Amisulbrom

466.311

466.31

RM460IQC3A

DTXSID0058063

Fine powder

124

4.4

1.61 at 20 deg C

128.6-130.0 deg C

651.5±65.0 °C at 760 mmHg

347.8±34.3 °C

1.718

In hexane 0.2643; toluene 88.63; dichloromethane >250; acetone >250; ethyl acetate >250; methanol 10.11; octanol 2.599 (g/L at 20 deg C)

1.8X10-5 mPa /1.35X10-10 mm Hg/ at 25 deg C

Odorless

Henry's Law constant = 2.8X10-5 Pa /2.1X10-7 atm-cu m/mol/ at 25 °C

UN 3077 9 / PGIII

3

50

61

N

P273

H400

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.

USEPA Office of Prevention, Pesticides and Toxic Substances, Pesticide Fact Sheet for Amisulbrom (September 16, 2011).[Available from, as of May 3, 2012: http://www.epa.gov/opprd001/factsheets/]

|Warning|H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]|P201, P202, P264, P273, P280, P281, P305+P351+P338, P308+P313, P337+P313, P391, P405, and P501|H319 (61.46%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]|P201, P202, P261, P264, P271, P273, P280, P281, P304+P312, P304+P340, P305+P351+P338, P308+P313, P312, P337+P313, P391, P405, and P501|Aggregated GHS information provided by 192 companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Danger|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P273, P280, P281, P301+P312, P302+P352, P304+P340, P305+P351+P338, P308+P313, P312, P314, P321, P330, P333+P313, P337+P313, P363, P391, P403+P233, P405, and P501

Amisulbrom's production may result in its release to the environment through various waste streams; its use as a fungicide(1) will result in its direct release to the environment(SRC). The compound is currently (2012) not manufactured in the U.S., nor is it registered for use in the US , but food products imported into the U.S. may contain residues of amisulbrom(2).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 5100(SRC), determined from a log Kow of 4.4(2) and a regression-derived equation(3), indicates that amisulbrom is expected to be immobile in soil(SRC). Volatilization of amisulbrom from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 2.1X10-7 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Amisulbrom is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.8X10-10 mm Hg at 25 °C(5). Biodegradation data in soil were not available(SRC, 2012).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 5100(SRC), determined from a log Kow of 4.4(2) and a regression-derived equation(3), indicates that amisulbrom is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon a Henry's Law constant of 2.1X10-7 atm-cu m/mole(2). According to a classification scheme(5), an estimated BCF of 370(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is high, provided the compound is not metabolized by the organism(SRC). Hydrolysis is expected to be an important environmental fate process since this compound contains functional groups that hydrolyze under environmental conditions(6). An aqueous half-life of 5 days at pH 9 and 25 °C has been reported(2). Biodegradation data in water were not available(SRC, 2012).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), amisulbrom, which has a vapor pressure of 1.35X10-10 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase amisulbrom may be removed from the air by wet or dry deposition(SRC). Amisulbrom absorbs light at wavelength 254 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Amisulbrom expected to undergo hydrolysis in the environment due to the presence of functional groups that hydrolyze under environmental conditions(1). An aqueous half-life of 5 days at pH 9 and 25 °C has been reported(2). Amisulbrom absorbs light with a lambda max of 254 nm reported(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 370 was calculated in fish for amisulbrom(SRC), using a log Kow of 4.4(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC), provided the compound is not metabolized by the organism(SRC).

The Koc of amisulbrom is estimated as 5100(SRC), using a log Kow of 4.4(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that amisulbrom is expected to be immobile in soil.

The Henry's Law constant for amisulbrom is 2.1X10-7 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that amisulbrom is expected to be essentially nonvolatile from water and moist soil surfaces(2). Amisulbrom is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.8X10-10 mm Hg(1).

Occupational exposure to amisulbrom may occur through inhalation and dermal contact with this compound at workplaces where amisulbrom is produced or used. (SRC)

