The term “vesicant” is commonly applied to chemical agents that cause blistering of the skin. Direct contact with these agents can also result in damage to the eyes and respiratory system. Systemic absorption may affect the gastrointestinal (GI), hematologic, and central nervous systems as well.
The four compounds historically included in this category—sulfur mustard, the nitrogen mustards, lewisite, and phosgene oxime—were all manufactured initially as potential chemical warfare agents. Phosgene oxime is technically not a true vesicant because the skin lesions it causes are urticarial as opposed to vesicular. The nitrogen mustards, although first synthesized in the 1930s for anticipated battlefield use, were found to be less effective for chemical warfare than the already existing sulfur mustard. Subsequent development for of nitrogen mustards for weapons use was therefore largely abandoned. However, one form of nitrogen mustard, HN2, became a highly used and effective chemotherapeutic agent. Lewisite was first synthesized during the latter part of World War I, but other than reports of its use by Japan against China between 1937 and 1944, it is not known to have ever been used on the battlefield. An antidote, British antilewisite (BAL, or dimercaprol), can minimize its effects if given promptly. Because so little is known about the toxicity and mechanisms of action of phosgene oxime and lewisite, and because anticipated medical management issues of these agents are somewhat similar, the following section focuses on the clinical effects and management issues regarding sulfur mustard exposure—historically the most frequently used and available of this class of chemical agent.
Sulfur mustard has been the most widely used of all chemical warfare agents over the last century. Approximately 80% of chemical casualties in World War I were due to sulfur mustard, and its use has been verified in multiple military conflicts since then. In addition, Iraq used sulfur mustard on numerous occasions during its war against Iran from 1980 to1988 and as a weapon of terror against thousands of Kurdish civilians, including children, by using aerially dispersed mustard bombs in 1988.
Sulfur mustard is stockpiled both in the United States and in several other countries as well. It is not difficult to manufacture, making it even more favorable for use by terrorists. In addition to its accessibility and ease of production, several other factors enhance its suitability as a terrorist or warfare agent. Although mortality associated with sulfur mustard is considerably lower than that caused by other chemical weapons such as nerve agents, sulfur mustard exposure results in significant and prolonged morbidity that may potentially overwhelm health care resources. The risk of direct contamination either from patient contact or from the agent';s persistence in the environment may force health care providers to wear bulky protective gear, which makes it difficult to administer care, particularly to children. Although tissue damage occurs within minutes of exposure, clinical symptoms are delayed for hours, potentially rendering the victim ignorant of exposure until the opportunity for effective decontamination has passed. Lastly, unlike the case for lewisite, there is no known antidote for sulfur mustard exposure.
Sulfur mustard is an alkylating agent that is highly toxic to rapidly reproducing and poorly differentiated cells. Under normal environmental conditions, it is an oily liquid that varies in color from yellow to brown, depending on amounts and types of impurities. Its odor has been described as similar to garlic or to mustard itself. In warmer climates, mustard vapor is a particular concern due to its low volatility, while at lower temperatures (<14°C or 58°F); it becomes a solid and may persist in the environment for an extended time. On contact with tissue surfaces, mustard vapor or liquid is rapidly absorbed and exerts its cellular damage within minutes. Both vapor and liquid readily penetrate most clothing, although rubber overgarments may be protective for several hours.
After exposure to sulfur mustard, skin findings do not appear for 2-48 hours, depending on the mode of exposure, the sensitivity of the individual, and the environmental conditions (Table 5.5). The most common early sign in exposed areas is erythema resembling sunburn, which may coincide or even be preceded by significant pruritus. If the exposure is mild, this may be the only skin manifestation. More typically, yellowish blisters begin to form over the next 24 hours. Penetration of the agent is enhanced by thin skin, warmth, and surface moisture, rendering areas such as the groin, axillae, and neck particularly susceptible. Once they appear, the vesicles frequently coalesce to form bullae. Although largely painless, these fragile bullae commonly rupture, resulting in painful ulcers that may take weeks or months to heal. The fluid from the blisters does not contain free mustard and is therefore not hazardous. If skin exposure has been severe, these earlier stages of developing lesions may be bypassed altogether with the direct appearance—albeit delayed—of skin sloughing similar to that seen in a full-thickness thermal burn.
