg/kg/day, males at 20,000 ppm until day 259) and 3.1, 30.4, 314.1 or 1,296.5 mg/kg/day (females). At 5,000 ppm, increased incidence/severity of abnormal crystals in the urine (both sexes, 70-100% affected vs. 10-40%, controls); slight, possibly treatment-related decrease in serum albumin in males (-20%); gross lesions of the urinary tract in females (calculi of kidney/bladder, dilatation of renal pelvis, 5 to 8.3% vs. 0 to 1.7%, controls) were observed. Microscopic findings in males included renal/urinary bladder calculi (3.3% and 5% vs. 0%, controls); dilatation of the renal pelvis (20% vs. 14%, controls); urinary bladder mucosal epithelial hyperplasia and dilatation (5% and 15% vs. 0% and 11%, controls); and increased incidence of mineralization in the heart, lung, pancreas and skeletal muscle (3.3% to 17% vs. 0 to 10%). In females, kidney pelvic epithelial hyperplasia (28% vs. 13%, controls), pelvic dilatation (13% vs. 0%), renal calculus (1.7% vs. 0%) and gastric pyloric erosions (10% vs. 1.7%) were observed. Females at interim sacrifice showed a slightly increased incidence of urinary tract calculi and related lesions. At 20,000 ppm, the following were observed: decreased survival in males (-33%, day 259) and possibly in females (-16%, termination); increased occurrence of blood-colored urine in males (37%, beginning on day 51) and intra-abdominal swelling (25%, day 135); decreased body weight/weight gain (-9%/-12% by sacrifice in males, up to -12%/-19%, days 51 to 485 in females); possible increased BUN at all time points in females (+20% to +60%); emaciated appearance in females (22% vs. 5%, controls); gross and microscopic lesions of the urinary tract in both sexes, including kidney or bladder calculi, dilatation, mineralization of renal cortex/medulla, bladder mucosal epithelial hyperplasia, pyelonephritis (females), squamous metaplasia of renal pelvic epithelium (females), increased severity of nephropathy (females), renal suppurative inflammation (females), necrosis of renal papilla (males) and hemorrhage of renal pelvis or bladder (males). In females, parathyroid hyperplasia (9% vs. 0%, controls), fibrous osteodystrophy of the femur and sternum (12% vs. 0%), and mineralization the aorta, cornea, heart, lungs, mesentery, pancreas, skeletal muscle, thyroid and spleen (3.7 to 18% vs. 0 to 1.7%, controls) were observed. The LOEL is 5,000 ppm (244.2 mg/kg/day), based on increased incidence of urinary tract gross/microscopic lesions, mineralization in several tissues (males), abnormal urine crystals and possibly decreased albumin (males, termination). The NOEL is 500 ppm (24.4 mg/kg/day). At 5,000 ppm, urinary bladder transitional cell carcinoma and papilloma were observed in females (1/50 each, vs. 0/50, controls) and were considered treatment-related because these tumors occur rarely. /SRP: No reported findings in males./ Dosing was adequate for both sexes based on increased urinary tract lesions and abnormal crystals in the urine at 5,000 ppm. Dosing at 20,000 ppm in males resulted in excessive toxicity.

Hydrolysis half-lives of 9.3, 40.6, 13.9 and 35.0 days at pH values of 4.0, 7.0, 9.2, and 6.8 (distilled water), respectively, were measured. Alkaline hydrolysis yielded 1-(2-ethylsulfonylimidazo[1,2-a]-pyridin-3-yl-3-(4,6-dimethoxypyrimidin-2-yl) amine(1). Hydrolysis half-lives of 7 (pH 4), 48 (pH 5), 168 (pH 7), and 156 days (pH 9) (all 25 °C) have also been reported(2). Under acidic conditions, 1-(2-ethylsulfonylimidazo[1,2-a]pyridin)-3-sulfonamide and 4,6-dimethoxy-2-aminopyrimidine were identified as hydrolytic degradation products(1). After irradiation for 11 days, the compound, present as an acetonitrile solution, decomposed with first-order rate kinetics, exhibiting a half-life of 9.1 days under sunlight. Photodegradation involved breaking of the sulfonylurea bridge as does acidic hydrolysis(1). Therefore sulfosulfuron may be susceptible to direct photolysis by sunlight(SRC).

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

DRINKING WATER: Sulfosulfuron was tested for in 206 surface drinking-water supplies of 15 communities in Manitoba, Saskatchewan, and Alberta, Canada in midsummer (July 2003). The source of drinking water in reservoirs was primarily from snowmelt runoff from crop lands. Sulfosulfuron was detected in 21 of 206 reservoir samples with a maximum concentration of 36.1 ng/L; detection limit = 1.0 ng/L. Positive detections were found in two of four reservoirs in Manitoba, exhibiting mean concentrations of 1.4 and 25 ng/L; it was not detected in six reservoirs in Saskatchewan and five reservoirs in Alberta(1).

Tolerances are established for residues of the herbicide sulfosulfuron, 1-(4,6-dimethoxypyrimidin-2-yl)-3-[(2-ethanesulfonyl-imidazo[1,2-a]pyridine-3-yl) sulfonyl]urea and its metabolites converted to 2-(ethylsulfonyl)-imidazo[1,2-a]pyridine and calculated as sulfosulfuron in or on the raw agricultural commodities. [Table#7815]

Reregistration Eligibility Decision (RED) Scheduled for 2011

For sulfosulfuron (USEPA/OPP Pesticide Code: 085601) ACTIVE products with label matches. /SRP: Registered for 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./

Herbicide

Controls annual and perennial grass and broadleaf weeds in noncrop areas.

Premix Partners: Metsulfuron-methyl

Wettable granule

Water dispersible granule

Mon 37500 Technical (Monsanto Company) Sulfosulfuron 98%

For more Formulations/Preparations (Complete) data for Sulfosulfuron (9 total), please visit the HSDB record page.

Herbicides

Environmental transformation -> Pesticides (parent, predecessor)

Pharmaceuticals