Nerve agents are highly toxic chemical compounds developed as chemical weapons, designed to severely disrupt the nervous system. These human-made agents do not occur naturally and exist as liquids at room temperature. Though commonly called “nerve gas,” many are liquids rather than true gases. Even small exposures can cause rapid, severe health effects, making them among the most dangerous chemical warfare agents.
Mechanism of Action
Nerve agents primarily exert their harmful effects by interfering with the normal function of the nervous system. They specifically target an enzyme called acetylcholinesterase (AChE), which plays a crucial role in nerve signal transmission. Normally, when a nerve impulse is sent, the neurotransmitter acetylcholine carries the message across a synapse to a muscle or organ. Acetylcholinesterase then quickly breaks down this acetylcholine, allowing the muscle or organ to relax and prepare for the next signal.
When nerve agents enter the body, they irreversibly bind to acetylcholinesterase, preventing it from breaking down acetylcholine. This leads to an excessive accumulation of acetylcholine at nerve endings, continuously stimulating nerves, muscles, and glands. The constant overstimulation prevents muscles from relaxing, leading to uncontrolled contractions and eventually paralysis. This disruption can rapidly lead to respiratory failure and cardiac arrest, as the body loses control over essential functions.
Categorization of Nerve Agents
Nerve agents are broadly categorized into different series based on their chemical structure and properties. The G-series agents, including Tabun (GA), Sarin (GB), Soman (GD), and Cyclosarin (GF), were developed in Germany during World War II. These agents are typically watery liquids with high volatility, meaning they evaporate easily and pose a significant threat through both skin contact and inhalation. Sarin, for instance, evaporates almost as quickly as water and is odorless.
The V-series agents, such as VX, were synthesized after World War II and represent a later generation. Unlike G-series agents, VX is a persistent liquid with an oily consistency, evaporating slowly and posing a primary hazard through skin contact. It is more potent than G-series agents. Additionally, a group known as A-series agents, or Novichok agents, developed in the Soviet Union, are even more persistent and potent than V-series agents. The production and use of these chemicals are banned under the 1993 Chemical Weapons Convention.
Signs and Symptoms of Exposure
The effects of nerve agent exposure can vary depending on the specific agent, the amount absorbed, and the route of exposure. Inhalation of nerve agent vapor can cause symptoms to appear within seconds to minutes, while skin contact with liquid agents may delay symptoms for minutes or even up to 18 hours. Miosis, characterized by constricted, pinpoint pupils, is a hallmark ocular symptom and early indicator of exposure.
Other immediate effects include a runny nose, tightness in the chest, and difficulty breathing, accompanied by wheezing and increased bronchial secretions. Gastrointestinal symptoms are common, including nausea, vomiting, abdominal pain, and involuntary urination and defecation. Muscles may twitch uncontrollably, then become weak and paralyzed. In severe cases, individuals can experience seizures, loss of consciousness, and ultimately death due to respiratory failure.
Emergency Response and Treatment
Immediate action is critical due to the rapid onset of severe symptoms. First, move the affected individual to fresh air and rapidly remove contaminated clothing to prevent further absorption and secondary exposure. Skin should be thoroughly washed with soap and water, and eyes flushed with water or saline solution. First responders and assistants must wear appropriate personal protective equipment.
Medical treatment focuses on administering specific antidotes to counteract the effects of the nerve agent. Primary medications are atropine and pralidoxime chloride (2-PAM chloride). Atropine works by blocking the excessive acetylcholine at muscarinic receptors, reducing symptoms like increased secretions and bronchospasm. Pralidoxime chloride reactivates the acetylcholinesterase enzyme by removing the nerve agent from its binding site, restoring normal nerve function, particularly at nicotinic receptors affecting skeletal muscles. These antidotes are often administered via autoinjectors, and benzodiazepines like diazepam may also be given to control seizures.