Although skin findings may be dramatic, the organ most sensitive to mustard exposure is the eye, with mild symptoms occurring at concentrations 10-fold lower than those needed to produce effects on the skin. Like the skin findings, ocular symptoms are also delayed, usually for 4-6 hours. The first symptoms are usually pain and irritation, followed progressively by photophobia, worsening conjunctivitis, corneal ulceration, and perforation of the globe with severe exposures. Although visual impairment is common, it is usually transient and simply reflects eye closure from intense pain and reflex blepharospasm as opposed to true damage to the optic nerve. Severe lid edema caused by inflammation of soft tissue around the eyes is also common.
With inhalation of mustard vapor, both the proximal and distal respiratory tract may be affected. Proximal involvement usually manifests after several hours and consists of rhinorrhea, hoarseness, a dry and painful cough with expectoration, and eventually a characteristic toneless voice due to vocal cord damage. With more significant inhalational exposures, necrosis of the airway mucosa can lead to a sterile tracheobronchitis with the necrotic epithelium forming pseudomembranes that may obstruct the airway. Bacterial superinfection may develop as well, usually days later, facilitated by a weakened immune response. Respiratory failure can be the end result of either early mechanical obstruction from laryngospasm or pseudomembrane formation or later by overwhelming bacterial infection enhanced by the denuded respiratory mucosa and necrotic tissue. Early onset of dyspnea, along with other signs of impaired peripheral gas exchange, such as hypoxia, is a sign of severe inhalational exposure and indicates a poor prognosis.
All cellular elements of the bone marrow can be affected by sulfur mustard due to its DNA alkylating effects, which impair replication in rapidly dividing stem cells. Megakaryocytes and granulocyte precursors are more susceptible than those of the erythropoietic system, and therefore the presence of anemia along with leukopenia indicates significant exposure and a poorer outcome. During the first few days after exposure, there may be a reactive leukocytosis that may or may not progress to leukopenia, depending on the level of exposure.
Gastrointestinal symptoms can develop from the general cholinergic activity of sulfur mustard, resulting in nausea and vomiting that occurs after several hours and is rarely severe. Direct injury to the GI mucosa from ingestion of mustard either directly or from contaminated food or water can lead to a later onset of more severe vomiting, diarrhea, abdominal pain, and prostration.
Although historically a large percentage of battlefield victims have reported central nervous system (CNS) findings such as lethargy, headaches, malaise, and depression, the role of the mustard agent itself in development of symptoms, as opposed to that of other environmental stressors, is unclear. Clinicians should be aware that, regardless of their etiology, these symptoms are a frequent presentation. In addition, absorption of high doses of sulfur mustard can result in CNS hyperexcitability, convulsions, abnormal muscular activity, and coma.
The most effective treatment is decontamination, because once sulfur mustard penetrates tissues, its effects are irreversible. Unfortunately, sulfur mustard is rapidly absorbed on contact, usually exerting damage within 3-10 minutes of exposure. Effectiveness of decontamination is therefore extremely time dependent. Self-decontamination may be the quickest method and should include removing clothing and physically eliminating any mustard residue on the skin.
Anyone providing aid to an exposed person should take proper precautions including ocular, respiratory, and skin protection, ideally with a chemical protection overgarment, rubber boots, and gloves. Exposed individuals should be washed with soap and warm water, or just rinsed with water, as soon as possible. The use of bleach is not recommended in children because it can cause liquefactive epithelial damage to their thin skin, which may in fact promote further penetration of the agent.
Other methods of physical removal, particularly if the mustard is predominately in solid form, include scraping or plucking the agent from the skin, as well as using adsorptive agents such as earth, powdered soap, or flour, followed by rinsing with water.
Regardless of decontamination method, the most important aspect is speed. While ideally all victims should be decontaminated before entering a medical treatment facility, if exposed individual arrive via personal transportation or on foot, they may first need to be taken to a separate area for decontamination. Even if delayed, decontamination should be done to protect others from exposure, to avoid further absorption, and to prevent spread to other areas of the body.
After decontamination and basic life-support issues and other life-threatening concomitant injuries have been addressed, it is important to remain aware of the latency of most symptoms of vesicant exposure. Even if no symptoms are seen at presentation, exposed patients should be observed for at least 8 hours before being discharged. Because of the lack of a specific antidote, the remainder of therapy is supportive.
