Organophosphorus nerve agent response

Pyridostigmine bromide competitively binds to nerve tissue AchE. The binding is reversible and has been shown to protect AchE against irreversible inhibition by organophosphorus nerve agents. Pyridostigmine is a quarternary compound and does not readily cross the blood-brain barrier. Thus, it is not expected to affect or protect brain AchE. Cholinesterase inhibition, which is a mechanism of action, is also responsible for toxicity. 

In the lead-up to World War II, the Germans forever changed chemical warfare with the discovery of the organophosphorus nerve agents (Goebel, 2008). These agents inhibit cholinesterase enzymes in the nerve synapse responsible for the breakdown of the neurotransmitter acetylcholine (ATSDR, 2008). This results in the accumulation of the neurotransmitter in the synapse and overstimulation of the nervous system. This can result in subsequent respiratory failure and death (ATSDR, 2008). 

As mentioned, nerve agents designed for use as CWAs are mostly derivatives of organophosphorus compounds that have high proton affinities. Thus, the sensitivity and specificity of response and the high speed of measurement make mobility spectrometers superb instruments for in-field or on-site determinations. In addition, blister agents and related breakdown products can be detected in the negative polarity. 

The principal nerve agents. Sarin (GB), Soman (GD), Tabun (GA) and V-agents, are all organophosphorus compounds that inhibit the enzyme cholinesterase which is responsible for breaking down acetylcholine, a neurotransmitter. Nerve agents are toxic both by inhalation and by absorption through the skin. Symptoms include droohng, dilated pinhead pupils, headache, involuntary defecation, and a runny nose. Death is caused by cardiac arrest or respiratory failure. 

Acoustic analysis detects changes in the properties of acoustic waves as they travel at ultrasonic frequencies in piezoelectric materials. The interaction between the waves and the phase-matter composition facilitates chemical selectivity and, thus, the detection of CWA s. These are commonly known as surface acoustic wave (SAW) sensors. Reported studies indicate detection limits as low as 0.01 mg m for organophosphorus analytes within a 2 min analysis [1]. There are several commercially available SAW instruments, which can automatically monitor for trace levels of toxic vapors from G-nerve agents and other CWAs, with a high degree of selectivity. A major advantage of SAW detectors is that they can be made small, portable and provide a real-time analysis of unknown samples. One of the drawbacks of these instruments is that sensitivity and a rapid response time are inversely related. In an ideal instrument, both parameters would be obtained without sacrificing one for the other. 

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