メチルカルバミド酸m-トリル

Procedures for carbamate pesticides, solid, include the following. Stay upwind and keep out of low areas. Wear positive pressure breathing apparatus and special protective clothing. Move container from fire area if you can do it without risk. Fight fire from maximum distance. Dike fire control water for later disposal; do not scatter the material.

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]

Avoid inhalation. For solid carbamate pesticides, use the following procedures. For small spills, take up with sand or other noncombustible absorbent material and place in containers for later disposal. For small dry spills, with clean shovel place material into clean, dry container and cover; move container from spill area. For large spills, dike far ahead of spill for later disposal. Do not touch spilled material. Use water spray to reduce vapors. (EPA, 1998)

0.44 [mg/m3]

4.8 [mg/m3]

53 [mg/m3]

For emergency situations, wear a positive pressure, pressure-demand, full facepiece self-contained breathing apparatus (SCBA) or pressure- demand supplied air respirator with escape SCBA and a fully-encapsulating, chemical resistant suit. (EPA, 1998)

When handling metolcarb, a respirator with gas absorbent should be used.

/Protective clothing includes/ Gloves, gas mask or respiratory, goggles, and clothing. When handling, wear a respiratory with gas absorbent. Avoid skin and eye contact.

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.

The combined toxicity of malathion, 2-sec-butylphenylmethylcarbamate, m-tolymethylcarbamate, and 3,4-xylyl-methylcarbamate was studied in mice and rats. ICR mice and male Fischer 344 rats were exposed orally to a suspension of insecticides at five dose concentrations to determine the median lethal dose (LD50); animals were observed for mortality at least 7 days after dosing. ... Mice were killed, brains were homogenized, and brain acetylcholinesterase activity was determined. Of all combinations tested, only malathion plus 2-sec-butylphenylmethylcarbamate exhibited a marked synergism in acute toxicity in male mice; other combinations with m-tolymethylcarbamate, or 3,4-xylyl-methylcarbamate did not show any significant potentiation of toxicity in male mice. Female mice responded similarly to insecticide synergism. In rats, the synergism was relatively less potent than in mice. Symptoms of muscle fasciculation, increased salivation, urination, convulsion, and dyspnea were similar in mice and rats. Significant time differences in mortality after dosing were observed among the insecticides and between rats and mice. ...

Succinylcholine, other cholinergic agents, and aminophylline are contraindicated. /Carbamates and related compounds/

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).

TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated Koc value of 200(SRC), determined from a measured log Kow of 1.7(2) and a regression-derived equation(3), indicates that metolcarb is expected to have moderate mobility in soil(SRC). Volatilization of metolcarb from moist soil surfaces is not expected to be important(SRC) given an estimated Henry's Law constant of 8.4X10- 10 atm-cu m/mole(SRC) from its experimental values for vapor pressure, 1.0X10-5 mm Hg(4), and water solubility, 2.6X10+3 mg/l(5). Metolcarb is not expected to volatilize from dry soil surfaces based on a measured vapor pressure of 1.0X10-5 mm Hg(4). Biodegradation of metolcarb in soil is expected to be an important process(SRC), based on microbial hydrolysis half-lives in six different soils ranging from 3.8 to 55 days(6).

AQUATIC FATE: Based on a recommended classification scheme(1), an estimated Koc value of 200(SRC), determined from a measured log Kow of 1.7(2) and a recommended regression-derived equation(3), indicates that some adsorption of metolcarb to suspended solids and sediment in water is expected(SRC). Metolcarb is not expected to volatilize from water surfaces(3,SRC) based on an estimated Henry's Law constant of 8.4X10-10 atm-cu m/mole(SRC) from its experimental values for vapor pressure, 1.0X10-5 mm Hg(4), and water solubility, 2.6X10+3 mg/l(5). According to a classification scheme(6), an estimated BCF of 12(3,SRC), from a measured log Kow(2), suggests that bioconcentration in aquatic organisms is low(SRC). Hydrolysis of metolcarb is expected to be an important process in aquatic systems where the pH is greater than 7(SRC); half-lives of 2.5 and 25 days were estimated for metolcarb at pHs 8 and 7, respectively(7). Biodegradation of metolcarb in aquatic systems may be important(SRC); metolcarb reached 36 to 41% of its theoretical BOD over a period of 4 weeks using an activated sludge inoculum(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), metolcarb, which has a measured vapor pressure of 1.0X10-5 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase metolcarb 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 about 1.8 days(3,SRC). Particulate-phase metolcarb may be physically removed from the air by wet and dry deposition(SRC).

Metolcarb 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)

The Koc of metolcarb is estimated as approximately 200(SRC), using a measured log Kow of 1.7(1) and a regression-derived equation(2,SRC). According to a recommended classification scheme(3), this estimated Koc value suggests that metolcarb is expected to have moderate mobility in soil(SRC).

Metolcarb's production and use as an insecticide to control leafhoppers, planthoppers, citrus mealybugs, onion thrips, Mediterranean fruit flies, pink bollworms, cotton aphids(1), and codling moths(2) will result in its release to the environment(SRC).

Metolcarb reached 36 to 41% of its theoretical BOD over a period of 4 weeks using an activated sludge inoculum(1). Microbial hydrolysis half-lives (days) for metolcarb in 6 different soils were (soil type, pH): 7.9 (silt, 7.85); 14 (silt loam, 7.20); 15 (silt loam, 7.05); 3.8 (silt loam, pH 6.85); 7.6 (sand, 5.20); and 55 (peat, 5.90)(2).

P190; As stipulated in 40 CFR 261.33, when metolcarb, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).