Skin lesions are treated similarly to those of burn victims. However, fluid losses tend to be less. For this reason, traditional formulas for fluid replacement in burn victims often overestimate losses in vesicant-exposed patients. Erythema and symptoms such as pruritus should be treated with topical and systemic analgesia and antipruritics, as well as soothing lotions such as calamine. Small vesicles (<2 cm) should be left intact, but larger vesicles and bullae should be incised and treated with frequent irrigation and topical antibiotics such as silver sulfadiazine. Widespread and severe partial or full-thickness involvement should be managed in a burn unit if possible.
Eye treatment should center on removing the agent and on preventing scarring and infection. After irrigation of the eye with copious amounts of water, cyclopegic agents should be applied for comfort and to prevent formation of synechiae. Topical antibiotics should then be applied directly along with lubricating ointments such as petroleum jelly to the eyelids to prevent adhesions and subsequent scarring.
Mild respiratory symptoms involving the upper airway can be treated with cough suppressants, throat lozenges, and cool mist vapor. More severe lower respiratory involvement generally requires ventilation with positive end-expiratory pressure. The patient should be intubated promptly if there are any signs of laryngeal spasm or edema. Direct bronschoscopy may be necessary for removal of obstructive pseudomembranes. The need for prolonged intubation (>5-10 days) is a sign of significant proximal airway damage and suggests a poor prognosis. The temptation to use systemic antibiotics during the first 3-4 days despite the not uncommon findings of fever, leukocytosis, and cough should be avoided to prevent the growth of resistant organisms. However, if these signs and symptoms persist beyond this period and there is radiographic evidence of consolidation, systemic antibiotics may then be indicated.
For severe GI effects, in addition to fluid replacement, antiemetics or anticholinergics may be helpful. In the rare case of vesicant ingestion, gastric lavage may be useful if performed within 30 minutes; vomiting should never be induced.
If anemia from bone marrow involvement is severe, blood transfusions may be of benefit. Other therapies, such as administration of hematopoietic growth factors and bone marrow transplantation, although used successfully in animal studies, have never been used in people exposed to vesicants.
The unique susceptibilities of children (Chapter 1, Children Are Not Small Adults) emphasize the need to consider a number of practical treatment issues after vesicant exposure. The first consideration is the time from exposure to onset of skin manifestations, which is shorter in children than in adults. As a result, children may be overrepresented in the initial index cases in a mass civilian exposure. Because a child's skin is more delicate, the caustic effects of decontamination agents (such as bleach) on an already damaged skin surface are potentially much greater; consequently, these agents should probably be avoided altogether in children. Soap and water used for washing and rinsing should be warmed if possible to prevent the greater likelihood of hypothermia in children. In addition, low water pressure (60 psi preferred; if not available, <100 psi) should be used if possible to minimize potential further penetration of the agent into the thinner skin of the child.
Because mustard vapor is denser than air, it tends to settle close to the ground, which has obvious ramifications for small children. In addition to more common facial and eye involvement, pulmonary involvement can also be more extensive, ostensibly from the lower breathing zones and increased respiratory rates of children. Therefore, intubation may be needed earlier, and more aggressive ventilatory management may be necessary in the vapor-exposed child who has lower respiratory tract symptoms.
Fluid replacement may also need to be more aggressive in children because of the greater potential for dehydration secondary to their lower volume reserve. Pain management is another important consideration, particularly in the very young child who is preverbal.
Toxic industrial chemicals used as terrorist weapons are a potentially significant threat to civilian populations. The Chemical Weapons Convention, a disarmament and nonproliferation treaty with 145 signatory countries, identifies 33 chemical and chemical precursors that can be used as weapons. Although some of the chemicals are well-known weapons (e.g., sarin, VX, sulfur mustard), others are more familiar as common industrial chemicals such as chlorine, phosgene, and others. In the United States today, millions of tons of these chemicals are manufactured yearly for the production of dyes, textiles, medicines, insecticides, solvents, paints, and plastics.
The potential terrorist threat posed by industrial chemicals is well known. A January 2002 report to Congress by the Central Intelligence Agency reports that terrorist groups “have expressed interest in many other toxic industrial chemicals—most of which are relatively easy to acquire and handle—and traditional chemical agents, including chlorine and phosgene.” Although of clear interest to terrorist groups, traditional nerve agents require a greater degree of technical sophistication to manufacture and deliver as weapons.
