Carbosulfan

Pesticide -> EPA IRIS

Insecticides, Nematicides

Active substance -> EU Pesticides database: Not approved

Pesticides -> Carbamate Insecticides

Insecticides, Nematicides

Environmental transformation -> Pesticides (parent, predecessor)

Carbosulfan is a viscous brown liquid.

Brown viscous liquid; [Merck Index] Medium yellow viscous liquid; Odorless to slight amine odor; [EFSA: DAR - Vol. 1]

188.3 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID5023950]

190.66 Ų [M+H]+ [CCS Type: TW; Buffer gas: N2; Ionization: GC-APCI+]

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P320, P321, P330, P333+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P320, P321, P330, P333+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Commission Regulation (EC) No 451/2000

2007/415

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Carbamate cholinesterase inhibitor; Hydrolyzed to carbofuran in the soil; [Merck Index] Insecticidal activity from the in vitro cleavage of the N-S bond forming carbofuran; Not irritating to skin or eyes; May cause skin sensitization; Developmental toxicity and teratogenicity observed in rats and rabbits at doses not overtly maternally toxic; No evidence of carcinogenicity or organophosphorus induced delayed neurotoxicity [EFSA: DAR - Vol. 1] A mild skin irritant; [RTECS] A mild skin irritant; May cause skin sensitization; Toxic by ingestion and inhalation; [Sigma-Aldrich MSDS] See Carbofuran. See CARBAMATE INSECTICIDES.

CARBOSULFAN is a thiocarbamate. Flammable gases are generated by the combination of thiocarbamates and dithiocarbamates with aldehydes, nitrides, and hydrides. Thiocarbamates and dithiocarbamates are incompatible with acids, peroxides, and acid halides.

Acute Tox. 3 (100%)

Acute toxicity - category 2

Acute toxicity (Oral) - Category 3

Acute Tox. 2 *

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

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.

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 nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).

Carbosulfan 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 inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

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)

Carbosulfan

1 x 10 ^-2 mg/kg-day

0.01

IRIS Current

6.30e+02

8.20e+03

5.10e+01

5.00e+00

1.20e+00

1.00e-02

1.90e+03

2.50e+04

1.50e+02

5.00e+00

1.00e-02

Volatile

Carbosulfan has known human metabolites that include (2,2-dimethyl-3H-1-benzofuran-7-yl) N-dibutylsulfinamoyl-N-methylcarbamate, dibutyl(sulfanyl)amine, and Carbofuran.

The carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (L793)

No active pesticide product registrations in the US; [NPIRS] Used as an insecticide; [Merck Index] Approved in the EU for use on maize, sugarbeet, cotton, and citrus; [EFSA: DAR - Vol. 1]

Farming (Pesticides) [Category: Industry]

Carbosulfan is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.

Environmental transformation -> Pesticides (parent, predecessor)

Insecticides, Nematicides