化合物详情

USDA APHIS Chemical Effects: collection=usda_chemeffect&query_type=synonym&query='^65907-30-4$'

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), furathiocarb, which has a vapor pressure of 2.9X10-8 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase furathiocarb is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 10 hours(SRC), calculated from its rate constant of 3.8X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase furathiocarb may be removed from the air by wet and dry deposition(SRC). Thiodicarb, a chemical that is structurally similar to furathiocarb, is susceptible to photolysis in...

Using a structure estimation method based on molecular connectivity indices(1), the Koc for furathiocarb can be estimated to be 1,600(SRC). According to a classification scheme(2), this estimated Koc value suggests that furathiocarb is expected to have low mobility in soil.

In soil, furathiocarb is rapidly decomposed to carbofuran(1). The half-life of [14C-methyl]-furathiocarb in Montardon soil after pretreatment with various methylcarbamates is 3-6 days(2). Within a week, all of the furathiocarb applied to a carbofuran adapted soil was degraded, compared with 10% degradation in unadapted soil after a week(3).

An estimated BCF of 830 was calculated for furathiocarb(SRC), using a log Kow of 4.70(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 altered physically or chemically after being released into the environment(SRC).

The Henry's Law constant for furathiocarb is 1.3X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 2.9X10-8 mm Hg(1), and water solubility, 11 mg/l(1). This Henry's Law constant indicates that furathiocarb is expected to be essentially nonvolatile from water surfaces(2). Furathiocarb's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Furathiocarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

The rate constant for the vapor-phase reaction of furathiocarb with photochemically-produced hydroxyl radicals has been estimated as 3.8X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 10 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The half-life for furathiocarb in water at pH 9 is 4 days(2). Thiodicarb, a chemical that is structurally similar to furathiocarb, is stable in water at pH 6, and is rapidly hydrolyzed at pH 9 and slowly at pH 3(2). Aqueous suspensions of thiodicarb are decomposed in sunlight(2).

Furathiocarb was analyzed for but not detected (detection limit=0.2 mg/kg) in the Danish National Pesticide Monitoring Program 1995-1996 for selected food commodities(1).

/OTHER TERRESTRIAL SPECIES/ Toxic to bees.

Furathiocarb's production may result in its release to the environment through various waste streams; its use as an insecticide(1) results in its direct release to the environment(SRC). It is not registered for use in the US(2).

Occupational exposure to furathiocarb may occur through inhalation and dermal contact with this compound at workplaces where furthiocarb is produced or used. Monitoring data indicate that exposure to the general public is limited. (SRC)

Furathiocarb's production may result in its release to the environment through various waste streams; its use as an insecticide results in its direct release to the environment. It is not registered for use in the US. If released to air, a vapor pressure of 2.9X10-8 mm Hg at 25 °C indicates furathiocarb will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase furathiocarb will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 10 hours. Particulate-phase furathiocarb will be removed from the atmosphere by wet and dry deposition. Thiodicarb, a chemical that is structurally similar to furathiocarb, is susceptible to photolysis in aqueous suspension; however,...

As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

LC50 (rat) = 214 mg/m3/4h

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central...

Other Poison - Carbamate

Inhalation (L793); oral (L793); dermal (L793)

Furathiocarb is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine este...

/SIGNS AND SYMPTOMS/ Principal effects /of anticholinesterases as toxic components of insecticides/ on eye, whether from local contact or systemic poisoning, are miosis and spasm of accommodation for near vision. /Anticholinesterases/

No indication of carcinogenicity to humans (not listed by IARC).

LC50 Rat inhalation 0.214 mg/l air/4 hr

/GENOTOXICITY/ The carbamate insecticides benfuracarb, carbosulfan and furathiocarb were investigated in the mouse bone marrow micronucleus assay to establish whether they show cytogenetic activity in vivo. Two doses of each substance were administered intraperitoneally to NMRI mice. All of the three substances led to a positive micronucleus response in polychromatic erythrocytes of the bone marrow at different expression times. While furathiocarb and carbosulfan showed similar patterns of the time-dependence of the micronucleus formation with maximum values after 72 hr, benfuracarb exhibited a different behavior with the maximum increase taking place within 24 hr after substance application. In furathiocarb-treated animals the ratio of normochromatic to polychromatic erythrocytes showe...

The clinical approach to carbamate toxicity is similar to that for organophosphate poisoning; the major exception is that pralidoxime usually is not recommended. /Carbamates/