|2009-06-17 23:53:05 UTC
|2014-12-24 20:23:02 UTC
|Propamocarb hydrochloride is a carbamate pesticide. Carbamate pesticides are derived from carbamic acid and kill insects in a similar fashion as organophosphate insecticides. They are widely used in homes, gardens and agriculture. The first carbamate, carbaryl, was introduced in 1956 and more of it has been used throughout the world than all other carbamates combined. Because of carbaryl's relatively low mammalian oral and dermal toxicity and broad control spectrum, it has had wide use in lawn and garden settings. Most of the carbamates are extremely toxic to Hymenoptera, and precautions must be taken to avoid exposure to foraging bees or parasitic wasps. Some of the carbamates are translocated within plants, making them an effective systemic treatment. (3)
- Organic Compound
- Synthetic Compound
|propyl [3-(dimethylamino)propyl]carbamate hydrochloride
|Average Molecular Mass
|CAS Registry Number
|propyl N-[3-(dimethylamino)propyl]carbamate hydrochloride
| belongs to the class of organic compounds known as trialkylamines. These are organic compounds containing a trialkylamine group, characterized by exactly three alkyl groups bonded to the amino nitrogen.
|Organic nitrogen compounds
- Tertiary aliphatic amine
- Organic 1,3-dipolar compound
- Propargyl-type 1,3-dipolar organic compound
- Carboximidic acid derivative
- Organic oxygen compound
- Organopnictogen compound
- Hydrocarbon derivative
- Organooxygen compound
- Aliphatic acyclic compound
|Aliphatic acyclic compounds
|Detected and Not Quantified
|1000 mg/mL at 20°C [TOMLIN,C (1997)]
|Predicted LC-MS/MS Spectrum - 10V, Positive
|Predicted LC-MS/MS Spectrum - 20V, Positive
|Predicted LC-MS/MS Spectrum - 40V, Positive
|Predicted LC-MS/MS Spectrum - 10V, Negative
|Predicted LC-MS/MS Spectrum - 20V, Negative
|Predicted LC-MS/MS Spectrum - 40V, Negative
|Mass Spectrum (Electron Ionization)
|Route of Exposure
|Inhalation (2) ; oral (2); dermal (2)
|Mechanism of Toxicity
|Propamocarb hydrochloride 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.
|The carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (2)
|Carcinogenicity (IARC Classification)
|No indication of carcinogenicity to humans (not listed by IARC).
|Propamocarb hydrochloride is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.
|Minimum Risk Level
|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 (1).
|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. (3)
|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.
|PubChem Compound ID
- Roldan-Tapia L, Nieto-Escamez FA, del Aguila EM, Laynez F, Parron T, Sanchez-Santed F: Neuropsychological sequelae from acute poisoning and long-term exposure to carbamate and organophosphate pesticides. Neurotoxicol Teratol. 2006 Nov-Dec;28(6):694-703. Epub 2006 Aug 30. [17029710 ]
- IPCS Intox Database (1987). Antimony pentoxide. [Link]
- Fishel F (2009). Pesticide Toxicity Profile: Carbamate Pesticides. University of Florida, IFAS Extension. [Link]