Carbamate poisoning

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Carbamate poisoning is poisoning due to exposure to carbamates, which are commonly sold as pesticides around the world. In most respects, it is similar to organophosphate poisoning, though typically less severe or requiring a larger amount of the chemical before symptoms appear.

Contents

Symptoms

The array of symptoms typically seen in carbamate poisoning include both muscarinic and nicotinic symptoms. [1] Muscarinic receptor effects include:

Bronchospasm is a potential life threat, especially when combined with nicotinic effects on the respiratory muscles. Bradycardia can be life-threatening in people with preexisting heart conditions. The combination of sweating, diarrhea, and vomiting can lead to severe dehydration, hypovolemia, and death from hypovolemic shock. [1]

Nicotinic symptoms of carbamate poisoning are caused by weakness, tremors, and fasciculations of muscles across the body. The most notable consequence of this is usually respiratory failure, as the diaphragm and other muscles become too weak to facilitate normal breathing. [1] [2]

Symptoms of the central nervous system are possible, but are less frequent and severe than those associated with organophosphate poisoning. Possible symptoms include: [1] [3]

Similarity to organophosphorus

Symptoms are overall similar to organophosphate poisoning. [4] However, several notable differences exist: unlike organophosphates, carbamates do not cause covalent bonds to form between the chemical and acetylcholinesterase. [1] This means that organophosphates, but not carbamates, can cause respiratory failure several days or weeks after exposure to the chemical, [2] while also resisting antidote administration. [1] Carbamate poisoning does not cause long-term effects. [3]

Pathogenesis

Most cases of carbamate poisoning are due to exposure to pesticide products containing the chemical. The most common carbamate chemicals in use are captan, ferbam, carbofuran, carbaryl, and aldicarb. Suicidal and homicidal poisonings also occur, but are rare, due to the lower lethality of carbamates in humans compared to other toxic substances. [5]

Like organophosphates, carbamates are toxic because of their ability to bind to and inhibit acetylcholinesterase (AChE). AChE is an enzyme found throughout the human body that breaks down acetylcholine (ACh), a neurotransmitter that causes muscle cells to contract, among other functions. Without AChE, acetylcholine builds up in the neuromuscular junction, eventually saturating the receptors in the junction and causing the muscle cell to contract uncontrollably. In large muscles such as the diaphragm, the muscle cells may use up their energy reserves and be unable to contract any more, resulting in weakness and tremors. [1]

Treatment

The primary treatment for carbamate poisoning involves decontamination and supportive care, with a focus on keeping the airway open. This is often achieved with the use of nasopharyngeal or oropharyngeal airway devices. Activated charcoal is often administered in cases where the substance was ingested, to limit further absorption of the toxin. In severe cases, atropine may be used as an antidote to counteract the effects of carbamates on the nervous system. Pralidoxime, another antidote, can be considered to reactivate inhibited acetylcholinesterase enzymes, although this is often less important for carbamate poisoning than it is for organophosphate poisoning. [1]

The most common cause of death following carbamate poisoning is respiratory failure. [3] Because of this, the most urgent treatment approaches center around ensuring that the patient's airway remains open. This may also involve the use of vacuum suction devices to remove saliva, which (due to the effects of the poison) can be produced in a high enough volume to drown the patient. Intubation and ventilation are sometimes used, in severe cases. [1] [3]

Atropine and pralidoxime are often packaged together in an auto-injector device, and are thus used together in the treatment of most cases. [1]

See Also

Related Research Articles

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<span class="mw-page-title-main">Atropine</span> Anticholinergic medication used as antidote for nerve agent poisoning

Atropine is a tropane alkaloid and anticholinergic medication used to treat certain types of nerve agent and pesticide poisonings as well as some types of slow heart rate, and to decrease saliva production during surgery. It is typically given intravenously or by injection into a muscle. Eye drops are also available which are used to treat uveitis and early amblyopia. The intravenous solution usually begins working within a minute and lasts half an hour to an hour. Large doses may be required to treat some poisonings.

