VG is the common name for a highly toxic organophosphate compound, officially classified as O,O-Diethyl S-[2-(diethylamino)ethyl] phosphorothioate, which belongs to the V-series of nerve agents. The V-series agents are recognized as chemical weapons due to their extreme potency and ability to severely disrupt the nervous system. VG, also known as Amiton or Tetram, was originally developed in the 1950s during research into new types of pesticides. VG represents a significant chemical warfare threat, despite being less commonly discussed than its relative, VX.
Understanding the Chemical Structure
VG is chemically categorized as an organophosphate compound, an organic molecule that contains phosphorus. This chemical group is known for interfering with biological processes, which is why similar compounds were initially explored for use as insecticides. The agent’s classification as a V-series nerve agent signifies its high persistence and low volatility.
As an oily liquid at room temperature, VG does not easily evaporate, allowing it to remain active on surfaces for an extended period. This property makes it dangerous primarily through skin contact, as it is readily absorbed through the dermis. The low volatility contributes to its designation as a “persistent” agent, unlike the more volatile G-series agents like Sarin.
How VG Disrupts the Nervous System
VG functions as a potent inhibitor of the enzyme acetylcholinesterase (AChE). Acetylcholinesterase is responsible for breaking down the neurotransmitter acetylcholine (ACh) after it has transmitted a signal. By inactivating this enzyme, VG prevents the natural termination of nerve impulses.
The organophosphate molecule in VG binds covalently to the active site of the AChE enzyme, effectively blocking its function. This binding process leaves the enzyme unable to hydrolyze acetylcholine. The resulting buildup of acetylcholine at nerve junctions causes continuous, uncontrolled signaling throughout the nervous system. This constant overstimulation affects both muscarinic and nicotinic receptors, leading to a state known as cholinergic crisis.
Recognizing the Physical Symptoms of Exposure
VG exposure causes severe physical symptoms across multiple body systems due to massive overstimulation. Initial symptoms following inhalation can appear within seconds to minutes, including a runny nose and tightness in the chest due to bronchial muscle constriction. Skin contact with the liquid agent delays the onset of systemic symptoms for several hours, often starting with localized sweating and muscle twitching at the contact site.
Systemic poisoning results from the overactivity of the parasympathetic nervous system. Patients experience profound glandular effects, including excessive salivation, tearing (lacrimation), and profuse sweating.
Vision is affected by miosis (pinpoint pupils) and blurred vision.
Gastrointestinal distress is prominent, causing abdominal cramps, nausea, vomiting, and involuntary urination and defecation.
Uncontrolled signaling leads to muscle fasciculations (involuntary twitches), followed by general muscle weakness. In severe cases, this progresses to flaccid paralysis of the entire body, including the respiratory muscles, which is the primary cause of death. Central nervous system effects include confusion, restlessness, and seizures. The combination of bronchial constriction, massive secretions, and paralysis leads to respiratory failure. Rapid intervention is necessary because death from asphyxiation or cardiac arrest can follow in minutes, particularly after high-dose exposure.
Immediate Medical Intervention and Treatment
Immediate medical response focuses on rapid decontamination and the administration of specific pharmacological antidotes. Decontamination requires removing contaminated clothing and washing the skin with soap and water or specialized agents to halt ongoing absorption of the oily liquid. Rescuers must wear appropriate personal protective equipment to prevent secondary exposure.
The pharmacological treatment involves a combination of two types of antidotes, often delivered via autoinjector systems. Atropine is administered to block the effects of excess acetylcholine at the muscarinic receptors. This action helps to manage life-threatening symptoms like excessive secretions and bronchoconstriction, which threaten the airway.
The second antidote is an oxime, such as pralidoxime (2-PAM). Pralidoxime works to reactivate the inhibited acetylcholinesterase enzyme by cleaving the nerve agent molecule from its active site. This restores the body’s natural mechanism for breaking down acetylcholine, but it is most effective if administered soon after exposure before the enzyme-agent bond “ages.” If seizures are present, a benzodiazepine, such as diazepam, is also used to control central nervous system overstimulation.