In a rat metabolism study, Han Wistar rats were treated with a single gavage dose of (indole- (14)C) or (triazole- (14)C) amisulbrom (radiochemical purity > or = 95.2%) at 10 and 1000 mg/kg in aqueous 0.5% methy1cellulose. A series of experiments were then performed (4/sex/dose group) evaluating the excretion and tissue distribution of radioactivity at each dose level at up to 120 hours post-dose, and plasma and whole blood kinetics were determined. An additional experiment was conducted examining the excretion of radioactivity from bile duct-cannulated rats following a single oral dose of (indole-(14)C) NC-224 at 10 or 1000 mg/kg. To examine the distribution of radioactivity in tissues over time, rats were also dosed with (indole- (14) C) amisulbrom at 10 or 1000 mg/kg and 3 rats/sex/time point were then sacrificed at 2 and 24 hours post-dose (10 mg/kg) or 12 and 72 hours post-dose (1000 mg/kg). Excreta and tissue/organ samples from these experiments were radioassayed, and selected pooled samples of feces, urine, bile, liver, and plasma were analyzed to determine the metabolic profile. Radioactivity was not detectable in expired air in a preliminary study. The overall recovery of the radioactivity was 90-108% of the administered dose for both the 10 and 1000 mg/kg doses, and the pattern of excretion was similar between sexes for the two (14)C-labels. Fecal excretion was the major route of elimination. For the 10 mg/kg dose groups, fecal excretion accounted for 80-98% of the administered dose, while urine accounted for 10-14%. Radioactivity remaining in the carcass and tissues at 120 hours post-dose accounted for <0.5%. For the 1000 mg/kg dose groups, fecal excretion accounted for 89-100% of the administered dose, urine accounted for 1-3% of the administered dose, and radioactivity remaining in the carcass at 120 hours post-dose accounted for 0.05%. At both dose levels, the majority of excretion occurred from 0-48 hours post-dose. The overall total recovery from bile duct cannulated rats was 92-97% of the administered dose, and the patterns of absorption and excretion were similar between sexes. Data from the bile duct cannulated rats indicate that 49-50% of the administered dose was absorbed from the gastro-intestinal tract at 10 mg/kg; however, in contrast, only 5% of the administered dose was absorbed at the 1000 mg/kg dose level, indicating that gastro-intestinal absorption was saturated at the high dose. In the 10 mg/kg dose group, biliary excretion accounted for 40-41 % of the administered dose and 44% of the administered dose was unabsorbed test material eliminated in the feces. Only 9% of the administered dose was in the urine. At the 1000 mg/kg dose, feces accounted for 85-86% of the administered dose, and bile and urine each accounted for 1-3% of the administered dose. The time to maximum concentration in plasma (T max) occurred at 2-6 hours post -dose for the 10 mg/kg groups and 6-12 post-hours in the 1000 mg/kg group, and maximum plasma concentrations (Cmax) were 2-6 Ilg equiv./g for the 10 mg/kg group and 12-30 Ilg equiv./g in the 1000 mg/kg group. The elimination half-life was 18-35 hours at 10 mg/kg and 8-13 hours at 1000 mg/kg. For the triazole labeled material the T max was delayed especially at the 1000 mg/kg dose group. At all the time points, the concentrations of (14)C-residues in tissues (excluding the GI tract) were typically highest in liver followed by kidneys, and the distribution of (14)C-residues among tissues was generally similar between sexes. Residue levels increased with dose, but the increases were not proportional to the increase in the dose level. By 120 hours post-dose, only minor amounts of radioactivity "0.5% administered dose) were detectable in a few organs, such as kidneys and liver.

In a rat metabolism study, Han Wistar rats were treated with a single gavage dose of (indole- (14) C) or (triazole- (14)C) amisulbrom (radiochemical purity > or = 95.2%) at 10 and 1000 mg/kg in aqueous 0.5% methy1cellulose. A series of experiments were then performed (4/sex/dose group) evaluating the excretion and tissue distribution of radioactivity at each dose level at up to 120 hours post-dose, and plasma and whole blood kinetics were determined. An additional experiment was conducted examining the excretion of radioactivity from bile duct-cannulated rats following a single oral dose of (indole-(14)C) NC-224 at 10 or 1000 mg/kg. To examine the distribution of radioactivity in tissues over time, rats were also dosed with (indole- (14) C) amisulbrom at 10 or 1000 mg/kg and 3 rats/sex/time point were then sacrificed at 2 and 24 hours post-dose (10 mg/kg) or 12 and 72 hours post-dose (1000 mg/kg). Excreta and tissue/organ samples from these experiments were radioassayed, and selected pooled samples of feces, urine, bile, liver, and plasma were analyzed to determine the metabolic profile. ... Parent compound was the major (14)C-residue identified in feces of both sexes and (14)C-labels, accounting for 40-52% of the administered dose at 10 mg/kg and 83-89% at 1000 mg/kg. Other components/metabolites isolated from feces, urine and bile each accounted for <5% of the administered dose, with the exception of one component isolated from the bile of the low-dose rats that accounted for 5.3% of the administered dose. This component was tentatively identified as an unspecified conjugate of Metabolite IT-2. In addition to parent, nine primary metabolites and a glucuronide conjugate of one metabolite were identified in urine, feces and/or bile. Two of these metabolites (IT-4 and IT-5) were also identified as being the major (14)C-residues in liver (each 12-20% of the total radioactive residues; TRR in liver) and plasma (each 14-56% of the TRR in blood) at Tmax. Based on the metabolic profile, the metabolism of amisulbrom in the rat involves a series of reactions including cleavage of the sulfonyl amino side chain on the triazole ring, debromination, oxidation/hydroxylation, limited cleavage of the sulfonyl bridge between the indole and triazole moieties, indole ring opening, and conjugation of primary metabolites. The major route of metabolism of amisulbrom in rats appears to involve the initial cleavage of the sulfonylamino side to form IT-4 and it subsequent hydroxylation to IT-5, followed by further degradation or conjugation of these primary metabolites.

In a rat metabolism study, Han Wi star rats were treated with a single gavage dose of (indole- (14) C) or (triazole- (14)C) amisulbrom (radiochemical purity > or = 95.2%) at 10 and 1000 mg/kg in aqueous 0.5% methy1cellulose. ... The elimination half-life was 18-35 hours at 10 mg/kg and 8-13 hours at 1000 mg/kg.

Amisulbrom ... is an oomycete-specific fungicide which acts by inhibiting the mitochondrial respiration within the fungus target species.

/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 /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's 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/

1H-1,2,4-triazole-1-sulfonamide, 3-((3-bromo-6-fluoro-2-methyl-1H-indol-1-yl)sulfonyl)-N,N-dimethyl-

The active ingredient for use on grape and tomato is formulated as a suspension concentrate for foliar applications.|Technical is 99% (nominal)|Suspension concentrates.

Amisulbrom is not currently registered in the United States; however tolerances have been established for commodities imported into the US. Amisulbrom is registered for use on grape and potatoes grown in several European countries, and a tomato use is currently under review in the European Union.

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

Amisulbrom has known environmental transformation products that include 3-bromo-6-fluoro-2-methyl-1-(1H-1,2,4-triazole-3-ylsulfonyl)indole.|Amisulbrom has known environmental transformation products that include IT-11, IT-14, IT-2, IT-4, IT-5, and IT-9.