<span class="mw-page-title-main">VX (nerve agent)</span> Chemical compound and chemical warfare nerve agent

VX is an extremely toxic synthetic chemical compound in the organophosphorus class, specifically, a thiophosphonate. In the class of nerve agents, it was developed for military use in chemical warfare after translation of earlier discoveries of organophosphate toxicity in pesticide research. In its pure form, VX is an oily, relatively non-volatile liquid that is amber-like in colour. Because of its low volatility, VX persists in environments where it is dispersed.

Anticholinergics are substances that block the action of the acetylcholine (ACh) neurotransmitter at synapses in the central and peripheral nervous system.

<span class="mw-page-title-main">Chlorfenvinphos</span> Chemical compound

Chlorfenvinphos is an organophosphorus compound that was widely used as an insecticide and an acaricide. The molecule itself can be described as an enol ester derived from dichloroacetophenone and diethylphosphonic acid. Chlorfenvinphos has been included in many products since its first use in 1963. However, because of its toxic effect as a cholinesterase inhibitor it has been banned in several countries, including the United States and the European Union. Its use in the United States was cancelled in 1991.

Obidoxime is a member of the oxime family used to treat organophosphate poisoning. Oximes are drugs known for their ability to reverse the binding of organophosphorus compounds to the enzyme acetylcholinesterase (AChE).

<span class="mw-page-title-main">Diazinon</span> Chemical compound

Diazinon, a colorless to dark brown liquid, is a thiophosphoric acid ester developed in 1952 by Ciba-Geigy, a Swiss chemical company. It is a nonsystemic organophosphate insecticide formerly used to control cockroaches, silverfish, ants, and fleas in residential, non-food buildings. Diazinon was heavily used during the 1970s and early 1980s for general-purpose gardening use and indoor pest control. A bait form was used to control scavenger wasps in the western U.S. Diazinon is used in flea collars for domestic pets in Australia and New Zealand. Diazinon is a major component in the "Golden Fleece" brand sheep dip. Residential uses of diazinon were outlawed in the U.S. in 2004 because of human health risks but it is still approved for agricultural uses. An emergency antidote is atropine.

A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh), as a result of the inactivity of the AChE enzyme, which normally breaks down acetylcholine.

<span class="mw-page-title-main">Pralidoxime</span> Chemical compound as an antidote

Pralidoxime or 2-PAM, usually as the chloride or iodide salts, belongs to a family of compounds called oximes that bind to organophosphate-inactivated acetylcholinesterase. It is used to treat organophosphate poisoning in conjunction with atropine and either diazepam or midazolam. It is a white solid.

<span class="mw-page-title-main">Azinphos-methyl</span> Chemical compound

Azinphos-methyl (Guthion) is a broad spectrum organophosphate insecticide manufactured by Bayer CropScience, Gowan Co., and Makhteshim Agan. Like other pesticides in this class, it owes its insecticidal properties to the fact that it is an acetylcholinesterase inhibitor. It is classified as an extremely hazardous substance in the United States as defined in Section 302 of the U.S. Emergency Planning and Community Right-to-Know Act, and is subject to strict reporting requirements by facilities which produce, store, or use it in significant quantities.

<span class="mw-page-title-main">Phosmet</span> Organophosphate non-systemic insecticide

Phosmet is a phthalimide-derived, non-systemic, organophosphate insecticide used on plants and animals. It is mainly used on apple trees for control of codling moth, though it is also used on a wide range of fruit crops, ornamentals, and vines for the control of aphids, suckers, mites, and fruit flies.

<span class="mw-page-title-main">Dioxathion</span> Chemical compound

Dioxathion, systematically known as p-dioxane-2,3-diyl ethyl phosphorodithioate, is an organophosphate pesticide. It is used as an insecticide on livestock and as an acaricide on citrus fruits, deciduous fruits and nuts.

<span class="mw-page-title-main">Organophosphate poisoning</span> Toxic effect of pesticides

Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents. Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion. While onset of symptoms is often within minutes to hours, some symptoms can take weeks to appear. Symptoms can last for days to weeks.

<span class="mw-page-title-main">Chlorethoxyfos</span> Chemical compound

Chlorethoxyfos is an organophosphate acetylcholinesterase inhibitor used as an insecticide. It is registered for the control of corn rootworms, wireworms, cutworms, seed corn maggot, white grubs and symphylans on corn. The insecticide is sold under the trade name Fortress by E.I. du Pont de Nemours & Company.

