Neurological aspects of chemical terrorism

Abstract

This review describes the neurological aspects of chemical terrorism with a focus on the civilian perspective. This review defines chemical threats as highly toxic chemicals that could be used in a terrorist attack, or those that could be released at toxic levels from transportation vehicles and storage facilities during an accident or natural disaster. Chemical threats can be categorized based on the target tissues and types of primary acute effects they produce (Table). Probably the most easily recognizable chemical terrorism threats are the traditional chemical warfare agents (CWAs) developed during the first and second World Wars. These include the organophosphorus (OP) nerve agents, such as sarin and VX, and the mustard blister agents. As a consequence of previous state-sponsored CWA programs, several stockpiles remain around the world. Sulfur mustard and OP nerve agents were used against Iraqi Kurdish villages in the late 1980s, and more recently, the OP nerve agents were used by the Japanese cult organization Aum Shinrikyo in two separate attacks against civilians in Japan.

Role of muscarinic signal transduction and CREB phosphorylation in dichlorvos-induced memory deficits in rats: An acetylcholine independent mechanism

“…In developing countries, over 3 million poisonings occur annually due to these pesticides, out of which 220,000 are fatal (Eddleston et al, 2002). In addition to their use in the control of insects and pests, some cholinesterase inhibitors are used as therapeutic agents (Cummings et al, 2008) as well as chemical warfare agents (Balali-Mood and Balali-Mood, 2008;Jett, 2007). Dichlorvos (DVPP), an organophosphorus pesticide, has been used as a crop protectant and as a general public health insecticide since 1961.…”

Inhibition of the prostaglandin EP2 receptor is neuroprotective and accelerates functional recovery in a rat model of organophosphorus induced status epilepticus

“…Exposure to high levels of organophosphorus compounds induces status epilepticus (SE, an unremitting seizure lasting longer than 5 to 30 min, or a series of seizures without intervening regain of consciousness) in humans and rodents, leading to brain injury and long-term cognitive deficits. The current treatments following toxic OP exposure in man such as pralidoxime (2-PAM) and atropine, must be given soon after OP exposure for optimal effectiveness (Jett, 2007). Delay in atropine administration results in decreased heart rate, increased bronchial secretions, lacrimation, and other features of cholinergic stimulation.…”

“…Delay in atropine administration results in decreased heart rate, increased bronchial secretions, lacrimation, and other features of cholinergic stimulation. The administration of an oxime such as 2-PAM helps to remove OP agents from acetylcholinesterase and prevent aging in which the bond between the OP and AChE is strengthened thus destroying the enzyme (Jett, 2007). Diazepam is administered to terminate seizures that may develop following OP exposure (Jett, 2007).…”

Intranasal delivery of obidoxime to the brain prevents mortality and CNS damage from organophosphate poisoning

“…Military and industrial organophosphates are also potential chemical threat agents (CTA) that can pose risks for both military personnel and civilian populations (Jett, 2007). Organophosphate based CTA exert their toxic effects by inhibiting acetylcholinesterase (AChE) leading to the accumulation of acetylcholine at synaptic and neuromuscular junctions.…”