2,3-ジヒドロ-2,2-ジメチル-7-[N-(N-メチル-N-ブトキシカルボニルアミノチオ)-N-メチルカルバモイルオキシ]ベンゾフラン

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

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

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

The protective clothing should be kept in separate places where it cannot be contaminated with toxic chemicals. It should be forbidden to keep this clothing in living quarters. Protective clothing must be washed at least once a week and each time it is contaminated with pesticides. Before washing the clothing should be soaked for several hours in a calcium carbonate solution. /Pesticides/

Smoking, eating, and drinking before washing should be absolutely prohibited when any pesticide ... is being handled or used. /Pesticides/

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.

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 nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).

LD50 Quail oral <25 mg/kg

LD50 Duck oral <25 mg/kg

LC50 Daphnia 1.8 ug/l/48 hr

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1600(SRC), determined from a structure estimation method(2), indicates that furathoicarb is expected to have low mobility in soil(SRC). Volatilization of furathiocarb from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 1.3X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 2.9X10-8 mm Hg(3) and water solubility, 11 mg/l(3). Furathiocarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). In soil, furathiocarb is rapidly decomposed to carbofuran(3). The half-life of [14C-methyl]-furathiocarb in Montardon soil after pretreatment with various methylcarbamates is 3-6 days(4).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1600(SRC), determined from a structure estimation method(2), indicates that furathiocarb is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon a Henry's Law constant of 1.3X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 2.9X10-8 mm Hg(4), and water solubility, 11 mg/l(4). According to a classification scheme(5), an estimated BCF of 830(SRC), from its log Kow of 4.70(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is high(SRC). The half-life for furathiocarb in water at pH 9 is 4 days(4). 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(4). Aqueous suspensions of thiodicarb are decomposed in sunlight(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 aqueous suspension(2); however, no data were found regarding the direct photolysis of either of these chemicals by sunlight in air(SRC).

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 esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

/BIRDS and MAMMALS/ As a rule, birds are not very sensitive to carbamates... . /Carbamate pesticides/

/AQUATIC SPECIES/ Although carbamates are not very stable under aquatic conditions, and will not persist long in this environment, some carbamates are highly toxic for invertebrates and fish, others /are/ much less /toxic/. Some /carbamates/ bioaccumulate in fish, mainly because the metabolism is slow in /these animals/. /Carbamate pesticides/

/OTHER TERRESTRIAL SPECIES/ Toxic to bees.

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)

SRP: Workers should undergo an annual medical exam. Contraindications for work with organophosporous pesticides are organic diseases of the CNS, mental disorders and epilepsy, and pronounced endocrine disorders. Blood cholinesterase, both plasma and RBC, must be determined before work starts. In the event of prolonged work periods, this activity should be determined at intervals of 3-4 days. Persons exhibiting a fall in cholinesterase activity of 25% or more must be transferred to other work where they are not exposed until cholinesterase activity is restored. /Organophosphorous pesticides; Anticholinesterase pesticides/

Measurement of whole blood-AChE is the most widely adopted method for monitoring the effects of occupational exposure to organophosphorus insecticides. Physiological variations in blood ChE levels occur in a healthy person and are seen among a population. It has been estimated that the coefficient of variation for AChE activity in samples from an individual is 8-11%, and that a decrease of 23% below pre-exposure level may, therefore, be considered significant. If the average of several pre-exposure values were available, then a decrease of 17% would be significant. It has been recommended that, if measured activity is reduced by 30% or more of the pre-exposure value, AChE measurements should be repeated at appropriate intervals to confirm the results. Depressions of AChE or ChE in excess of 20-25% are considered diagnostic of exposure but not, necessarily, indicative of hazard. Depressions of 30-50% or more are considered indicators for removal of an exposed individual from further contact with pesticides until levels return to normal. /Organophosphorus pesticides; Anticholinesterase pesticides/

...Organophosphorus pesticides may undergo hydrolysis in vivo to yield substituted phosphoric acids that are subsequently excreted in urine. Advances in gas chromatography and combined gas chromatography/mass spectrometry (GC/MS) have made it possible to analyse the urine of exposed persons for the presence of appropriate metabolites. It is usually necessary to preserve the sample by the addition of chloroform, to concentrate or extract the metabolite(s), and to convert them to suitably-volatile derivatives that can be detected by GC. Obviously, access to a well-equipped analytical laboratory, capable of the quick processing of samples, is a necessary factor if monitoring by urine analysis is proposed. However, in some cases, simpler and sensitive colorimetric tests are available for screening the urine of exposed persons. Thus, 4-nitrophenol can be measured directly in the urine of workers exposed to parathion. Consideration of the concentration of metabolite(s) in the urine can be helpful in determining patterns of exposure, and these concentrations can be calibrated against the effects on AChE for a particular pesticide. However, the time-course and peak of excretion of metabolites appears to vary according to dose, so that serial sampling and analyses of urine are desirable. Levels of metabolite alone cannot be considered a guide to hazard. This is obvious when it is realized that pesticides that have very different toxicities may yield identical acidic metabolites. Thus, the level of metabolites in urine, after exposure to sufficient amounts of the very toxic parathion-methyl to depress blood-AChE to 50%, will be much lower than that of the identical metabolites, following exposure to the related fenitrothion, which is about 40 times less toxic. /Organophosphorus pesticides; Anticholinesterase pesticides/

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.

Used as systemic soil insecticide in maize, oilseed rape, sorghum, sugar beet, sunflowers, and vegetables; [HSDB]

Banned in the EU for use as a biocide and agricultural insecticide; [eChemPortal: ESIS]

Farming (Pesticides) [Category: Industry]

Systemic insecticide. For soil-dwelling insects and early season pests.

Control of soil-dwelling insects in maize, oilseed rape, sorghum, sugar beet, sunflowers, and vegetables. Applied as a foliar, soil, or seed treatment.

Furathiocarb is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.

Granules, emulsifiable concentrate, capsule suspension

Liquid seed treatment

Tradenames: 'Deltanet' (Syngenta); 'Promet' (Syngenta).