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

Medical Aspects of Chemical Warfareusually requiring more than 60% mutant genes forsymptoms to present. Patients with LHON are normaluntil the sudden onset of blindness between the agesof 15 and 35. 158 The stressor leading to cell death of thehighly aerobic optic nerve is the elevated blood cyanidelevel associated with smoking and the associated bloodcyanide level. 159Given the likely acute high-level exposure expectedin a military environment, it is reasonable to ask whethercyanide exposure can lead to blindness in someindividuals. This is theoretically possible in the smallfragment of the population with LHON mutations,although no cases have been reported. There is onlyone case of blindness from acute cyanide poisoning inthe literature, a temporary case caused by a sodiumnitroprusside overdose. 160Cyanide can also be responsible for some cases ofgoiter. Elevated levels of thiocyanate as well as thyroidabnormalities have been documented in individualson cyanogenic food diets and those in industries withchronic exposures such as electroplating. 161 Thiocyanateprevents uptake of iodine into the thyroidgland. 162Patients with chronic renal failure who smoke havebeen known to develop a condition known as uremicneuropathy, a result of the accumulation of thiocyanate,the major detoxification metabolite of cyanide.In these patients, thiocyanate cannot be removedfrom the body, even with dialysis. Treatment involvesadministration of hydroxocobalamin antidote, whichuses a different chemical pathway. 163Several conditions were previously thought to beassociated with cyanide, including lathyrism, a neurologicaldisorder associated with grass pea ingestion.Subacute combined degeneration of the spinal cord,attributed to cyanide in the past, is now well knownto be related to vitamin B12 metabolism.In summary, the long-term effects of cyanide exposureare highly variable. Severe exposures and caseswith delayed treatment may manifest in a Parkinsonianakinetic syndrome. Long-term exposure to cyanideis likely in areas where cassava is the staple foodand represents a likely risk to future prisoners of warin these areas. Long-term cyanide exposure combinedwith poor protein intake leads to neuromotor andneurosensory disorders. Smoking represents a chroniccyanide exposure that may lead to permanent blindnessin rare individuals. Most importantly, the majorityof cyanide-exposed individuals who receive prompttreatment may expect no long-term sequelae followingan acute cyanide exposure. This fact emphasizes theimportance of prompt casualty care.TOXIC INHALATION INJURYThe pulmonary agents are absorbed almost exclusivelyby inhalation. They readily penetrate to thelevel of the respiratory bronchioles and alveoli, thatis, to the peripheral compartment of the respiratorytree. However, most of these agents are essentiallyconsumed by reactions occurring at the alveolar-capillarymembrane, or more proximally in the respiratorytract, and are not systemically distributed to a clinicallysignificant extent.Inhalation of selected organohalides, oxides ofnitrogen, and other compounds can result in varyingdegrees of pulmonary edema, usually after a symptomfreeperiod that varies in duration with the amountinhaled. Chemically induced acute lung injury by theseagents involves a permeability defect in the blood–airbarrier (the alveolar-capillary membrane); however,the precise mechanisms of toxicity remain an enigma.The United States produces over a billion pounds ofphosgene per year for industrial uses; however, it isnot stockpiled for military use.Perfluoroisobutylene (PFIB) is a toxic pyrolysisproduct of tetrafluoroethylene polymers encounteredin military materiel (eg, Teflon [DuPont, Wilmington,Del] found in the interior of many military vehicles).The oxides of nitrogen are components of blast weaponsor may be toxic decomposition products. Smokes(eg, HC) contain toxic compounds that cause the sameeffects as phosgene. 164 The long-term health effects ofphosgene exposure also apply to casualties from agentssuch as PFIB and oxides of nitrogen. 165PhosgenePhosgene produces pulmonary edema following aclinical latent period of variable length that dependsprimarily on the intensity of exposure (ie, the Ct), butalso partly on the physical activity of the exposed individual.After the latent period, the patient experiencesworsening respiratory distress that at first is unaccompaniedby objectively verifiable signs of pulmonarydamage, but may progress relentlessly to pulmonaryedema and death.During the time preceding the appearance of shortnessof breath, individuals exposed to particularly highconcentrations of organohalides may report symptomsassociated with mucous membrane irritation.Exposure to large quantities of phosgene may irritatemoist mucous membranes, presumably because of thegeneration of hydrochloric acid from the hydrolysis ofphosgene. Transient burning sensation in the eyes with324