化合物详情

CAS59669-26-0
分子式C10H18N4O4S3
分子量354.46 g/mol
非危品

Thiodicarb can cause cancer according to The Environmental Protection Agency (EPA).

科学粮草官-词典编辑部,修订于:2026-07-06

化合物详情

Toxicity

Toxicity
28
EPA Ecotoxicity
Pesticide Ecotoxicity Data from EPA: 47
Ecotoxicity Values
LC50; Species: Anas platyrhynchos (Mallard duck) dietary >5620 ppm for 5 days /99% ai/ /from table/
Fate Summary
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), thiodicarb, which has a vapor pressure of 4.3X10-5 mm Hg at 20 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase thiodicarb 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 9.7 hours(3), calculated from its rate constant of 1.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(4). Particulate-phase thiodicarb may be removed from the air by wet and dry deposition(SRC). Thiodicarb contains chromophores that absorb at wavelengths >290 nm(5) and, therefore, is susceptible to di...
Soil Adsorption / Mobility
Thiodicarb has Koc values of 64 to 1,167, with a mean value of 351, reported for sand, silt loam, clay, sand, and sandy loam(1-3). Thiodicarb has a soil distribution coefficient, Kd = 3.30(4). According to a classification scheme(5), the average Koc value suggests that thiodicarb is expected to have moderate mobility in soil.
Environmental Biodegradation
ANAEROBIC: Thiodicarb degrades under anaerobic conditions in aqueous environments with a reported half-life of 3 hours(1).
Environmental Bioconcentration
In a fish bioaccumulation study, acetic acid was the major metabolite in fish tissue and 46-74% of the accumulated residues in the fish tissues were eliminated after 28 days(1). A whole body BCF of 5.7 was reported for thiodicarb in bluegill fish (Lepomic macrochirus) exposed for 28 days, in the EPA bioconcentration guideline 165-4/OPPTS 950.1730 test(2). According to a classification scheme(3), this BCF suggests the bioconcentration in aquatic organisms is low.
Volatilization from Water / Soil
The Henry's Law constant for thiodicarb is estimated as 1.1X10-6 atm-cu m/mole(SRC) derived from its vapor pressure, 4.3X10-5 mm Hg(1), and water solubility, 19.1 mg/L(2). This Henry's Law constant indicates that thiodicarb is expected to volatilize slowly from water surfaces(3). 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)(3) is estimated as 63 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 1.3 years(SRC). Thiodicarb's estimated Henry's Law constant indicates that volatilization from moist soil surfaces may occur slowly(SRC). Thiodicarb is not expected to volatilize from dry soil surfaces(SRC) based upon it...
Environmental Abiotic Degradation
The rate constant for the vapor-phase reaction of thiodicarb with photochemically-produced hydroxyl radicals has been estimated as 1.3X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 9.7 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(2). Thiodicarb has hydrolysis half-lives of 78 days, 32 days, and 12 hours at pH values of 5, 7, and 9, respectively(3). Thiodicarb contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, is susceptible to direct photolysis by sunlight(SRC). Reported aqueous and soil photolysis half-lives for thiodicarb are 8 days and 37 days, respectively(3).
Environmental Water Concentrations
SURFACE WATER: Water quality data compiled from the Retrieval (STORET) Data Warehouse report 2006 monitoring data from the Idaho State Department of Agriculture indicating that thiodicarb was not detected in surface water samples collected from April 2006 to July 2006(1). Water quality data compiled from the Retrieval (STORET) Data Warehouse report 2013, 2014, and 2015 monitoring data from the California Department of Water Resources indicating that thiodicarb's major degradation product, methomyl, was detected in surface water samples, at concentrations ranging from 0 to 1.2 ug/L, collected in March, June, and Sept 2013, Feb, March, Apr, Jun and Aug 2014, and March and June 2015(1).
Food Survey Values
Thiodicarb residue was detected in unwashed, washed, and washed and salted potato tuber samples at concentrations of 0.008 to 0.038 mg/kg, but was not detected in peeled samples, potato samples were collected from local markets in Egypt in 2013(1).
Ecotoxicity Excerpts
