3,5-크실릴 메틸카르밤산염

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]

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).

LC50 Carp > 40 mg/l/48 hr

LD50 Wild bird species 75 mg/kg

Terrestrial fate: in soil, hydrolyzed to 3,5-xylenol and N-methylcarbamic acid.

TERRESTRIAL FATE: 3,5-xylyl methylcarbamate degrades in soil both by biological and abiotic hydrolysis of the carbamate linkage, producing carbon dioxide and the corresponding phenol(1-2). The rate of hydrolysis is dependent both on the nature of soil and soil pH(1-2). The half-life of 3,5-xylyl methylcarbamate has been estimated to 12.8 days in a silt soil of pH 7.85 and 750 days in a peat soil of pH 5.90(2). Since the compound is stable towards sunlight(6), photolysis in soil should not be important. The estimated Koc value of 389(3,SRC) suggests that the insecticide will be moderately adsorbed onto soil(4). However, adsorption of 3,5-xylyl methylcarbamate onto soil has been experimentally found to be stronger than would be expected from the estimated Koc value(1). It has been postulated that 3,5-xylyl methylcarbamate forms a complex with humus materials in soil and the complex remains irreversibly adsorbed in soil(1). Therefore, leaching of the compound will become less and less important as the carbon content of the soil increases. Based on an estimated Henry's Law constant (H) of 3.91X10-8 atm-cu m/mole(5) and the relationship between H and volatility(3), volatilization of 3,5-xylyl methylcarbamate from moist soil will not be important(SRC).

AQUATIC FATE: As in the case of soil, both biotic and abiotic hydrolysis are expected to degrade 3,5-xylyl methylcarbamate in water, but no quantitative data on the rate of hydrolytic degradation are available. Due to its ability to bind strongly with humus materials(1-2), 3,5-xylyl methylcarbamate is expected to be present predominantly adsorbed onto suspended solids and sediment in water. Because 3,5-xylyl methylcarbamate is stable to sunlight(5), photodegradation is not important in water. Based on its estimated value of the Henry's Law constant(4), volatilization of 3,5-xylyl methylcarbamate from water may be unimportant(3,SRC). The bioconcentration factors for 3,5-xylyl methylcarbamate in catfish (Ictalurus punctatus), crayfish (Procambaru sp.) and snail (Physa sp.) have been determined to be 550, 104 and 260(2).

ATMOSPHERIC FATE: 3,5-Xylyl methylcarbamate in the vapor phase may react with photochemically produced hydroxyl radicals with an estimated half-life of 5.6 hrs(1,SRC). Particle-bound 3,5-xylyl methylcarbamate is likely to be removed from the atmosphere by dry deposition(SRC).

3,5-Dimethylphenyl methylcarbamate 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.

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)

Based on a log Kow of 2.23(1) and a regression equation(2), the Koc value for 3,5-xylyl methylcarbamate has been estimated to be 389(SRC). This Koc value suggests that the insecticide will be moderately adsorbed to soils(3). However, due to formation of strong complexes with humic matter in soils, 3,5-xylyl methylcarbamate has been found to remain strongly adsorbed onto soils(4-5).

With carbamate poisoning, plasma and red blood cell cholinesterase may be depressed, but usually return to normal within a few hours after exposure. /Carbamate poisoning/

Symptoms and signs of carbamate poisoning: Constriction of pupils; Salivation; Profuse sweating; Lassitude; Muscle incoordination; Nausea; Vomiting; Diarrhea; Epigastric pain; Tightness in chest. /Carbamates; from table/

Used as an insecticide on rice and tea; [HSDB]

Farming (Pesticides) [Category: Industry]

... Insecticide

Control of leafhoppers and planthoppers on rice, and tea green leafhoppers on tea.

3,5-Dimethylphenyl methylcarbamate is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.

Emulsifiable concentrate (200 g ai/l), wettable powder (500 g/kg), dustable powder (20 g/kg), microgranule (30 g/kg)

Mixed formulations: (XMC +) carbaryl; malathion; fenthion; edifenphos; diazinon; kasugamycin.