化合物详情

Pesticide Ecotoxicity Data from EPA: 48

LD50 Bobwhite quail (gavage) 28 mg/kg

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), chlorethoxyfos, which has a vapor pressure of 7.95X10-4 mm Hg at 20 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase chlorethoxyfos 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 4.2 hours(SRC), calculated from its rate constant of 9.2X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Chlorethoxyfos is not expected to absorb light with wavelengths >290 nm and is not expected to be susceptible to direct photolysis by sunlight(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc for chlorethoxyfos can be estimated to be 890(SRC). According to a classification scheme(2), this estimated Koc value suggests that chlorethoxyfos is expected to have low mobility in soil.

AEROBIC: Half-lives in soil at 25 °C of chlorethoxyfos in laboratory studies were 7 days in Handord sandy loam and 20 days in Flanagan loam(1). Field soil dissipation half-lives were reported in the range of 2-3 days(1).

An estimated BCF of 680 was calculated for chlorethoxyfos(SRC), using a log Kow of 4.59(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC).

The Henry's Law constant for chlorethoxyfos is estimated as 4.2X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that chlorethoxyfos is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 10 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 9 days(SRC). Chlorethoxyfos' Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). However, volatilization may be attenuated by adsorption to soil(SRC). Chlorethoxyfos is not expected to volatilize from dry soil surfaces...

The rate constant for the vapor-phase reaction of chlorethoxyfos with photochemically-produced hydroxyl radicals has been estimated as 9.3X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 4.2 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Half-lives for the hydrolysis of chlorethoxyfos are 4.3, 59, and 72 days at pH 5, 7, and 9, respectively(2). Chlorethoxyfos is not expected to absorb light with wavelengths >290 nm and is not expected to be susceptible to direct photolysis by sunlight(SRC).

Many of the organophosphorus insecticides are excreted in the milk ... /Organophosphorus insecticides/

The substance is very toxic to aquatic organisms. 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.

Chlorethoxyfos' production may result in its release to the environment through various waste streams; its use as an insecticide(1) will result in its direct release to the environment(SRC).

Secondary exposure of children through contact with their parents' contaminated clothing can also occur. /Organophosphorus pesticides/

Chlorethoxyfos' production may result in its release to the environment through various waste streams; its use as an insecticide will result in its direct release to the environment. If released to air, a vapor pressure of 7.95X10-4 mm Hg at 20 °C indicates chlorethoxyfos will exist solely as a vapor in the ambient atmosphere. Vapor-phase chlorethoxyfos 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 4.2 hours. If released to soil, chlorethoxyfos is expected to have low mobility based upon an estimated Koc of 890. Volatilization from moist soil surfaces is expected based upon an estimated Henry's Law constant of 4.2X10-6 atm-cu m/mole; however, volatilization may be attenuated by ad...

Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include 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. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.

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.

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LC50 (rat) = 0.58 ppm/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 - Organophosphate

The substance can be absorbed into the body in hazardous amounts by inhalation, through the skin and by ingestion.

Chlorethoxyfos is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. 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 inhibit...

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Oral Chronic Reference Dose Reference: OPP

/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).

LD50 Rat (male) oral 4.8 mg/kg

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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In a two-generation reproduction study, Crl:CD BR rats were fed diets containing Chlorethoxyfos at 0, 0.25, 1, 4 or 8 ppm. These doses were equivalent to 0,0.018, 0.074, 0.296 or 0.607 mg/kg/day in males and 0, 0.022, 0.09 1, 0.3 57 or 0.776 mg/kg/day in females, respectively. There was no increased sensitivity to pups over the adults. The parental/systemic NOEL was 4 ppm (0.296 mg/kg/day) and the LOEL was 8 ppm (0.607 mg/kg/day) based on increased incidence of tremors during lactation. For reproductive toxicity, the NOEL was 8 ppm (0.607 mg/kg/day); a LOEL was not established.

Pralidoxime. Before administration of pralidoxime, draw a blood sample (heparinized) for cholinesterase analysis (since pralidoxime tends to reverse the cholinesterase depression). Administration pralidoxime (Protopam, 2-PAM), a cholinesterase reactivator, in cases of severe poisoning by organophosphate pesticides in which respiratory depression, muscle weakness, and/or twitching are severe. When administered early (usually less than 48 hours after poisoning) pralidoxime relieves the nicotinic as well as the muscarinic effects of poisoning. Pralidoxime works by reactivating the cholinesterase and also by slowing the "aging" process of phosphorylated cholinesterase to a non-reactivatable form. ... Dosage of pralidoxime may be repeated in 1-2 hours, then at 10-12 hour intervals if needed....