As chemical weapons, chlorine and phosgene are commonly known as “pulmonary,” “inhalational,” or “choking” agents. These terms are ambiguous to the point of confusion, and it is better to conceptualize these compounds along a spectrum. Type I agents act primarily on the central, or tracheobronchial, components of the respiratory tract; Type II agents act primarily on the peripheral, or gas-exchange, regions (i.e., the respiratory bronchioles, alveolar ducts, and alveoli). Type I agents are typically water soluble and chemically reactive and attack the respiratory epithelium of the bronchi and larger bronchioles. The resultant pathologic effects are necrosis and denudation with or without the formation of pseudomembranes; the resultant clinical effects are mucosal irritation, with prominent components of noise (coughing, sneezing, hoarseness, inspiratory stridor, and wheezing). Type II agents cause noncardiogenic pulmonary edema initially manifested clinically by dyspnea without accompanying signs of either radiologic or laboratory anomalies.
Few agents are pure Type I or Type II agents, and high doses of either kind of agent can affect both central and peripheral compartments. For example, chlorine, which is intermediate in both aqueous solubility and chemical reactivity, typically produces a mix of both central and peripheral effects. Phosgene, however, has few Type I effects except at moderately high doses. Sulfur mustard has poor aqueous solubility, but once dissolved, it cyclizes to form such a powerfully reactive cyclic ethylene sulfonium oxide that it acts in the airways primarily as a Type I agent at low to moderate doses. Used as weapons of mass destruction, agents such as hydrogen cyanide and hydrogen sulfide would most likely be released as vapors or gases and, in that respect, would be “inhalational” agents. However, in contrast to Type I and Type II agents—the major pathologic and clinical effects of which are local on respiratory epithelium or alveolar septae—cyanides are widely distributed via the blood throughout the body and therefore merit a separate classification as Type III (systemically distributed) agents. Finally, some agents such as sulfur mustard exhibit both local (in this case, initially Type I) and systemic (Type III) effects, although the systemic effects of mustard (which may include bone-marrow depression and resulting pancytopenia) become clinically significant only after a delay.
Although not stockpiled in the United States for military purposes, chlorine, phosgene, and hydrogen cyanide are common components in industrial manufacturing. Primarily liquids, they are easily vaporized, allowing for widespread gaseous dispersion.
The significant morbidity from pulmonary agents is caused by pulmonary edema. With chlorine, edema may appear within 2-4 hours or even sooner with more significant exposures. Radiologic signs lag behind clinical symptoms: pulmonary interstitial fluid must be increased 5- to 6-fold to produce Kerley B lines on a chest radiograph. Pulmonary edema may be exceptionally profuse; in a study from the 1940s, pulmonary sequestration of plasma-derived fluid could reach volumes of up to 1 L/hr. This problem may be exceptionally profound in children, who have less fluid reserve and are at increased risk of rapid dehydration or frank shock with the pulmonary edema. Additionally, because children have a faster respiratory rate, there is exposure to a relatively higher toxic dose.
Chlorine is a greenish yellow gas that is denser than air and, therefore, settles closer to the ground and low-lying areas. This may have significant consequences for small children and infants, who would be exposed to higher concentrations of the vapor and thus receive higher inhaled doses of the agent. Chlorine has a strong, pungent odor that most people associate with swimming pools. Because the odor threshold (at 0.08 ppm) is less than the toxicity threshold, the odor may warn individuals that exposure is occurring.
The initial complaints in chlorine exposure may be either intense irritation or the sensation of suffocation, or both; the suffocating feeling is what led to its characterization as a “choking” agent. Low-level exposures to chlorine result in mucosal irritation of the eyes, nose, and upper airways. Higher doses lead to respiratory symptoms that progress from choking and coughing to hoarseness, aphonia, and stridor—classically Type I effects. Dyspnea after chlorine exposures indicates damage to the peripheral compartment (Type II insult) and incipient pulmonary edema.
Like chlorine, phosgene is also heavier than air, thus posing an increased risk for children who are exposed. Phosgene itself is colorless, but associated condensation of atmospheric water produces a dense white cloud that settles low to the ground. It has the characteristic odor of newly mown hay. However, the odor threshold for phosgene (at 1.5 ppm) is higher than the toxicity threshold, and unlike the case with chlorine, detection of the odor would be inadequate and too late to serve as a warning against toxic exposure.