/OTHER TERRESTRIAL SPECIES/ Bee: Moderately toxic as direct treatment; not toxic after spray residues have dried.
Artificial Pollution Sources
Thiodicarb's production may result in its release to the environment through various waste streams; its use as an insecticide and molluscicide(1) will result in its direct release to the environment(SRC).
Probable Routes of Human Exposure
Occupational exposure to thiodicarb may occur through inhalation and dermal contact with this compound at workplaces where thiodicarb is produced or used. (SRC)
Environmental Fate / Exposure Summary
Thiodicarb's production may result in its release to the environment through various waste streams; its use as an insecticide and molluscicide will result in its direct release to the environment. If released to air, a vapor pressure of 4.3X10-5 mm Hg at 20 °C indicates thiodicarb will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase thiodicarb 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 9.7 days. Particulate-phase thiodicarb will be removed from the atmosphere by wet and dry deposition. Thiodicarb contains chromophores that absorb at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, thiodic...
Symptoms
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)
Treatment
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.
Toxicity Data
LD50: 40 mg/kg (Oral, Guinea pig) LD50: 2540 mg/kg (Dermal, Rat) LC50: 0.0015-0.0022 mg/L over 4 hours (T58)
Health Effects
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...
Adverse Effects
ACGIH Carcinogen - Confirmed Animal.
Exposure Routes
Inhalation (L793); oral (L793); dermal (L793)
Toxicity Summary
Thiodicarb 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 estera...
RAIS Toxicity Values
Oral Acute Reference Dose Reference: OPP
Human Toxicity Excerpts
/CASE REPORTS/ ... A 40-year-old woman was found dead in her car. Empty packages of medicines and an open bottle of Larvin containing thiodicarb were found near her body. No signs of violence nor traumatic injuries were noticed upon autopsy, and police investigations strongly suggested a suicide. Systematic toxicological analysis performed on postmortem specimens revealed the presence of various sedatives, hypnotics, and antipsychotic drugs in blood, urine, and gastric content. Some of the compounds identified were determined at blood concentrations well above the known therapeutic concentrations: zolpidem (2.87 mg/L), bromazepam (2.39 mg/L), nordazepam (4.21 mg/L), and levopremazine (0.64 mg/L). Specific analysis of thiodicarb and of its methomyl metabolite was then performed on all fl...
Carcinogen Classification
No indication of carcinogenicity to humans (not listed by IARC).
Non-Human Toxicity Values
LD50 Mouse (female) oral 79 mg/kg
Non-Human Toxicity Excerpts
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Thiodicarb, a carbamate pesticide widely used on crops, may pose several environmental and health concerns. This study aimed to explore its toxicological profile on male rats using hematological, biochemical, histopathological, and flow cytometry markers. Exposed animals were dosed daily at 10, 20, or 40 mg/kg/body weight (group A, B, and C, respectively) during 30 d. No significant changes were observed in hematological parameters among all groups. After 10 d, a decrease of total cholesterol levels was noted in rats exposed to 40 mg/kg. Aspartate aminotransferase (AST) activity increased (group A at 20 d; groups A and B at 30 d) and alkaline phosphatase (ALP) (group B at 30 d) activity significantly reduced. At 30 d a decrease of...
Evidence for Carcinogenicity
Cancer Classification: Group B2 Probable Human Carcinogen
Antidote and Emergency Treatment
Consider pralidoxime in cases of mixed carbamate/organophosphate poisoning and cases of an unknown pesticide with muscarinic symptoms on presentation ... . Pralidoxime has been used in some cases of carbamate poisoning, although other cases have resolved from supportive care alone. Pralidoxime is probably of little value in N-methyl carbamate poisonings and is not indicated in isolated carbamate poisonings. Atropine alone usually is effective. /N-methyl carbamate insecticides/
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