Preparation by local authorities for a nerve-agent accident or attack is essential to managing risk.
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.
V-series nerve agents
The V-series agents include O-ethyl-S-[2-(diisopropylamino)ethyl] methylphosphonothioate (VX), which, at an LCt50 of 10 mg x min/m3, is the most toxic of the nerve agents. VX is approximately 10-fold more poisonous than sarin.
Information about other V-series nerve agents is less well known. These include V-gas, a Russian-produced equivalent of VX, as well as O-ethyl-S-[2-(diethylamino)ethyl] ethylphosphonothioate (VE), O-O-diethyl-S-[2-(diethylamino)ethyl] phosphorothioate (VG), and O-ethyl-S-[2-(diethylamino)ethyl] methylphosphonothioate (VM).
Researchers do know that all V-series compounds are persistent agents, allowing them to remain on skin, clothes, and other surfaces for long periods of time. The compounds have an oily consistency, making them extremely toxic upon contact. Just a tiny drop — 0.01 gram (approximately the size of a tear drop) of VX on a person — could be lethal.
Given its consistency, VX would seem to be less of a risk for inhalation. If a method of aerosolizing it were developed, however, the substance would be significantly more toxic than any of the G-series compounds. A concentration of just 0.002 PPM of VX in the air would be toxic.
VX is an odorless, thick, and clear-to-straw-colored liquid. It also is more persistent than G-series nerve agents; after deployment, it remains active in the environment for two to six days.
Release risks
Despite safety precautions, tens of thousands of accidental chemical releases or spills are reported each year in the United States, resulting in multiple deaths and injuries. One of the most infamous chemical accidents occurred in 1984 in Bhopal, India, when a gas leak at a Union Carbide plant released 40 tons of the pesticide methyl isocyanate. Although not a nerve agent, the release of methyl isocyanate killed at least 3,800 people and caused significant morbidity and premature death for many thousands more.
The availability of source chemicals for nerve agents, which are used in manufacturing and agriculture, raises concerns about the use of these compounds by terrorist organizations. In 1994 and 1995, the religious cult Aum Shinrikyo manufactured the nerve agent sarin and released it in two separate attacks, killing 19 people and injuring almost 1,300.
As a consequence, communities must prepare for a potential chemical emergency that could result from either a terrorist attack or the accidental release of toxic chemicals.
Total preparedness
Preparations for any chemical emergency must be made at the federal, state/regional, and local level. Although some responsibilities may intersect, an adequate and effective emergency-management plan demands the involvement of all three levels.
At the federal level, homeland security and health authorities provide guidance and information that aids state and local governments in instituting the protocols and plans that immediately address a chemical emergency. The federal government also must help to ensure that drugs, vaccines, and antidotes reach state and local governments.
One federal resource is the Strategic National Stockpile, which is jointly managed by the CDC and U.S. Department of Homeland Security. Through the SNS program, caches of drugs, vaccines, antidotes and medical supplies are placed in strategic locations throughout the United States. These stockpiles are intended to augment, or replenish, medical supplies already in the hands of state and local governments.
The CDC also has begun working with state and local authorities on a voluntary program to pre-position Chempacks, containing antidote and other essential medications, throughout the US so they can be immediately accessed in a chemical emergency. Certain antidotes are included on DHS' authorized equipment list and can be purchased using DHS grant funding.
In addition to obtaining necessary supplies, it is the responsibility of state and local governments, as well as health providers, to establish thorough preparedness plans to address potential disasters in their regions. Dealing effectively with a chemical attack requires simultaneous, coordinated effort on the part of first responders, including emergency medical services, fire, law enforcement, environmental protection and hospital personnel, both at the scene and at remote locations such as an emergency operations center.
As with any other mass-casualty incidents, preparing a response to the release of toxic chemicals requires a plan that reduces population exposure and prevents responders from becoming victims themselves.
Prior awareness of chemical threats in the community is essential for all responders, including emergency medical services, fire, law enforcement, environmental services and public health agencies. Local authorities need to communicate with federal and state governments, as well as chemical producers, chemical warehouses and end users, to understand the types of chemicals responders may encounter. Information should be shared with relevant local agencies and healthcare professionals.
Protocols must be developed by local governments for detection, rescue, decontamination, triage, field treatment and transportation of the contaminated and injured.
Logistics. The actual criteria and steps for identifying the nature of the incident should be thoroughly outlined to ensure that responders are protected, and for other important purposes, such as isolating the source, decontaminating victims, triage, administration of chemical antidotes, supportive field treatment and transport of victims to the hospital. Logistics should address every step, beginning with a dispatcher alerting responding units to a possible chemical incident and continuing with the first arriving units looking for indicators of multiple people exposed to a chemical, calling for the assistance of a hazmat unit and beginning the process of detecting the type of chemical involved (perhaps by assessing the symptoms that victims demonstrate or by using chemical detectors).
