Nerve agents ocular effects

Exposure to acutely toxic concentrations of nerve agents can result in excessive bronchial, salivary, ocular and intestinal secretions, sweating, miosis, bronchospasm, intestinal hypermotility, bradycardia, muscle fasciculations, twitching, weakness, paralysis, loss of consciousness, convulsions, depression of the central respiratory drive, and death (Grob and Harvey, 1953 Grob, 1956 Marrs, 2007 Sidell, 1997 Yanagisawa et al, 2006 many others). Minimal effects observed at low vapor concentrations... 

Nerve agents can be absorbed by any route (ocular, oral, inhalation, dermal) (RTECS, 2008 HSDB, 2008). Onset of signs and duration of effects depend on the form of nerve gas (vapor, hquid) and the route of exposure. With a vapor exposure and inhalation, local signs of nasal discharge and respiratory noise begin within one to several minutes and signs can last for a few hours (mild exposure) up to 1 to 2 days (severe exposure) (Pfaff, 1998). Inhalation of a large amount of the vapor will result in sudden loss of consciousness, apnea, flaccid paralysis, and seizures within seconds to 2 to 3 min (Sidell et al, 1997). Peak effects are seen within 20 to 30 min and death is usually due to respiratory failure (Berkenstadt et al, 1991). 

Toxic effects occur within seconds to 5 min of nerve agent vapor or aerosol inhalation. The muscarinic effects include ocular (miosis, conjunctival congestion, ciliary spasm), nasal discharge, respiratory (bronchoconstriction and increased bronchial secretion), gastrointestinal (anorexia, vomiting, abdominal cramps, and diarrhea), sweating, salivation, and cardiovascular (bradycardia and hypotension) effects. The nicotinic effects include muscular fa-sciculation and paralysis. CNS effects can include ataxia, confusion, loss of reflexes, slurred speech, coma, and paralysis. 

Casualties are caused both by inhalation and by dermal contact. Since VX is an oily liquid with low volatility, liquid droplets on the skin do not evaporate quickly, thus facilitating effective percutaneous absorption. Clothing can release VX for about 30 min after contact with VX vapor, which can lead to the exposure of other people. In addition to inhalation and percutaneous exposure, casualties can also be caused by ocular exposure, ingestion, and injection. Although VX does not mix with water as easily as nerve agents do, it could be released into water and lead to exposures via drinking contaminated water or dermal contact with contaminated water. People can also be exposed by eating food contaminated with VX. 

III. Ocular Effects of Nerve Agent Vapor/Aerosol Exposure.236... 

III. OCULAR EFFECTS OF NERVE AGENT VAPOR/AEROSOL EXPOSURE... 

Agent GA (tabun) is an organophosphate ChE inhibitor similar to other nerve agents in mode of action and toxic effects, and it is toxic by all possible exposure routes ingestion, inhalation, and ocular and percutaneous absorption (DA 1974). By the inhalation exposure route, GA is only half as toxic as GB however, at low concentrations it has a greater effect on the eyes (DA 1974). The acute toxicity of GA and other nerve agents has been reviewed in several earlier reports (Carnes and Watson 1989 Dacre 1984 Munro et al. 1994 Sidell 1992 ... 

Notably, the miotic effect of OPNAs is mainly due to ocular absorption rather than systemic distribution, since liquid agent on the skin will not cause miosis until near-lethal doses (Table 38.4 Romano et al., 2008). In contrast, a droplet of liquid in or near the eye will cause miosis at very low concentrations (Hurst et al., 2007). Together, these suggest that the relatively privileged environment of the inner eye is more susceptible to direct absorption of nerve agent and drugs than to systemically circulated compoxmds. Furthermore, they indicate that the onset... 

As demonstrated with fluorophotometry, timolol acts predominantly by decreasing the production of aqueous humor and does not significantly alter facility of outflow. Most studies support the view that both short-term and long-term administration of timolol do not alter optic nerve head circulation or produce retrobulbar hemodynamic changes. The ocular hypotensive effect of timolol is additive to most other therapies, including outflow agents (e.g., pilocarpine) and inflow agents (e.g., dorzolamide, brinzolamide, apraclonidine, and brimonidine). When added to latanoprost, timolol and most other P-blockers further reduce lOP approximately 2 mm Hg. This reduction is less than that attained by topical CAIs such as dorzolamide (Table 10-2). 

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