If a person is exposed to a high dose of nerve gas1, death ensues within minutes. Death is produced by respiratory arrest. With lower levels of exposure, fatalities can still occur within the first 24 hours. The victim will suffer many effects prior to succumbing by respiratory arrest. These include, intense constriction of the pupils (miosis) and severe eye pain, constriction of the bronchioles producing labored breathing, nausea and vomiting, lacrimation (tearing), salivation, sweating, urination, defecation, (basically everything oozes out!) and muscle twitching leading to muscle paralysis. Signs that the nerve gas gets into the brain include; anxiety, confusion, dizziness, nausea, vomiting, seizures and respiratory depression. Death is usually the result of respiratory failure. This occurs by 2 routes. The nerve gas acts directly on the diaphragm (smooth muscle) to paralyze it and it also inhibits the firing rate of neurons in an area of the brainstem that controls breathing. This area is called the respiratory center and it contains neurons that send their axons to the diaphragm to cause muscle contraction, and thus, breathing. After chronic exposure to low levels of nerve gas, victims suffer from a variety of neurological and mental disorders including; depression, insomnia, loss of memory, mental confusion and cognitive problems. This was typical in US soldiers exposed to nerve gas in Iraq during the dismantling of chemical weapons after the Gulf War.
1 a group of very lipophilic compounds (e.g. sarin, tabun, soman) that can exist as a vapor at room temperature. They contain phosphorus groups and bind avidly to acetylcholinesterase to inhibit its activity. The inhibition of acetylcholinesterase causes the accumulation of acetylcholine in all areas of the nervous system, causing excessive muscle contraction followed by paralysis, secretions, seizures and death by respiratory failure.