Attacks using chemicals, though not new to the military, have not been a concern for the general public or public safety personnel in the United States. Because of the vast number of potential chemicals that could be used, this topic is even more confusing. The CDC currently lists over 50 chemicals that could be a terrorist attack concern.

The first step in dealing with a chemical attack is identification of the chemical and protection of the public and responders. Identification may not be an easy task. Organized hazardous materials teams should be primarily responsible for the identification of the chemical agent used. The first clues, however, may come from the people exposed. The problem with using signs or symptoms is that the victim themselves, before being properly decontaminated, may present a hazard to responders even after being removed from the hazardous environment.

Protection and decontamination are two primary concerns. For the most part both must be performed before medical treatment can begin. This will make responding to a chemical attack an atypical response in that the treatment and transport will be delayed.

Chemical agents are grouped into one of eight different categories. They are:

This paper will focus on those agents most likely to be used in a chemical attack and agents with the most significant impact from an emergency medical perspective. It should be noted that there are a variety of chemicals, both weapons grade and industrial, that could be used in an attack.

Nerve agents will be discussed in depth because antidote agents are available and, in the event of a nerve agent attack, would be used in the pre-hospital setting. EMS providers may be more familiar with the effects of nerve agents than they think. That is because, though much more toxic, nerve agents are very closely related to the insecticide organophosphates used for agricultural purposes. Thus, many of the signs and symptoms will be the same. In fact, most nerve agents were originally produced in a search for insecticides, but because of their toxicity were evaluated for military use.

Sarin (GB) is odorless and the most volatile of the nerve agents. In 1995 Sarin was used to attack subway commuters in Tokyo. Some reports indicate that, because the people that were to deploy the Sarin in Tokyo, the concentration used was half of what was available to the terrorist and they chose not to use the most effective method of dissemination. We know today that many terrorist do not have the same concern for their own well being. Even at this reduced capability, the attack resulted in almost 6000 people being affected with 12 dead. Around 50 of the injured were first responders. Other nerve agents include Tabun (GA), Soman (GD) and V-Agent (VX).

                    Inhalation

The primary dissemination method is by aerosol spray. An aerosol is defined as a suspension or dispersion of small particles (solid or liquid) in a gaseous medium. Aerosol dissemination methods range from hand-held spray bottles to large powered generators.

Nerve agents inhibit acetylcholinesterase which results in excess acetylcholine. Acetylcholine is the chemical neurotransmitter that carries nerve impulses from one neuron (nerve cell) to another. Acetylcholinesterase is the enzyme that removes the acetylcholine after the impulse has been transmitted to prepare the synapse (junction) to transmit another impulse. When, because of the effects of the nerve agent, the synapse is not cleared, continual nerve impulses result.

Acetylcholine affects a number of body systems including the cardiovascular system by acting as a vasodilator, by decreasing cardiac rate, and by decreasing cardiac contraction; the gastrointestinal system by such activities as increasing peristalsis in the stomach and by increasing the amplitude of digestive contractions; and the urinary tract by such actions as decreasing the capacity of the bladder and increasing the voluntary voiding pressure. It also affects the respiratory system and stimulates secretion by all glands that receive parasympathetic nerve impulses.

The SLUDGE acronym, which is often associated with organophosphate poisoning, is also applicable to nerve agents. SLUDGE stands for Salivation, Lacrimination (tearing), Urination, Defecation, Gastro-intestinal distress (cramping) and Emesis (vomiting). Pinpoint pupils, twitching and seizures are also signs of nerve agent exposure.

Rapid decontamination is critical to preventing further absorption by the patient and to prevent exposure to others. Nerve vapors can be emitted from contaminated clothing for up to 30 minutes. Rescuers operating in the hot zone should be qualified and equipped with personal protective equipment including positive pressure breathing apparatus.

Victims that can walk should be lead out of the hot zone to the decontamination zone. Depending on resources, triage of remaining victims should be performed and victims removed from the hot zone.

Traumatic injuries and preexisting medical conditions may also be considered during triage.

The MARK I is the antidote kit used for nerve agent exposure. MARK I kits contain an auto-injector with 2 mg Atropine and an auto-injector with

600 mg 2-PAM (Pralidoxime) Chloride. MARK I kits have been widely distributed in the State of Illinois and available to emergency responders at the scene of a nerve agent emergency.