<span class="mw-page-title-main">Disulfoton</span> Chemical compound

Disulfoton is an organophosphate acetylcholinesterase inhibitor used as an insecticide. It is manufactured under the name Di-Syston by Bayer CropScience. Disulfoton in its pure form is a colorless oil but the technical product used in vegetable fields is dark and yellowish with a sulfur odor. Disulfoton is processed as a liquid into carrier granules, these granules are mixed with fertilizer and clay to be made into a spike, designed to be driven into the ground. The pesticide is absorbed over time by the roots and translocated to all parts of the plant. The pesticide acts as a cholinesterase inhibitor and gives long lasting control.

<span class="mw-page-title-main">Cholinesterase inhibitor</span> Chemicals which prevent breakdown of acetylcholine and butyrylcholine

Cholinesterase inhibitors (ChEIs), also known as anti-cholinesterase, are chemicals that prevent the breakdown of the neurotransmitter acetylcholine or butyrylcholine. This increases the amount of the acetylcholine or butyrylcholine in the synaptic cleft that can bind to muscarinic receptors, nicotinic receptors and others. This group of inhibitors is divided into two subgroups, acetylcholinesterase inhibitors (AChEIs) and butyrylcholinesterase inhibitors (BChEIs).

<span class="mw-page-title-main">Ethoprophos</span> Chemical compound

Ethoprophos (or ethoprop) is an organophosphate ester with the formula C8H19O2PS2. It is a clear yellow to colourless liquid that has a characteristic mercaptan-like odour. It is used as an insecticide and nematicide and it is an acetylcholinesterase inhibitor.

<span class="mw-page-title-main">Terbufos</span> Chemical compound

Terbufos is a chemical compound used in insecticides and nematicides. It is part of the chemical family of organophosphates. It is a clear, colourless to pale yellow or reddish-brown liquid and sold commercially as granulate.

<span class="mw-page-title-main">Triazofos</span> Chemical compound

Triazofos is a chemical compound used in acaricides, insecticides, and nematicides.

<span class="mw-page-title-main">Guanitoxin</span> Chemical compound

Guanitoxin (GNT), formerly known as anatoxin-a(S) "Salivary", is a naturally occurring cyanotoxin commonly isolated from cyanobacteria. It is a potent covalent acetylcholinesterase inhibitor, and thus a potent rapid acting neurotoxin which in cases of severe exposure can lead to death. Guanitoxin was first structurally characterized in 1989, and consists of a cyclic N-hydroxyguanine organophosphate with a phosphate ester moiety.

References

  1. 1 2 3 4 5 6 7 8 9 10 Vohra, Rais (2022). "Organophosphorus and carbamate insecticides". Poisoning & Drug Overdose (8th ed.). McGraw Hill.
  2. 1 2 Jayawardane, Pradeepa; Senanayake, Nimal; Buckley, Nick A.; Dawson, Andrew H. (2012). "Electrophysiological correlates of respiratory failure in acute organophosphate poisoning: Evidence for differential roles of muscarinic and nicotinic stimulation". Clinical Toxicology. 50 (4): 250–253. doi:10.3109/15563650.2012.670875. ISSN   1556-3650. PMC   3357897 . PMID   22455356.
  3. 1 2 3 4 King, Andrew M.; Aaron, Cynthia K. (2015-02-01). "Organophosphate and Carbamate Poisoning". Emergency Medicine Clinics of North America. Management of Hazardous Material Emergencies. 33 (1): 133–151. doi:10.1016/j.emc.2014.09.010. ISSN   0733-8627. PMID   25455666.
  4. ↑ Eddleston, Michael; Buckley, Nick A; Eyer, Peter; Dawson, Andrew H (February 2008). "Management of acute organophosphorus pesticide poisoning". The Lancet. 371 (9612): 597–607. doi:10.1016/S0140-6736(07)61202-1. PMC   2493390 . PMID   17706760.
  5. ↑ Kumar, Sachil; Baggi, Tulsidas R.; Zughaibi, Torki (2022-11-01). "Forensic toxicological and analytical aspects of carbamate poisoning – A review". Journal of Forensic and Legal Medicine. 92: 102450. doi:10.1016/j.jflm.2022.102450. ISSN   1752-928X. PMID   36399917. S2CID   253433639.
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