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

Toxic Inhalational Injury and Toxic Industrial Chemicalsbrotic pulmonary changes. Appropriate precautions,such as wearing protective masks, must be taken whenHC smoke is used. 95Chemicals That Act on Both the Central andPeripheral AirwaysChlorineChlorine is a good example of a combinationagent, one that acts on both airway compartments inlow doses because of its intermediate water solubility.Chlorine’s effectiveness as a warfare agent wasgreatly reduced once protective masks became widelyavailable in World War I, but it continues to be seenin industrial accidents. The Occupational Safety andHealth Administration’s permissible exposure levelof chlorine is 1 ppm. The National Institute for OccupationalSafety and Health has determined thatthe IDLH concentration is 25 ppm. Chlorine turns tohydrochloric acid when it contacts the moisture ofthe airway; the hydrochloric acid then causes tissueburns to the epithelia of the conjunctivae and upperrespiratory mucus membranes. 97 Chlorine producessigns and symptoms similar to those associated withexposure to both centrally and peripherally actingagents. A chest radiograph of a chemical worker 2hours after exposure to chlorine shows diffuse pulmonaryedema without considerable cardiomegaly(Figure 10-10). This person also experienced severeresting dyspnea and diffuse crackles on auscultation.Although the central lung damage of chlorine injurymay seem to be the primary concern in some patients(ie, they are coughing and wheezing), the healthcareprovider must anticipate treatment for potentialdevelopment of peripheral symptoms and take seriouslyany patient complaints about chest tightnessor breathing difficulty. 96Clinical EffectsCentrally Acting AgentsAlmost immediately after exposure to these gassesor vapors, the casualty can develop a laryngospasm,which could cause sudden death. As the airways areirritated and damaged, the individual may experiencea wide variety of symptoms including sneezing; developmentof rhinorrhea; tachypea; pain in the nasopharynx,indicating early inflammation; dysphagia fromthe pain of swallowing; oropharyngeal inflammation;hoarseness; a feeling of choking; noise with exhalationcaused by laryngeal edema (the hallmark sign of cen-Fig. 10-10. The chest radiograph of a female chemical worker2 hours postexposure to chlorine inhalant. On medical examinationshe had severe resting dyspnea during the 2ndhour, diffuse crackles/rhonchi on auscultation, and a Po 2of32 mm Hg breathing room air. The radiograph shows diffusepulmonary edema without significant cardiomegaly.trally acting agents); chest pain or retrosternal burning;coughing, which could be violent at times; wheezingduring breathing from the trachea and bronchi inflammation;and edema. If the exposure is severe enoughand the TIC has penetrated into the peripheral airway,the casualty may experience peripheral effects. Later,scarring of the central airway can cause permanentairway narrowing, depending on the agent involvedand the dose received.Peripherally Acting AgentsPeripherally acting agents exert a direct toxic effecton the peripheral compartment of the respiratory tract,leading to damage of the alveolar-capillary membraneand the hallmark clinical effect—dyspnea. The time toonset of clinical effects from peripherally acting agentsdepends on dose, duration, and concentration. Shortlyafter low concentration exposure to phosgene or otheragents affecting the peripheral airway, the casualtiesare typically asymptomatic for 30 minutes to 72 hours(although they may notice irritation of the eyes, nose,and throat). However, symptoms may progress tocomplaints of coughing and dyspnea on exertion. Themajor effects do not occur until hours later. More significantexposures have a latency period of less than 24hours. Chlorine, which can affect both compartmentsbut primarily affects the central compartment of therespiratory tract, can also exhibit delayed effects in theperipheral compartment.Approximately 2 to 24 hours after exposure, the ca-359