Lung Damaging Agents (Choking Agents)
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377 J R Army Med Corps: first published as 10.1136/jramc-148-04-07 on 1 December 2002. Downloaded from Lung Damaging Agents (Choking Agents) GENERAL lung damaging materials injury such as those in smoke or products of combustion may Introduction cause toxic inhalational injury following the Lung damaging agents are chemical agents, generation of particulate aerosols. which produce a toxic inhalational injury – Military dispersion of phosgene during they attack lung tissue and primarily cause World War I followed the explosion of liquid pulmonary oedema. Whether produced for filled shells with subsequent rapid military or industrial use, these chemical evaporation and formation of a white cloud agents pose a very real threat to military due to its slight solubility in an aqueous personnel. environment. It spontaneously converted to a The term choking agents has been colourless, low-lying gas four times as dense traditionally applied to the use of certain as air. Because of its relatively low boiling lung damaging agents as chemical weapons, point (7.5ºC), phosgene was often mixed with and includes phosgene (CG), diphosgene other substances. Chlorine was released from (DP), chlorine (CL), and chloropicrin (PS). pressurised cylinders to form a pungent Phosgene accounted for 80% of all chemical greenish-yellow gas that was heavier than air. fatalities in World War I, but at least 14 different respiratory agents were used, as well Detection as obscurants (smokes), harassing agents Although field-detection equipment for (chloracetone), and vesicants (mustard) that classical choking agents is currently could cause pulmonary injury. employed by some nations, and various Today, only a handful of such pulmonary commercial industrial detectors are available toxicants still exist in stockpiles around the for the wider of lung damaging agents, there world. Several however, such as chlorine and are no automatic detectors in service. The phosgene, are currently produced in large characteristic odour of some lung damaging quantities for industrial purposes; other toxic agents may be unreliable as a sure means of industrial chemicals which may cause toxic detection. For example, in low concentration http://militaryhealth.bmj.com/ inhalational injury include ammonia, phosgene has a smell resembling new mown isocyanates, mineral acids etc. hay, but the odour may be faint or lost after Other lung damaging materials – although accommodation. There is also considerable not likely to be used as CW agents - are still variation in the sense of smell between likely to be encountered on the battlefield. individuals. Perfluoroisobutylene (PFIB) is a toxic Similarly the eye irritation, coughing, pyrolysis product of tetrafluoroethylene sneezing, hoarseness, and other central polymers encountered in military materiel respiratory effects seen after exposure to high (e.g., Teflon®, found in the interior of many concentrations of some pulmonary toxicants are also unreliable indicators of exposure, as military vehicles). The oxides of nitrogen on September 29, 2021 by guest. Protected copyright. (NOx) are components of blast weapons or these may be transient or entirely absent at may be toxic decomposition products. lower but still potentially lethal Smokes (e.g. HC) contain toxic compounds concentrations. This is particularly true in that cause the same effects as phosgene. the case of phosgene. Similar substances encountered in fires, e.g. PFIB, isocyanates, phosgene, and HCl may Protection also produce lung damage. Chemical fire The activated charcoal in the canister of the extinguishers containing carbon dioxide chemical protective mask adsorbs phosgene, should not be used in confined spaces to and in-service respirators afford full extinguish thermite or magnesium types of protection from this and other choking incendiaries - carbon tetrachloride in contact agents. However, only limited or temporary with flame or hot metal produces a mixture protection against toxic products of of phosgene, chlorine, carbon monoxide and combustion or smoke can be assumed, and hydrochloric acid. may be complicated in addition by the presence of oxygen-depleted air. Physical and Chemical Properties Decontamination Choking agents are usually true gases in field No decontamination is required following environments, and stored and transported as exposure to classic choking agents or other a liquid under pressure. Other less volatile lung damaging agents in gas or vapour form. 378 J R Army Med Corps: first published as 10.1136/jramc-148-04-07 on 1 December 2002. Downloaded from Following exposure to high concentrations of centrally acting irritants, sufficient agent may penetrate into the peripheral lung to cause