CBRNE - Lung-Damaging Agents, Toxic Smokes - NOx, HC, RP, FS, FM, SGF2, Teflon Clinical Presentation

  • Author: Lanny F Littlejohn, MD; Chief Editor: Robert G Darling, MD, FACEP   more...
 
Updated: May 14, 2010
 

History

  • Oxides of nitrogen: Because of their insolubility in water, NOx tend not to cause immediate upper airway irritation. Unfortunately, this may allow a significant exposure to remain undetected for prolonged periods. As with most toxic inhalations, severity of disease and presentation are related to the concentration of the smoke or fumes, length of time of exposure, manner in which the exposure was delivered, and underlying health of the exposed individual.
    • Mild exposure to nitrogen dioxide results in upper airway and ocular irritation such as itching or burning eyes. Cough, dyspnea, fatigue, chest tightness, throat tightness, nausea, vomiting, vertigo, somnolence, and loss of consciousness also may occur from mild exposure. At weaker concentrations, the individual may experience very little discomfort, quickly accommodating to the cough, mild choking, or upper airway irritation. Because of this, symptoms may appear quickly or remain unnoticed for a few hours. Although the symptoms of mild exposure may become quite dramatic, once the patient is removed from the exposure, complete recovery is expected within 24 hours.
    • In more severe exposures, the clinical response may be described as triphasic.
      • During phase I, an intense respiratory symptom complex may occur. Severe cough, dyspnea, and rapid onset of pulmonary edema suddenly may arise. Physical exertion actually may be a precipitating factor, quickening the progression to pulmonary edema. If the patient survives this episode, spontaneous remission occurs within 48-72 hours postexposure. Fiercer exposures can cause acute bronchiolitis with severe cough, dyspnea, and weakness. This typically resolves 3-4 days postexposure.
      • Phase II lasts from 2-5 weeks and is relatively uneventful. A mild residual cough with malaise and perhaps dyspnea may linger, but the chest radiograph (CXR) typically remains clear.
      • In phase III, symptoms may recur 3-6 weeks after the exposure. Severe cough, fever, dyspnea, and cyanosis may develop in the setting of rales and increasing carbon dioxide retention.
    • More acutely severe exposures can result in immediate death from bronchiolar spasm, laryngeal spasm, reflex respiratory arrest, or simple asphyxia. Some exposures can progress from mild upper airway irritation to pulmonary edema in 3-30 hours.
    • Many studies have evaluated effects of NOx on individuals with healthy lungs and those with asthma or chronic obstructive bronchitis. Concentrations of 0.5 ppm or less generally have not affected people with preexisting airway disease. Levels from 0.5-1.5 ppm begin to bother patients with asthma, who notice minor airway irritation. With concentrations greater than 1.5 ppm, people with healthy lungs experience decreases in pulmonary function tests and decreased D LCO with widening of the alveolar-arterial gradient on arterial blood gas measurement.
  • Zinc oxide: Individuals exposed to HC smoke may complain of nose, throat, and chest irritation. They may experience cough and some nausea. Individuals with severe exposures may present in severe respiratory distress, and such exposures can be fatal. A thorough social history offers vital clues of exposure, since respiratory distress can mimic many different disease processes.
    • Fume fever typically presents in a delayed fashion 4-8 hours after exposure with a pattern of symptoms including dryness of the throat, coughing, substernal chest pain or tightness, and fever. Other symptoms include hoarseness, sore throat, retching, paroxysmal coughing, rapid pulse, malaise, shortness of breath, and abdominal cramps. Respiratory symptoms generally disappear in 1-2 days with supportive care.
    • Milder exposures are characterized by sensations of dyspnea without any radiologic, auscultatory, or blood gas abnormalities.
    • A patient with moderate exposure to HC may demonstrate rapid clinical improvement within 6 hours. These patients usually are sent home, only to return in 24-36 hours with rapidly worsening dyspnea and a CXR showing dense infiltrative processes. This usually clears, but significant hypoxia may persist during the time the CXR is abnormal.
    • Prolonged exposures or exposures to very high doses of HC may result in sudden early collapse and death. This may be due to laryngeal edema or glottal spasm. If severe exposure 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 acute tracheobronchitis.
    • Most individuals with HC inhalation injuries progress to complete recovery. Of exposed individuals, 10-20% develop fibrotic pulmonary changes. Distinguishing between those who will recover and those who will not is difficult, since both groups make an early clinical recovery.
  • Red phosphorus: Individuals with toxic inhalation usually have a history of exposure to the smoke either on the battlefield or in some other setting where phosphorus smokes are used.
    • Complaints of eye, nose, and throat irritation are common.
    • A severe exposure can be associated with an explosive persistent cough. If a person has come in contact with unoxidized phosphorus, chemical burns to the skin can cause pain and erythema.
    • Most often, the cough and irritating symptoms resolve after the individual is removed from the exposure source.
  • Sulfur trioxide: Because FS smoke is so irritating, those exposed do not remain in it for long.
    • FS-exposed individuals complain of cough; substernal ache or soreness; and a burning sensation in the eyes, nose, mouth, and throat. Blurry vision and photophobia also may be complaints.
    • If inhalant injury is severe enough, explosive cough and shortness of breath may develop.
    • The individual may complain of a prickling sensation of the exposed skin, which could be the prelude to pending chemical dermatitis.
    • A report by Steuven et al of 12 persons exposed to FS for approximately 2 hours elicited complaints such as pleuritic chest pain, chest tightness, vague chest discomfort, cough, an acidic taste in the mouth, and nasal irritation. Everyone was asymptomatic 6 hours postexposure.[2]
  • Titanium tetrachloride: Although several industrial exposures have occurred with FM liquid and smoke, only 1 death has been reported. This was a worker who accidentally was splashed over his entire body with liquid FM. He died from complications resulting from inhalation of FM fumes and overwhelming superinfection.
  • Oil fog: Individuals exposed to SGF2 or other oil mists may report mild irritation or slight cough, a sensation of shortness of breath, or headache. Those who have underlying pulmonary disease such as asthma or chronic obstructive pulmonary disease (COPD) may have symptoms triggered after exposure to SGF2.
  • Teflon particles: Clinical complaints of exposed individuals closely mimic influenzalike symptoms.
    • The individual complains of malaise, fever (at times to 104°F), chills, sore throat, sweating, and chest tightness 1-4 hours postexposure. These symptoms usually resolve 24-48 hours after the patient is removed from the source.
    • More intensely exposed individuals complain of dyspnea on exertion, orthopnea, and later, dyspnea at rest. Cough productive of bloody sputum occasionally is seen.
    • Some animal studies have demonstrated disseminated intravascular coagulation and other organ involvement, but this may be due to global hypoxia, since this only occurred in animals with severe lung damage.
    • Cases of PFF have been reported in persons exposed to pyrolyzed hairspray and horse-rug waterproofing spray and in one individual smoking hand-rolled cigarettes after working with dry lubricant.[7]
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Physical