Healthcare planning procedures need to be in place for rescue, triage, hot zone treatment, decontamination, and secondary triage prior to transportation to healthcare facilities. Stockpiles of antidotes and treatments should be immediately accessible to emergency responders in local communities. Treatment in the pre-hospital setting should be considered largely temporary until the patient can be transported to the hospital where definitive care can begin. The key to reducing morbidity and mortality is rapid assessment and treatment of victims, as well as protection of emergency workers. Healthcare facilities also should be prepared for a deluge of the "worried well," individuals who fear exposure, yet show no symptoms.
Communication: All parties must be coordinated and able to communicate easily and effectively, both at the scene and the command post. In addition, information must be relayed to all emergency departments in the region so they know what to expect. Ensuring good radio communications is fundamental to a hazardous materials response operation.
Responder protection and decontamination: Everyone entering the contaminated area — including those who are there to mitigate release of the chemical or to rescue, triage, and decontaminate victims — must have proper personal protective equipment. After leaving the area, decontamination of first responders' and health-care workers' clothing and protective gear is an important consideration, as chemicals can be brought home in clothing or on the skin of first responders, thereby becoming a hazard to those around them.
Antidotes and intervention
To be useful, antidotes need to be accessible to emergency responders and easy to administer in the pre-hospital setting. In a large-scale chemical emergency, it is not feasible to deliver antidote intravenously. First responders have only minutes to access, triage, and administer treatment to those affected, depending on the route and concentration of exposure to the chemical. In the event of nerve-agent exposure, intramuscular injection of the antidote, followed by evacuation and decontamination, is the preferred method of treatment. Follow-up use of benzodiazepines may be necessary to manage seizures, and definitive medical care should be sought to manage other symptoms of chemical exposure.
The two antidotes available for organophosphate poisoning, atropine and pralidoxime chloride, work in slightly different ways to counteract the effects of such poisoning. Atropine works by competing with excess ACh at nerve receptors, blocking its effect until normal function can return to nerves, muscles, and glands. Pralidoxime chloride helps reactivate AChE, thereby halting the continued buildup of ACh at receptors, and restores normal function to nerves, muscles and glands.
In a chemical emergency involving organophosphate poisoning, responders will have only minutes to administer both antidotes to individuals exhibiting symptoms. Consequently, the availability of atropine and pralidoxime chloride in a form that assures rapid administration is critical. The ideal antidote technology would be easy to use and would enable injection of medication through clothing, with virtually no preparation.
Atropine and pralidoxime chloride are included in the DuoDote auto-injector (atropine and pralidoxime chloride injection), a pre-filled, ready-to-use unit that is about the size of a penlight. The auto-injector device, manufactured by Meridian Medical Technologies, is included in the Chempack program. It allows rapid administration of medication through clothing and outer garments. Upon intramuscular injection, atropine is released first, followed by pralidoxime chloride. The unit is designed to provide rapid, peak blood levels of antidote to treat symptoms of organophosphate poisoning. After administration, the victim should be removed from the scene to receive more definitive medical care.
First responders should take care to administer organophosphate antidotes only when an individual experiences two or more symptoms of nerve-agent poisoning, and these symptoms have been identified in others in the same area. Extreme care should be made to prevent mistaken diagnosis of nerve-agent poisoning and antidote administration, as an overdose of the antidotes could result in temporary incapacitation. Furthermore, when symptoms of poisoning are not severe, DuoDote should be used with extreme caution in individuals with heart disease, arrhythmias, recent myocardial infarction, severe narrow angle glaucoma, pyloric stenosis, prostatic hypertrophy, significant renal insufficiency, chronic pulmonary disease, or hypersensitivity to any component of the product.
Given the widespread availability and use of chemicals throughout the United States and its territories, urban and rural areas are both vulnerable to an accidental or intentional chemical release. To adequately plan for, and respond to, a chemical emergency, communities must have the knowledge and resources on hand and in place. A plan can help mitigate morbidity, mortality, and damage to societal infrastructure that could occur as a consequence of a chemical emergency. In addition, communities should check the expiration dates of their current supply of antidotes and restock if inventory expires in three months or less. If a supply of antidotes does not exist or has expired, communities should check the availability of DHS domestic preparedness grants to obtain a new supply.
Jerome Hauer is former assistant secretary for Public Health Emergency Preparedness at the U.S. Department of Health and Human Services. He also served as director of Emergency Management for New York City, and as director of Emergency Medical Services and Fire Services for the State of Indiana. Hauer is CEO of the Hauer Group, a consulting firm whose clients include Meridian Medical Technologies.
Emergency Management Model
In the United States, the standard disaster-preparedness model analyzes a potential emergency in four ways:
Mitigation
What measures can be employed before an incident to minimize damage?
Preparedness
What activities should be conducted prior to a disaster to improve readiness?
Response
What actions will be necessary to deal with the consequences during the disaster?
Recovery
What procedures will help restore operations to normal?




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