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

Long-Term Health Effects of Chemical Threat Agentspostexposure, a particularly severe respiratory symptomcomplex may appear suddenly; exertion seemsto be a prominent precipitating factor. There may besevere cough, dyspnea, and rapid onset of pulmonaryedema. If the patient survives this stage, spontaneousremission occurs within 48 to 72 hours postexposure.More intense exposures produce a relatively rapid onsetof acute bronchiolitis with severe cough, dyspnea,and weakness, without the above-mentioned latentperiod. Again, spontaneous remission occurs at approximately3 to 4 days postexposure. 175Phase 2 is a relatively asymptomatic period lastingapproximately 2 to 5 weeks. A mild residual coughwith malaise and perhaps minimal shortness of breathmay occur, as well as a sense of weakness that mayprogress. The chest radiograph, however, typically isclear. In phase 3, symptoms may recur 3 to 6 weeksafter the initial exposure. Severe cough, fever, chills,dyspnea, and cyanosis may develop. Crackles areidentified on physical examination of the lung. Thepolymorphonuclear white blood cell count is elevated,and the partial pressure of carbon dioxide may be elevatedas well. 176 The chest radiograph demonstratesdiffuse, scattered, fluffy nodules of various sizes,which may become confluent progressively, with abutterfly pulmonary edema pattern and a prominentacinar component. At this point, pathological studydemonstrates classic bronchiolitis fibrosis obliterans,which may clear spontaneously or may progress tosevere, occasionally lethal respiratory failure. Thefluffy nodular changes noted in the chest radiographtypically show no clinical improvement. Pulmonaryfunction testing may show long-term persistence ofairways obstruction. 177–179Zinc OxideHexachloroethane (HC) smoke, a mixture of equalamounts of HC and zinc oxide with additional ingredients,is a toxic military smoke and obscurant. HC’stoxicity is attributed to the irritating effects of zincchloride. Most likely, carbon monoxide, phosgene,hexachloroethane, and other products contribute tothe observed respiratory effects. The damage to thepulmonary system is confined largely to the upperrespiratory tract, where zinc chloride acts much likea corrosive irritant. Studies reveal that HC exposurecan produce a gradual decrease in total lung capacity,vital capacity, and diffusion capacity of carbonmonoxide. HC is associated with the presence ofpulmonary edema, increased airway resistance, anddecreased compliance. When HC smoke exposure isdiscontinued, the pulmonary changes are reversible inall but 10% to 20% of those effected, who could developpulmonary fibrotic changes. 180In a study by Conner et al 181 performed withguinea pigs, exposure to ultrafine HC particles (0.05µm) in increasing degrees was associated with adose-response elevation in protein, neutrophils, andangiotensin-converting enzyme found in lavage fluid.A direct relationship also was observed with alkalinephosphatase, acid phosphatase, and lactate dehydrogenasein lavage fluid. Centriacinar inflammation wasseen histologically, indicating evidence of pulmonarydamage. A study by Marrs et al 182 involving mice, rats,and guinea pigs demonstrated a positive associationof alveologenic carcinoma in a dose-response trendto HC smoke, as well as a variety of inflammatorychanges. The article states that hexachloroethane andzinc, as well as carbon tetrachloride (which may bepresent in HC smoke), may be animal carcinogens incertain circumstances. This raises the suspicion of HCas a potential carcinogen.Metal fume fever is a well-documented acute diseaseinduced by intense inhalation of metal oxides,especially zinc oxide. The exact pathology is not understood,but the clinical syndrome is well describedand has been studied at length. A study by Kuschneret al 183 on human volunteers showed that pulmonarycytokines such as tumor necrosis factor, interleukin6, and interleukin 8 may play important initial rolesin mediating metal fume fever. Prolonged exposuresor exposures to very high doses of HC may resultin sudden early collapse and death, possible as aresult of laryngeal edema or glottal spasm. If severeexposure does not kill the individual immediately,hemorrhagic ulceration of the upper airway may occur,with paroxysmal cough and bloody secretions.Death may occur within hours secondary to an acutetracheobronchitis.Most individuals with HC inhalation injuriesprogress to complete recovery. Of exposed individuals,10% to 20% develop fibrotic pulmonary changes.Distinguishing between those who will recover andthose who will not is difficult, because both groupsmake an early clinical recovery.SUMMARYA wide variety of chemical agents and industrialproducts are associated with long-term health consequencesafter an acute insult. Others are knownto be harmful with prolonged low-level exposure.The linkage between these associations is sometimestenuous given the limitations of retrospective studiesand case reports up to 90 years old. Research laboratoryefforts and future case reports will continue327