化合物详情

Pesticide Ecotoxicity Data from EPA: 95

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), oxamyl, which has a vapor pressure of 0.00023 mm Hg at 20-25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase oxamyl 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 1.4 days(SRC), calculated from its rate constant of 2.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Oxamyl is not expected to absorb light at wavelengths >290 nm, and would not be expected to be susceptible to direct photolysis by sunlight in air(SRC).

An experimental study using Arrendondo, Cecil, and Webster soils found Koc values of 8, 6, and 10, respectively(1). According to a classification scheme(2), these Koc values suggest that oxamyl is expected to have very high mobility in soil. Laboratory experiments show that oxamyl is fairly mobile in muck, loamy sand, and 2 silt loam soils (with movement faster in the loamy sand and slowest in the muck)(3). However, field leachate studies in silt loam, loamy sand, and fine sand show that movement is not that extensive even after 3 to 5 months with very little oxamyl below 15 inches(3). This difference may be attributed to oxamyl degradation losses being greater than movement through soil despite large rainfall levels(3).

Using loamy sand (pH 6.8) from North Carolina and a sandy soil (pH 6.4) from Florida, half-lives for the degradation of oxamyl were 11 and 15 days, respectively, under aerobic conditions(1). Under anaerobic conditions, a half-life of 6 days was obtained with Keyport silt loam (pH 4.7)(1). The decomposition of oxamyl in soils followed first-order kinetics, the half-life ranging from 4-33 days in a Bet Dagan soil(2). Less than 5% of the oxamyl remained after one day in four water saturated, anaerobic subsoils at 10 °C(3). Half-lives in aerobic soils ranged from 21 days in loamy fine sand to 415 days in fine sand at 10 °C(3). Oxamyl in moist soils (Arrendondo sand, Cecil sandy loam, and Genada silt loam) was rapidly mineralized to CO2; mineralization half-lives for 14C oxamyl ranged from 2...

An estimated BCF of 3.1 was calculated for oxamyl(SRC), using a log Kow of -0.48(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).

The Henry's Law constant for oxamyl is 2.37X10-10 atm-cu m/mole(SRC), derived from its vapor pressure, 0.00023 mm Hg(1), and water solubility, 2.8X10+5 mg/l(2). This Henry's Law constant indicates that oxamyl is expected to be essentially nonvolatile from water surfaces(3). Oxamyl's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Oxamyl 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 oxamyl with photochemically-produced hydroxyl radicals has been estimated as 2.3X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1.4 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The half-lives for the hydrolysis of oxamyl in sterile water-ethanol (99:1) phosphate buffers at 25 °C were 300 weeks, 17 weeks, 1.6 weeks, and 1.4 days at pHs of 4.5, 6.0, 7.0 and 8.0 respectively(2). The rate constant for the hydrolysis of oxamyl has been determined to be 169 L/min-mol(3). Oxamyl was found to be stable at pH 4.7 for at least 11 days and hydrolyzed slowly in neutral solution (pH 6.9) with 3 and 9% hydrolysis occurring after 24 a...

SURFACE WATER: Oxamyl was found in 2% of samples with concentration >0.1 ug/l in estuaries and coastal waters in England and Wales in 1994(1).

In a study conducted from 1982-1984 sampling dietary intake of 25-30 yr old males, oxamyl was found in 2 of 201 adult foods sampled at a total of 0.012 ug; 83% of total the oxamyl intake was from cucumbers(1). Oxamyl was found in two ready-to-eat foods at an average concentration of 0.021 ug/g: once in cucumbers at 0.031 ug/g and once in raw sweet green pepper at 0.011 ug/g(2). Oxamyl was found in 4 out of 1219 samples of domestic (US) tomatoes at a maximum concentration of 0.12 ppm and twice in imported tomatoes at trace concentrations(3). Oxamyl has been detected as residues during the 1978-82, 1983-86, and 1994 US regulatory monitoring studies, however, concentrations were not reported(4,5,6). In a 1985-1991 US study of domestic foods which may be eaten by infants/children, oxamyl wa...

Radioactive thiocyanate was the major metabolite identified in the milk... /of lactating goats orally administered five consecutive daily doses of 31 ppm oxamyl/.

/FIELD STUDIES/ New Zealand white rabbits maintained in outdoor pens were exposed to three simulated field-spray applications of oxamyl at 3.36 kg/ha. No clinical signs of toxicity, behavioral alterations, or gross pathologies were observed in any rabbits 5 days after the last treatment.

Oxamyl's production may result in its release to the environment through various waste streams; its use as an insecticide, acaricide, and nematicide(1) and will result in its direct release to the environment(SRC).

Occupational exposure to oxamyl may occur through inhalation and dermal contact with this compound at workplaces where oxamyl is produced or used. Monitoring data indicate that the general population may be exposed to oxamyl via ingestion of food. (SRC)

Oxamyl's production may result in its release to the environment through various waste streams; its use as an insecticide, acaricide, and nematicide will result in its direct release to the environment. If released to air, a vapor pressure of 0.00023 mm Hg at 20-25 °C indicates oxamyl will exist solely as a vapor in the ambient atmosphere. Vapor-phase oxamyl 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 1.4 days. If released to soil, oxamyl is expected to have very high mobility based upon Koc values ranging from 6 to 10. Volatilization from moist soil surfaces is not expected to be an important fate process based upon a Henry's Law constant of 2.37X10-10 atm-cu m/mole. Half-lives...

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.

LD50: 2300 ug/kg (Oral, Mouse) (T14) LC50: 170 mg/m3 over 1 hour (Inhalation, Rat) (T14)

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)

Oxamyl 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 i...

Oral Chronic Reference Dose Reference: IRIS Current

/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...

Oral RfD: 0.025 mg/kg/day (UF: 100, MF: 1)

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

Fraction of Contaminant Absorbed Dermally from Soil: 0.1

Fraction of Contaminant Absorbed Dermally from Soil: 0.1

Reference: Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP