Medical Aspects of Chemical Warfare (2008) - The Black Vault

PROCESSToxic Inhalational Injury and Toxic Industrial Chemicalsif the exposure requires intensive care intervention. Bothlong-term effects and the potential for developing anARDS-like response must be taken into account in theadministration of therapeutic countermeasures.Clinical presentation and diagnosisThis section considers only TICs that pose a potentialthreat to military personnel. Although this list isnot complete, casualties from other lung-damagingagents are managed in the same way as these examples.In low doses, highly reactive TICs have agreater effect on the central airway; some TICs acton both the central and peripheral airways; and stillothers that are not as reactive in the central airwaycan defuse deeper into the respiratory tract and destroythe tissues of the alveoli-capillary membranein the peripheral airways, leading to noncardiacpulmonary edema. Any large inhaled dose of a TICcauses both central and peripheral airway damage(Figure 10-4).Centrally Acting Toxic Industrial ChemicalsCentrally acting chemicals affect the respiratory systemfrom the nasopharynx to the bronchioles. Centrallyacting TICs normally form strong acids or bases (alkali)with the water in the central airway tissues, whichleads to the destruction of these tissues. The damagedtissue swells, causing sloughing of the epitheliumlining into the airway and reactive smooth musclecontraction, causing restriction of breathing.Levels of exposure to toxic gases are defined by theshort-term exposure limit (STEL), time-weighted average(TWA), and concentrations at which toxic gassesare immediately dangerous to life or health (IDLH).STEL is the concentration of exposure that after 15minutes may cause immediate or chronic compromiseto health. TWA is the concentration for an 8-hour workdayof a 40-hour workweek that most workers can beexposed to without adverse effects. 91AmmoniaThis highly caustic and reactive gas has not beenused in warfare but may be encountered in industrialaccidents. Ammonia has a TWA of 25 ppm, an STEL of35 ppm and an IDLH of 500 ppm. Most injuries fromammonia are caused by inhalation. In low doses it isprimarily a centrally acting TIC (Table 10-6). Ammoniagas usually causes damage when it contacts the moist,watery tissues of the central airway, which results inthe formation of a strongly alkaline solution. This reactionis exothermic—capable of causing significantthermal burns and destruction to tissues —which couldlead to the victims presenting with a laryngospasmand airway collapse.In 1941 Caplin classified accidental ammonia inhalationas mild, moderate, and severe. Casualties withmild exposure present with pain and conjunctival andupper respiratory inflammation but no signs of respi-Table 10-6Gaseous ammonia effects at variousconcentrationsAmount(ppm)Effects25–50 Detectable odor; adverse effects unlikely50–100 Mild eye, nose, and throat irritation140 Moderate eye irritation400 Moderate throat irritation700 Immediate eye injury1,000 Directly caustic to airway1,700 Laryngospasm2,500 Fatal (after half-hour exposure)2,500–6,500 Sloughing and necrosis of airway mucosa,chest pain, pulmonary edema andbronchospasm5,000 Rapidly fatalFig. 10-4. Airway compartments: central and peripheral.Courtesy of: US Army Medical Research Institute of ChemicalDefense, Aberdeen Proving Ground, Md.Data source: Issley S. Toxicity, ammonia. eMedicine from WebMD.Available at: http://www.emedicine.com/EMERG/topic846.htm.Accessed August 6, 2007.355