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

Long-Term Health Effects of Chemical Threat Agentslacrimation and chemical conjunctivitis may coexistwith mild, early onset cough and a substernal achewith a sensation of pressure. Irritation of the larynxby very large concentrations of the agent may lead tosudden laryngeal spasm and death.A clinical latent period during which the patientis asymptomatic may follow low Ct exposure orthe transient irritation associated with substantialphosgene exposure. This asymptomatic period maypersist up to 24 hours after organohalide inhalation.The duration of the latent period is shorter followinga high dose and is shortened by physical exertionfollowing exposure.The most prominent symptom following the clinicallatent period is dyspnea, perceived as shortnessof breath, with or without chest tightness. Thesesensations reflect hypoxemia, increased ventilatorydrive, and decreased lung compliance, all of whichresult from the accumulation of fluid in the pulmonaryinterstitial and peripheral airways. Fine cracklescan be heard at the lung bases, but these may not beclearly audible unless auscultation is conducted aftera forced expiration. Later, auscultation reveals coarsecrackles and rales in all lung fields, and increasingquantities of thin, watery secretions are noted. Thebuildup of fluid in the lungs has two clinically pertinenteffects. First, developing pulmonary edemainterferes with oxygen delivery to alveolar capillariesand may lead to hypoxemia, and if a sufficientpercentage of hemoglobin is unoxygenated, cyanosiswill become apparent. Second, the sequestration ofplasma-derived fluid (up to 1 L per hour) in the lungsmay lead to hypovolemia and hypotension, interferingwith oxygen delivery to the brain, kidneys, andother crucial organs. Death results from respiratoryfailure, hypoxemia, hypovolemia, or a combinationof these factors. Hypoxia and hypotension mayprogress particularly rapidly, which suggests a poorprognosis. The development of symptoms and signsof pulmonary edema within 4 hours of exposure isan especially accurate indicator of a poor prognosis;in the absence of immediately available intensivemedical support, such patients are at high risk ofdeath. Complications include infection of damagedlungs and delayed deaths following such respiratoryinfections. 164 Several studies sponsored by theVeterans Administration using animals and humansreported that after phosgene exposure pulmonaryedema appeared very early. 166In July 1920, Winternitz’s 167 report on experimentalwork with dogs revealed acute changes in the cardiorespiratorysystem following exposure to lethal concentrationsof phosgene. The upper portion of the respiratorytract was not affected, but the alveoli of the lungsand the finer bronchi gave evidence of congestion,inflammation, and edema. The inflammatory reactionfollowing phosgene exposure resulted in congestionof the bronchial and spread into the surrounding aircells, indicative of an early bronchopneumonia witha marked edema of the lungs. Dilatation, reflex bronchiolarspasm, and plugging of the bronchiols withexudates led to patches of atelectasis and emphysema.A substantial amount of fibrin on alveolar walls, crossingand obstructing the capillaries, led to resistance inthe pulmonary circulation, with a consequent dilatationof the right heart. In the dogs, damage occurredprincipally in the respiratory tract, and lesions variedaccording to the length of survival after the exposure.Initial pulmonary edema associated with congestionreached a maximum intensity toward the end of thefirst 24 hours and gradually disappeared in animalssurviving 10 days or longer. With the edema, there wasan associated inflammatory exudation of fibrin andleucocytes. This cellular exudate was found especiallyin the finer bronchioles and extended into the alveolartissue. It was suggestive of a lobular pneumonia.The pneumonia was frequently complicated by necrotizationof the walls of the bronchioles, which alsoinvolved the adjacent alveoli and resulted in abscessformation. In some cases, although the inflammatoryprocess was succesesfully overcome, an obliterativebronchiolitis resulted.In the exposed dogs, the pathology was localized tothe trachea and bronchi. The epithelium of the tracheaand larger bronchi was damaged, while the smallerbronchi and bronchioles were the most seriously affected.In addition to changes in the mucosa, therewere contractions, distortions of the bronchioles, andmore or less obliteration of the lumina. All this led tomechanical disturbance in the air sacs, with restingatelectasis and emphysema.The Veterans Administration conducted a studyreviewing the histories of 10 veterans who had beengassed with phosgene and showed evidence of physicaleffects a number of years later. 166 This historicalstudy revealed that chronic bronchitis was the most frequentlong-term effect noted. Emphysema was notedin three of the veterans, pulmonary fibrosis was notedin two, chronic-active pulmonary tuberculosis wasfound in one case, and bronchial asthma was found inanother. This study also revealed that the symptoms ofthe pulmonary disabilities were observed immediatelyafter the phosgene gas exposure and continued to bethe causative factor the long-term pulmonary effectsat the time of the study. 166According to the Veterans Administration, the followingpathological changes were noted in soldierswho died following phosgene gas exposure 166 :325