Phosgene is primarily associated with the development of pulmonary edema. However, because in low to moderate doses it does not cause the mucosal irritation associated with Type I agents, the significance of the exposure may be underestimated. Exposure to progressively higher doses produces mild cough, sneezing, and other effects on the central compartment. Dyspnea is seldom present initially except when doses have been massive; instead, there is a clinically asymptomatic, or latent, period usually of several hours and inversely correlated with dose. Dyspnea and associated clinical deterioration have in several instances been triggered by slight to moderate exertion.
Decontamination consists primarily of removing the victim from the source of the pulmonary agent to fresh air. For first responders such as paramedics and fire-rescue workers, personal protective equipment (PPE) with self-contained breathing apparatus is required; however, because the gases are volatile, cross-contamination is unlikely. Victims of chlorine exposure may require copious water irrigation of the skin, eyes, and mucosal membranes to prevent continued irritation and injury.
Management is primarily supportive; there are no antidotes or specific postexposure treatments for inhalational agents. Victims should be observed and monitored for both central (Type I) and peripheral (Type II) acute effects, including development of pulmonary edema. Most deaths are due to respiratory failure and usually occur within the first 24 hours. Because of the delay in onset of pulmonary edema, prolonged observation of victims of phosgene and chlorine attacks is warranted.
Treatment of central, or Type I, damage involves administering warm, moist air and supplemental oxygen, and treating bronchospasm either produced de novo by the toxicant in normal airways or resulting from toxicant-induced exacerbation of airway hyperresponsiveness in individuals with underlying pathology such as asthma or reactive airways. Aggressive bronchodilator therapy with beta-agonists is appropriate. The value of corticosteroids is less clear, but they may be efficacious in victims with severe bronchospasm or a history of asthma. Nebulized lidocaine (4% topical solution) has been recommended to provide analgesia and reduce coughing. The possibility of laryngospasm should always be anticipated and the necessity and timing of intubation carefully assessed. Associated central damage from inhaled particles of smoke in situations involving fire should also be considered. Pseudomembrane formation may lead to airway obstruction and may require bronchoscopic identification and removal of pseudomembranous debris. Necrotic debris from central damage provides an excellent culture medium for secondary bacterial colonization and infection, and bacterial superinfections are commonly seen 3-5 days after exposure. Early aggressive antibiotic therapy directed against culture-identified organisms is imperative. Prophylactic antibiotics are of no value.
Treatment of peripheral (Type II) damage from pulmonary agents includes adequate oxygenation, establishment of effective intra-alveolar pressure gradients using positive end-expiratory pressure (for example, in conscious patients, with continuous positive airway pressure, or CPAP), and careful attention to fluid balance. In cases of florid pulmonary edema, using a central line to monitor hemodynamics in critically ill children may be necessary. The length of the latent period in a dyspneic patient can provide clinically valuable information about the intensity of exposure; patients who develop breathing difficulty within the first 4 hours after exposure may face a grave prognosis, and even patients with mild dyspnea, because of the timing of the dyspnea, may be candidates for urgent or priority evacuation. All patients at risk of pulmonary edema induced by pulmonary agents should be maintained on strict bed rest to avoid cardiopulmonary decompensation associated with exertion.
Modern riot control agents comprise a heterogeneous group of chemical compounds that have been used widely around the world since the 1950s (Table 5.6). These agents have the ability to incapacitate at low aerosol concentrations and have a high safety ratio (ratio of lethal dose to effective dose). However, prolonged exposure or release in enclosed areas can intensify the physical effects of these agents. CS (2-chlorobenzylidene), CN (1-chloroacetophenone, Mace®), and pepper spray (Oleoresin capsicum) are commercially available to the public in the United States.
Mode of transmission varies by agent. Common means include spraying a solution, release of pressurized canisters, explosive dispersion (smoke “grenades”), and burning. Explosive modes of transmission may cause traumatic injuries in addition to the incapacitating effects. CS is very flammable and poses a fire hazard. Most agents disperse soon after release, although persistent forms of CS exist. Riot control agents may contaminate clothing, buildings, and furniture and may cause ongoing symptoms in continued or repeat exposure.
When dispersed, riot control agents are chemical irritants of the skin and mucous membranes of the eyes, nose, mouth, airways, and GI tract. CS and CN incapacitate through direct chemical irritation, acting like chemical thorns. Due to its low vapor pressure, CR (dibenzoxazepine) has limited effects on the respiratory tract. In addition to direct irritation, pepper spray also induces local release of the neurotransmitter substance P in peripheral afferent sensory nerves. This mechanism causes pain, capillary leakage, and vasodilation.
