化合物详情

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), butocarboxim, which has a vapor pressure of 7.95X10-5 mm Hg at 20 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase butocarboxim 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 15 hours(SRC), calculated from its rate constant of 2.5X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase butocarboxim may be removed from the air by wet and dry deposition(SRC). Butocarboxim was found to photodegrade on sterilized soil surfaces when exposed to sunlight(4), but...

Using a structure estimation method based on molecular connectivity indices(1), the Koc for butocarboxim can be estimated to be 37(SRC). According to a classification scheme(2), this estimated Koc value suggests that butocarboxim is expected to have very high mobility in soil.

Half-lives in soils were reported as 1-8 days(1).

An estimated BCF of 1.4 was calculated for butocarboxim(SRC), using a log Kow of 1.1(1) and a regression-derived equation(2). A BCF of 42 has been reported for aldicarb(4), a pesticide with a similar structure to butocarboxim. According to a classification scheme(3), BCF values <30 suggest a low potential for bioconcentration in aquatic organisms and values of 30-100 suggests the potential for bioconcentration in aquatic organisms is moderate (SRC), provided the compound is not altered physically or chemically after being released into the environment (SRC).

The Henry's Law constant for butocarboxim is 5.70X10-10 atm-cu m/mole(SRC) derived from its vapor pressure, 7.95X10-5 mm Hg(1), and water solubility, 35,000 mg/l(1). This Henry's Law constant indicates that butocarboxim is expected to be essentially nonvolatile from water surfaces(2). This Henry's Law constant indicates that volatilization from moist soil surfaces is not expected(SRC). Butocarboxim is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

Chemical and physical properties of butacarboxim are similar to those of other oximcarbamates, e.g. thiofanox and aldicarb. On and in foliage in the field, butocarboxim oxidizes rapidly to the sulfone via the sulfoxide. Simultaneously, the carbamate group is hydrolysed to the corresponding oximes

/OTHER TERRESTRIAL SPECIES/ In laboratory tests the active ingredient of Co 755 proved harmless to predators such as lady bugs. The preliminary LD5O per os for bees lies at approximately 1 mug/animal.

Butocarboxim's former production in the US(1) may have resulted in its release to the environment through various waste streams; its former use as an insecticide(2) will have resulted in its direct release to the environment(SRC).

Occupational exposure to butocarboxim may have occurred through inhalation and dermal contact with this compound at workplaces where butocarboxim was produced or used. Occupational exposure and general population exposure should be low or non-existent since butocarboxim is no longer produced or used in the US. (SRC)

Butocarboxim's former production in the US may have resulted in its release to the environment through various waste streams; its former use as an insecticide will have resulted in its direct release to the environment. If released to air, a vapor pressure of 7.95X10-5 mm Hg at 20 °C indicates butocarboxim will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase butocarboxim 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 15 hours. Particulate-phase butocarboxim will be removed from the atmosphere by wet and dry deposition. If released to soil, butocarboxim is expected to have very high mobility based upon an estimated Koc of 37. Volatilization from...

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.

LC50 (rat) = 1,000 mg/m3/4h

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)

Butocarboxim 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/ Principal effects /of anticholinesterases as toxic components of insecticides/ on eye, whether from local contact or systemic poisoning, are miosis and spasm of accommodation for near vision. /Anticholinesterases/

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

LC50 Rat inhalation 1 mg/l air/4 hr