The benefits of antidote administration are reduced as the time from exposure to antidote administration increases. In the presence signs and symptoms of nerve agent exposure, initial antidote administration should be preformed immediately. This includes administration in the hot-zone prior to decontamination.

Both antidote medications reach peak effectiveness within 10 minutes when delivered by auto injector (3-10 minutes for Atropine and 6-8 minutes for 2 PAM Cl). Atropine use should continue until symptoms subside. In the presence of severe nerve agent exposure, as much as 50 mg of Atropine may be required in a 24 hour period. There is generally no benefit from administration of more than 1800 mg of 2-PAM Cl. Assistance with ventilations may also be required until antidote effectiveness can be obtained. The primary cause of death with nerve agent exposure is respiratory and airway complications.

Also useful, but not included in the MARK I kit, is the use of Diazepam for central nervous system (CNS) effects, particularly seizures. Unlike Atropine, Diazepam readily crosses the blood-brain barrier to block the effects of acetylcholine. In cases of severe exposure Diazepam is sometimes given to prevent seizures.

Exposure to blister agents can be through contact with either the liquid or the vapor. Like nerve agents, blister agents exist as a liquid. Aerosolizing and/or heating must be used to produce significant vapors.

Blister agents include Mustard (H), Distilled Mustard (HD), Nitrogen Mustard (HN1-HN3) and Lewisite (L). The primary effects of blister agents occur in the eyes, airway, mucous membranes and skin. Absorbed mustard may produce effects in other body systems.

Vesicants are generically referred to as "Mustard gas". What does mustard have to do with vesicants? In some forms it is yellowish and reputedly smells like mustard, but its aroma has also been likened to the smell of horseradish, garlic, and apples. At room temperature, it’s actually a liquid rather than a gas, but the name "mustard gas" has stuck since it was used in notorious gas attacks during World War I.

Symptoms of exposure may appear 1 to 6 hours after initial contact. This makes mustard gas especially insidious, since victims can suffer tissue damage before they even realize they need treatment. Mustard gas also attacks a cell’s DNA, so it can cause cancer and birth defects.

Reddening (Erythema) is the mildest and earliest form of injury appearing after exposure to mustard. It resembles sunburn, and is associated with itching or burning pain. It may begin 2 to 24 hours post vapor exposure.

Blistering appears later and can be quite severe. While nerve agents act in a manner similar to insecticides, vesicants act more like acids or caustics in their

effect.

The primary airway lesion from mustard is necrosis of the mucosa with later damage to the musculature of the airways if the inhaled exposure is large. The most common cause of death in mustard poisoning is respiratory failure; however, mustard is not commonly used to inflict death but to cause injury. In World War I there was a less than 5% mortality rate associated with Mustard exposure.

The eyes are the most sensitive to mustard vapor injury. The time between exposure and visible injury is shorter for the eyes than for skin. The GI tract is also very susceptible to damage, either from systemic absorption or ingestion. However, GI exposure is infrequent.

Central nervous system effects are poorly defined. In high doses mustards may be convulsants. In human exposures, people who were heavily exposed reportedly experienced neurological effects within several hours of exposure just prior to death. Small exposures have, in some cases, also reportedly resulted in victims appearing sluggish, apathetic and lethargic.

Lewisite is another blister agent that is similar to that of mustards, but far more immediate. Lewisites cause almost immediate pain and irritation of the skin and mucous membranes. Delayed symptoms, including reddening of the skin and blisters on the skin and eyes, as well as airway damage develop later. Lewisite has not been known to have been used on humans.

The proper response for exposure to Mustard is immediate decontamination then supportive medical care. Personal protective equipment before patient decontamination includes Level A protection. Decontamination within 1 to 2 minutes following exposure is the only effective means for decreasing tissue damage. Later decontamination is not likely to improve the victim’s condition but will protect other personnel from exposure.

There is no antidote for mustard exposure. There is an antidote for exposure to lewisite call The British Anti-Lewisite Cream, however I am not aware of its availability in Central Illinois.

In addition to the chemicals, there are a variety of agents, many that are commonly in industrial settings, which could be used in an attack. An example of this is chlorine or ammonia, both choking agents. As mentioned before there are also riot control agents, vomiting agents, and incapacitating agents which are not intended to be of a lethal nature. For industrial agents, poison control or common hazardous materials references should be used.