Riot control agents have specific effects on the eyes, nose, mouth, and airway, with variation in intensity depending on mode of exposure and agent used. Symptoms occur quickly after exposure and typically resolve in 1-2 hours once the victim has been removed from the agent. On contact, these agents induce eye burning, eye pain, tearing, conjunctival infection, blepharospasm, periorbital edema, and photophobia. Exposures at close range, particularly to exploding CS and CN grenades or canisters, may cause serious damage to the eye including corneal edema, conjunctival laceration, hyphema, vitreous hemorrhage, and secondary glaucoma. Permanent effects such as cataracts and traumatic optic neuropathy may also be seen.
After dispersal of riot control agents, nasal burning and pain, copious rhinorrhea, and persistent sneezing begin along with oral irritation and salivation. Pulmonary effects include chest tightness and burning, bronchorrhea, bronchospasm, and coughing. Gagging, retching, and vomiting frequently accompany mucosal and airway irritation. Exposed skin stings and may progress to erythema, vesiculation, and bullae depending on the conditions of exposure; prolonged exposure, high ambient temperature, and humidity favor worsening skin effects. These manifestations may occur hours to days after exposure to CS. Skin exposed to CR may become painful in water for up to 2 days after exposure. CN and CS can cause allergic contact dermatitis in people who are repeatedly exposed.
Severe clinical effects from riot control agents are uncommon. Intense exposure to CS, CN, and pepper spray has caused laryngospasm, pneumonitis, bronchospasm, and noncardiogenic pulmonary edema. Often, the agent was released in an enclosed space, or the victim was not able to leave the vicinity of the agent. Individuals with asthma are predisposed to serious pulmonary symptoms. Experience with a 4-week-old infant who was unintentionally exposed to pepper spray at close range suggests that severe lung injury from Oleoresin capsicum is reversible in young children, provided that intensive medical support is provided. Deaths caused by pulmonary effects have occurred after CN exposure in victims who had previously normal lung function. Pepper spray was implicated in the death of one asthmatic prisoner in custody. Prolonged reactive airway disease has also been described after CS exposure in a previously healthy person with no prior history of atopy. In general, riot control agents are incapacitating but rarely lethal, especially relative to other deployable chemical agents such as the nerve agents, vesicants, and pulmonary agents.
Some physical characteristics of the compounds can assist in detection when riot control agents are used. The most common agents (CS, CN, and pepper spray) are deployed in identifiable canisters. CS and pepper spray have a pungent pepper odor. CN has a flowery apple odor. Pepper spray frequently contains fluorescein dye that becomes readily apparent on exposed skin under a Wood';s lamp. No environmental monitoring systems currently exist for riot control agents.
Differentiation of clinical effects caused by riot control agents from those of other chemicals can be a challenge during early management. Tearing, salivation, bronchorrhea, bronchospasm, and vomiting suggest the cholinergic effects of nerve agent exposure. Intense exposure to riot control agents with pneumonitis and pulmonary edema mimic symptoms of exposure to pulmonary agents, such as chlorine and phosgene. The potential for delayed skin effects, including vesiculation and bullae, with riot control agents makes them similar to vesicants such as sulfur mustard. However, symptoms rapidly resolve once contact with the agent ceases. Lack of progression to more severe symptoms such as bone marrow failure, paralysis, and seizures, combined with negative results from field detection systems and the physical characteristics mentioned above make identification of riot control agent release ultimately possible.
Decontamination requires that all victims be moved to a well-ventilated, uncontaminated space and have their outer clothing removed. Clothing should be double bagged to prevent secondary exposure. Medical treatment of riot control agent exposure focuses on ending contact, assessing for serious pulmonary effects, and addressing ongoing eye and skin irritation (Table 5.7).
In most instances, clinical signs and symptoms resolve over 30-60 minutes, and specific medical treatment is not needed. Pulmonary effects may be delayed. Victims who exhibit prolonged dyspnea or have other objective lung findings should be admitted to a medical facility for ongoing monitoring and treatment.
All first responders should wear PPE including, but not limited to, a full-face gas mask, properly rated outer clothing, gloves, and boots. Field incident command should identify a hot zone, decontamination area, and cold zone. Ideally, decontamination should begin in the field and be complete before entry into a medical facility.