pulmonary oedema. Similarly, high conc- entrations of peripherally-acting agents can release enough hydrochloric acid to cause significant central airway irritation and epithelial damage. Because chlorine is intermediate in its solubility and reactivity, chlorine-exposed soldiers in World War I usually exhibited both central airway damage and pulmonary oedema, even from moderate concentrations of the gas. Phosgene is only slightly soluble in water and aqueous solutions; once dissolved, it rapidly hydrolyses to form carbon dioxide and hydrochloric acid. The early-onset ocular, nasopharyngeal, and central airway irritation from high concentrations of phosgene appears to result from the release of Fig 26. Phosgene induced injury to pig lungs. hydrochloric acid during phosgene hydrolysis by water in the upper airways. Mechanism of Action Chemicals that are highly reactive and/or Toxicity highly soluble in aqueous solutions tend to The odour threshold for phosgene is about act in the conducting, or central 1.5 mg/m3, and phosgene irritates mucous compartment of the respiratory tract. membranes at 4 mg/m3. The LCt50 of Centrally-acting irritants such as sulphur phosgene is approximately 3200 mg.min.m-3, mustard, ammonia, and hydrochloric acid, which is half the LCt50 (6,000 mg.min.m-3) cause pronounced irritation of the epithelial of chlorine, the first gas used on a large scale cells lining the upper airway. Additionally, at in World War I. Phosgene is twice as toxic as low concentrations, centrally-acting chlorine; although it is less potent than compounds are essentially consumed by almost all of the subsequently developed deposition and reaction in the conducting chemical warfare agents, this should not lead airways before they reach the peripheral to an underestimation of its danger - deaths portion of the respiratory tract. have occurred after the inhalation of only a In contrast, most of the pulmonary agents, few breaths of high concentrations of http://militaryhealth.bmj.com/ such as phosgene, oxides of nitrogen, and phosgene. Perfluoroisobutylene (PFIB) is PFIB, are relatively insoluble and said to be ten times more toxic than nonreactive, readily penetrating to the level phosgene. of the respiratory bronchioles and the alveoli. There they undergo acylation reactions and are essentially consumed at that site, causing CLINICAL-PATHOLOGICAL the damage that may eventually lead to pulmonary oedema. EFFECTS Chemically induced, acute lung injury by these peripherally-acting agents involves a Pathology permeability defect in the blood-air barrier The outstanding feature of acute lung injury on September 29, 2021 by guest. Protected copyright. (the alveolar-capillary membrane); however, caused by lung damaging agents is massive the precise mechanisms of toxicity remain pulmonary oedema. This is preceded by largely unknown. Leakage of fluid from damage to the bronchiolar epithelium, capillaries into the pulmonary interstitium is development of patchy areas of emphysema, normally compensated by lymphatic partial atelectasis, and oedema of the drainage from the parenchyma, but as the perivascular connective tissue. The trachea fluid leakage increases, normal drainage and bronchi are usually normal in mechanisms become progressively over- appearance. This contrasts with the findings whelmed. After an asymptomatic or latent in chlorine and chloropicrin poisoning in period of 20 min to 24 h (depending on the which both structures may show serious exposed dose), fluid leakage into the damage to the epithelial lining with pulmonary interstitium decreases comp- desquamation. The lungs are large, liance producing a stiff lung and increasing oedematous and darkly congested. Oedema complaint of tight chest, shortness of breath, fluid, usually frothy, pours from the bronchi and dyspnoea. Fluid eventually invades the and may be seen escaping from the mouth alveoli and produces clinically evident and nostrils (Figure 26). With exposure to pulmonary oedema. very high concentrations, death may occur The distinction between centrally and within several hours; in most fatal cases peripherally acting agents is not strict. pulmonary oedema reaches a maximum in 379 J R Army Med Corps: first published as 10.1136/jramc-148-04-07 on 1 December 2002. Downloaded from 12h, followed by death in 24 to 48h. If the support, such patients are at high risk of casualty survives, resolution commences death. Complications include infection of within 48h and, in the absence of comp- damaged lungs and delayed deaths following licating infection, there may be little or no such respiratory infections. residual damage. Condition of Exposed Tissues Clinical Effects Pre-existing airway damage (such as that Exposure to high concentrations of lung caused by prior exposure to a lung damaging damaging agent may