Nerve gases

Nerve agents, or nerve gases, are a class of organic chemicals that disrupt the nerves transfer messages to organs. 


Nerve gases block acetylcholinesterase, an enzyme that catalyzes the breakdown of acetylcholine, a neurotransmitter. 



Nerve agents are acetylcholinesterase inhibitors used as poison.



Nerve gas poisoning leads to constriction of pupils, profuse salivation, convulsions, and involuntary urination and defecation.



Nerve gas poisoning symptoms 


appearing in seconds after exposure. 



Death may follow in minutes due to the loss of the body’s control over respiratory and other muscles with


asphyxiation or cardiac arrest.



Some nerve agents are vaporized, aerosolized with the primary portal of entry into the body is the respiratory system. 



Nerve agents can also be absorbed through the skin.



Nerve gasses are generally colorless to amber in color.



They are tasteless liquids that may evaporate to a gas. 



Agents sarin and VX are odorless.



Nerve agents attack the nervous system,  resulting in cholinergic crisis by inhibit the enzyme acetylcholinesterase.



Acetylcholinesterase is responsible for the breakdown of acetylcholine (ACh) in the synapses between nerves that control muscle contraction. 



If acetylcholine cannot be broken down, muscles are prevented from relaxing and they are effectively paralyzed: includes the heart and respiratory muscles.



Following nerve gas exposure, the first symptoms usually appear within seconds of exposure and death can occur via asphyxiation or cardiac arrest in a few minutes.



Following nerve gas exposure initial symptoms are a runny nose, tightness in the chest, and constriction of the pupils, followed by difficulty breathing nausea and salivation. 



With deteriorating control of bodily functions: involuntary salivation, lacrimation, urination, defecation, gastrointestinal pain and vomiting are experienced. 



Skin blisters, burning of the eyes and/or lungs may occur.



Subsequently, myoclonic jerks followed by status epilepticus occur.



Death then comes respiratory depression, most likely via the excessive peripheral activity at the neuromuscular junction of the diaphragm.



Nerve agents are long lasting and toxicity increases with continued exposure. 



Survivors of nerve agent poisoning suffer from chronic neurological damage and related psychiatric effects: blurred vision, tiredness, declined memory, hoarse voice, palpitations, sleeplessness, shoulder stiffness and eye strain for up to 2-3 years following exposure.



Exposure to nerve agents is associated with lowered serum and erythrocyte acetylcholinesterase levels in the long-term.



Lowered acetylcholinesterase levels is worse in patients with persistent symptoms.



Motor nerves stimulation releases the neurotransmitter acetylcholine, which transmits the impulse to a muscle or organ. 



Subsequently the enzyme acetylcholinesterase breaks down the acetylcholine in order to allow the muscle or organ to relax.



Nerve agents disrupt inhibit the function of the enzyme acetylcholinesterase by forming a covalent bond with its active site, preventing  acetylcholine breakdown and hydrolysis.



Acetylcholine build up continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop, there is uncontrolled drooling, lacrimation and rhinorrhea.



Treatment for nerve agent poisoning requires a combination of an anticholinergic agent to manage the symptoms, and an oxime antidote.



Anticholinergics reduce the effects of acetylcholine.



The standard anticholinergic drug used to manage the symptoms of nerve agent poisoning is ((atropine)).



Atropine acts as an antagonist to muscarinic acetylcholine receptors, blocking the effects of excess acetylcholine.



Atropine administration is continued until the clearing of bronchial secretions.



Synthetic anticholinergics, are available, to counteract the central symptoms of nerve agent poisoning more effectively than atropine, passing  the blood–brain barrier better than atropine.



Oximes displaces phosphate molecules from the active site of the cholinesterase enzymes.



This displacement allows the breakdown of acetylcholine. 



((Pralidoxime)) chloride is the standard oxime used to treat nerve agent poisoning.



Pralidoxime chloride reactivates the poisoned acetylcholinesterase by scavenging the phosphoryl group counteracting the nerve agent itself.



Pralidoxime chloride works more effectively on nicotinic receptors while blocking acetylcholine receptors with atropine is more effective on muscarinic receptors.



Anticonvulsants may be necessary to manage seizures, to improve long term prognosis and reducing risk of brain damage.



There are two main classes of nerve agents. 



The G series of nerve agents are known as non-persistent, while the V series are persistent. 



The V-series is the second family of nerve agents and contains five members: VE, VG, VM, VR, and VX, along with several more analogues.



All of the V-agents are persistent agents, they do not degrade or wash away easily and can therefore remain on clothes and other surfaces for long periods. 



V-agents to be used to blanket terrain to curtail the movement of enemy ground forces. 



The contact hazard for V-agents is primarily dermal. 



VX was the only V-series agent that was fielded by the US as a munition



The Novichok agents, are series of organophosphate compounds.



A large group of  nerve agents are carbamates, Which are about three times more toxic than VX.



Some insecticides, including carbamates and organophosphates such as dichlorvos, malathion and parathion, are nerve agents. 



Insecticides have little effect on humans at proper doses, but there is concern about the effects of long-term exposure to these chemicals by farm workers and animals alike. 



At high doses, acute toxicity and death can occur through the same mechanism as other nerve agents. 



Organophosphate pesticide poisoning is a major cause of disability in many developing countries and is often the preferred method of suicide.



Methods for spreading nerve agents such as:



uncontrolled aerosol munitions



smoke generation



explosive dissemination



atomizers, humidifiers and foggers



Laser photoacoustic spectroscopy (LPAS) is a method of detecting gaseous nerve agents in the air.



LPAS technology can identify gases in parts per billion (ppb) concentrations.



The following nerve agent simulants have been identified with multiwavelength LPAS:



dimethyl methyl phosphonate (DMMP)


diethyl methyl phosphonate (DEMP)


diisopropyl methyl phosphonate (DIMP)


dimethylpolysiloxane (DIME), triethyl phosphate (TEP)


tributyl phosphate (TBP)


acetone (ACE)


isopropanol (ISO)
















Ethylene Glycol







Non-dispersive infrared techniques have been used for gaseous nerve agent detection, as have traditional IR absorption, and Fourier transform infrared spectroscopy.




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