化合物详情

LD50 Quail oral 43 mg/kg.

ATMOSPHERIC FATE: Based on a reported vapor pressure of 1.7X10-4 mm Hg at 25 °C(1), thiofanox should exist almost entirely in the vapor phase in the ambient atmosphere(2,SRC). Vapor-phase thiofanox is expected to degrade rapidly in the ambient atmosphere by reaction with photochemically produced hydroxyl radicals; the half-life for this reaction is about 5.1 hr(3,SRC).

Based on a reported water solubility of 5.2X10+3 mg/l at 22 °C(1,2) and a recommended regression derived equation(3), a Koc for thiofanox can be estimated to be approximately 39.5(SRC) indicating that thiofanox has very high mobility in soil and will leach(4).

Based on a reported water solubility of 5.2X10+3 mg/l at 22 °C(2,3) and a recommended regression derived equation(1), the BCF for thiofanox can be estimated to be approximately 4.96(SRC). This BCF value suggests that bioconcentration in aquatic organisms is not significant(SRC).

Based on a reported vapor pressure of 1.7X10-4 mm Hg at 25 °C(1) and water solubility of 5.2X10+3 mg/l at 22 °C(1,2), a Henry's Law constant can be estimated to be approximately 9.39X10-7 atm cu-m/mole at 25 °C(3,SRC). This value of Henry's Law constant suggests that thiofanox will slowly volatilize from environmental waters(3). Based on this value of Henry's Law constant, the volatilization half-life from a model river (1 m deep flowing 1 m/sec with a wind velocity of m/sec) can be estimated to be approximately 15.8 yrs(3,SRC).

In acidic & neutral solutions, thiofanox was stable. At pH 10, oxidation to the sulfoxide occurred. Hydrolysis of thiofanox to the corresponding oxime (3,3-dimethyl-1-methylthio-2-butanone oxime) was insignificant. Partial hydrolysis of thiofanox sulfoxide to the corresponding oxime occurred. Hydrolysis of the thiofanox sulfone apparently occurred to a greater extent & was the principal source of the oxime-sulfone (3,3-dimethyl-1-methylsulfonyl-2-butanone oxime). Loss of oxime was detected after 5 days with formation of a keto-sulfone.

Thiofanox is a systemic acaricide and insecticide(1); however, it is not registered for use in the U.S.(2).

Thiofanox is a systemic acaricide and insecticide; however, it is not registered for use in the U.S.(2). Workers involved in the application of the chemical will probably be exposed through inhalation or through dermal contact(SRC).

Thiofanox is released to the environment through its use as a pesticide. If released to the atmosphere, vapor-phase thiofanox is expected to degrade relatively rapidly by reaction with photochemically produced hydroxyl radicals (estimated half-life of 5.1 hrs). If released to soil, thiofanox is expected to leach significantly based on an estimated Koc value of 39.5. The major route of metabolism for thiofanox in soil is oxidation to its sulfoxide and further, to the sulfone. Subsequently, hydrolysis to the oxime may take place by analogy to the structurally similar carbamate, aldicarb; however, thiofanox is relatively stable to hydrolysis under environmental conditions. In water, bioconcentration (BCF of 4.96), adsorption to sediment and volatilization are not expected to be significant...

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.

WHEN 2,2-DIMETHYL-1,3-BENZODIOXOL-4-YL-N-METHYLCARBAMATE WAS APPLIED SIMULTANEOUSLY WITH GRANULAR 3,3-DIMETHYL-1-METHYLTHIO-2-BUTANONE O-METHYLCARBAMOYLOXIME ON SUGAR BEETS IT CONTROLLED APHIS FABAE AND HAD A SYNERGISTIC ACTION BETTER THAN DID EITHER CMPD APPLIED INDIVIDUALLY.

LC50 (rat) = 70 mg/m3

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)

Thiofanox 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 esteras...

Oral Subchronic Chronic Reference Dose Reference: HEAST Current

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

LD50 Sylvilagus (Rabbit) dermal 39 mg/kg.

Fraction of Contaminant Absorbed Dermally from Soil: 0.1

Fraction of Contaminant Absorbed Dermally from Soil: 0.1