Companies in the United States formulate, manufacture and transport more than 75,000 different toxic chemicals used in manufacturing, agriculture and commercial products. The sheer prevalence of these substances throughout the United States, and the ease with which they can be transported by road, rail and ship, require that emergency management authorities at federal, regional and local levels consider and prepare for the risk of a chemical emergency.

The Centers for Disease Control and Prevention defines a chemical emergency as a situation in which release of a hazardous chemical, either as a consequence of an accident or a terrorist attack, has the potential for harming human health. Typically, hazardous chemicals are categorized either by chemical type or by the effects the substance would have on individuals exposed to it. Among the chemicals that the CDC has categorized are biotoxins, such as ricin or strychnine; blister agents/vesicants, such as mustard gas; blood agents, such as cyanide and arsine; pulmonary agents, such as chlorine, phosgene and phosphorous; and nerve agents, such as sarin or VX.

Of these chemicals, nerve agents are considered to be among the most hazardous when released upon human populations. The term "nerve agent" applies to a group of highly toxic chemicals called organophosphates, which are used as insecticides. Militarized, or highly potent, versions of organophosphates can be produced through the reaction of alcohol and phosphoric acid, using readily available source chemicals. A thorough understanding of the health threats of nerve agents can help to minimize injuries or loss of human life in a chemical emergency involving these compounds.

Nerve-agent toxicity is due to the agents' ability to bind and permanently block acetylcholinesterase (AChE), an enzyme present throughout the nervous system. AChE controls the concentration of the neurotransmitter acetylcholine (ACh) at synapses or neuromuscular junctions. By blocking AChE, nerve agents cause excessive levels of ACh to build up at cholinergic receptors, leading to a wide range of seemingly unrelated clinical effects observed in victims of nerve-agent exposure.

Common symptoms at the onset of organophosphate poisoning are excessive salivation and tearing, involuntary urination and defecation, as well as eye pain, miosis (constriction of the pupil), dim vision, rhinorrhea (runny nose), and chest pain. Contact with all organophosphates, including common insecticides, is associated with these effects, which are controlled by the ACh muscarinic receptors. Symptoms progress to further muscarinic effects that potentially are more deadly for victims of exposure, including a build up of mucus in the lungs as well as a rapid heart beat.

Exposure to highly potent nerve agents also can stimulate effects that are controlled by ACh nicotinic receptors, including muscle twitching, weakness, and eventually muscle paralysis. In addition, nerve-agent exposure has been shown to cause strange or confused behavior, convulsions, and unconsciousness. Nerve-agent poisoning can be fatal if treatment is not received within minutes of symptom onset, with death typically resulting from respiratory or cardiac failure.

Nerve agents present a special challenge to homeland-security organizations because of the threat they pose to civilian populations. These compounds are categorized into two main classes: G-Series and V-Series. Typically, individual agents are given either a common or chemical name as well as a two-character NATO identifier.

G-series nerve agents

G-series compounds include sarin (GB), tabun (GA), soman (GD), and cyclosarin (GF). G-series organophosphates are volatile compounds that can be dispersed as liquid or vapor. G-series nerve agents in liquid form could be aerosolized through dispersal devices, such as commercial insect foggers or an explosive blast. Because nerve-agent vapors are denser than air, the risk for inhalation is particularly hazardous for individuals in low areas or underground shelters. G-series agents dispersed in such an environment may remain persistent, or active, from two to 72 hours. In open air, the nerve agents in vapor form would be less effective and their endurance would be subject to meteorological factors, such as wind and humidity.

Although all of the G-series agents are lethal at low levels, soman may be the most toxic of such agents, requiring only minute traces of the agent in the air or on skin to exert a toxic effect.

Upon inhaling nerve-agent vapors, symptoms can appear 30 to 120 seconds after exposure. Exposure to just 0.008 parts per million (PPM) of soman and 0.03 PPM of sarin or tabun in the air is immediately dangerous to life and health. At such concentrations, inhalation results in immediate loss of consciousness, followed shortly by convulsions, paralysis, and respiratory failure due to rapid absorption through the respiratory tract.

Dermal contact of G-series agents also is dangerous. Nerve agents are soluble in fat and water and are easily absorbed through the eyes, respiratory tract and skin. Depending on the agent, just one gram or less of the liquid on skin will cause symptoms after the liquid has been absorbed; however, onset of symptoms may be delayed as long as 18 hours after exposure.

G-series agents share many physical and chemical properties. However, while GB and GD are colorless, GA can range in color from clear to brown. GB is odorless, while GA and GD smell fruity.