化合物详情

LC50 Daphnia 0.22 mg/L/48 hr /Conditions of bioassay not specified/

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ethiofencarb, which has a vapor pressure of 7.1X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase ethiofencarb 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 16 hours(SRC), calculated from its rate constant of 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase ethiofencarb may be removed from the air by wet and dry deposition(SRC). While ethiofencarb was found to photodegrade in aqueous and nonaqueous solution(4,5) and on soil(6),...

Using a structure estimation method based on molecular connectivity indices(1), the Koc for ethiofencarb can be estimated to be 230(SRC). According to a classification scheme(2), this estimated Koc value suggests that ethiofencarb is expected to have moderate mobility in soil.

Five weeks after application of a 10% 14C-carbonyl-labeled ethiofencarb granular formulation to soil under greenhouse conditions, the metabolites (sulfoxide and sulfone) were found in the soil, and the parent compound was no longer detectable(1). Radiochemical determination of the degradation rate showed that ethiofencarb had a half-life of about 2 weeks under greenhouse conditions(1). Similar rates of degradation were determined under field conditions(1).

An estimated BCF of 7.4 was calculated for ethiofencarb(SRC), using a log Kow of 2.04(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC). In addition, ethiofencarb undergoes hydrolysis(4,5) and photolysis(6) in aquatic environments, and bioconcentration is not expected to be a significant fate process(SRC).

The Henry's Law constant for ethiofencarb is 1.2X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 7.1X10-6 mm Hg(1), and water solubility, 1820 mg/l(2). This Henry's Law constant indicates that ethiofencarb is expected to be essentially nonvolatile from water surfaces(3). Ethiofencarb's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Ethiofencarb 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 ethiofencarb with photochemically-produced hydroxyl radicals has been estimated as 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 16 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). At pH 6, the half-life of ethiofencarb was 3.2X10+4 seconds (8 hours) at 50 °C and was not degraded at 20 °C(2). At pH 9, the half-lives of ethiofencarb were 1.1X10+6 seconds (300 hours) at 20 °C and 1.1X10+3 seconds (3.0 hours) at 50 °C(2). At pH 2, ethiofencarb was not degraded at any of the studied temperatures(2). At pH 12, degradation was instantaneous at 20 and 50 °C(2). The half-lives of ethiofencarb by photodegradation in water were...

...Milk collected from the /Holstein/ cow 6 hr after treatment /with a single oral dose (0.5 mg/kg) of ring (14C) croneton/ contained 128 ppb 14C residues; 60% of this was as the free carbamate metabolites, croneton sulfoxide and sulfone. ...

/PLANTS/ Phytotoxic to anthurium and begonias.

The substance is very toxic to aquatic organisms. This substance may be hazardous to the environment. Special attention should be given to birds. This substance does enter the environment under normal use. Great care, however, should be taken to avoid any additional release, for example through inappropriate disposal.

Ethiofencarb's former production may have resulted in its release to the environment through various waste streams; its use as an insecticide(1) resulted in its direct release to the environment(SRC).

Occupational exposure and general population exposure should be low or non-existent since ethiofencarb is no longer produced or used. (SRC)

Ethiofencarb's former production may have resulted in its release to the environment through various waste streams; its former use as an insecticide resulted in its direct release to the environment. If released to air, a vapor pressure of 7.1X10-6 mm Hg at 25 °C indicates ethiofencarb will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase ethiofencarb 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 16 hours. Particulate-phase ethiofencarb will be removed from the atmosphere by wet and dry deposition. While ethiofencarb was found to photodegrade in aqueous and nonaqueous solution and on soil, no data were found regarding the direct photolysis of e...

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.

LCLo (rat) = 97 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)

Ethiofencarb 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/ The clinical picture of carbamates intoxication results from accumulation of ACh at nerve endings. ...The signs and symptoms can be categorized into the following 3 groups: (a) Muscarinic manifestations - increased bronchial secretion, excessive sweating, salivation, and lachrymation; pinpoint pupils, bronchoconstriction, abdominal cramps (vomiting and diarrhea); and bradycardia. (b) Nicotinic manifestations - fasciculation of fine muscles (in severe cases, diaphragm and respiratory muscles also involved); and tachycardia. (c) Central nervous system manifestations- headache, dizziness, anxiety, mental confusion, convulsions, and coma; and depression of respiratory center. All these signs and symptoms can occur in different combinations and can vary in onset and sequ...

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