  • Oxides of nitrogen: The severity of physical examination findings depends on the severity of exposure.
    • In a mild exposure, an individual may have injected conjunctivae and normal to mildly erythematous-appearing mucous membranes.
    • After a more severe exposure, signs may range from mild respiratory distress (eg, tachypnea, accessory muscle use) to more severe signs of wheezes and rales, yellow frothy sputum, and yellow staining of the mucous membranes. This may be followed by cyanosis, lethargy, convulsions, coma, and death.
  • Zinc oxide
    • Like other inhalation injuries, physical examination findings depend on the time of exposure, concentration of the gas, method of gas distribution, and underlying general health of the exposed individual.
    • Physical examination findings may range from slight dyspnea and increased work of breathing to severe respiratory distress, convulsions, coma, or death. Hoarseness and cough are common findings. Retching, fever, tachycardia, hypoxia, and cyanosis may be present, as well as pulmonary wheezes and rales.
  • Red phosphorus: Physical examination findings are those associated with irritation of mucosal surfaces. A cough or chemical burns to exposed skin surfaces from direct contact with unoxidized phosphorus may be present.
  • Sulfur trioxide
    • Conjunctivitis, corneal erosion with uptake of fluorescein, and lacrimation may be present. Erythema of exposed skin surfaces and an inflammatory reaction of mucosal surfaces also may be present. Intense salivation may follow. The individual may have an explosive cough with bloody sputum, dyspnea, hypoxia, rales, or wheezes.
    • Obviously, physical examination findings vary due to length of exposure, concentration of FS smoke, environment of the exposure, and underlying health of the exposed individual.
    • FS smoke is known to exacerbate symptoms of asthma or COPD and significantly worsen pulmonary function test numbers in these patients
  • Titanium tetrachloride: Physical examination findings are expected to be the same as for FS smoke.
  • Oil fog: After an intense and prolonged exposure, a patient may have mild dyspnea, basilar rales, or evidence of bronchoconstriction (eg, wheezing, prolonged expiratory phase).
  • Teflon particles
    • Physical examination is similar to that of patients with chemical inhalation injury, but fever often is present as well. Dyspnea, increased work of breathing, and rales are common. Pulmonary edema usually is mild and typically does not require oxygen supplementation.
    • More intense toxicity and hypoxia may be seen, requiring more invasive methods of oxygenation and ventilation. Pulmonary edema is also worse if the individual exercises postexposure.
    • CXR findings of pulmonary edema worsen for up to 12 hours and then typically clear by 72 hours.
    • Deaths have been reported with severe pulmonary edema, hypotension, and gram-negative superinfection.
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Causes

  • Oxides of nitrogen
    • At ground level, NOx are produced during electric or arc welding, combustion of fuels, detonation of nitrate-based explosives, combination of nitrogen-containing products, and decomposition of organic matter. Recently filled farm silos have high nitrogen dioxide levels for approximately 10 days, peaking at 4000 ppm. Significant quantities of nitrogen dioxide also are found in diesel engine exhaust.
    • Severe pulmonary reactions have been reported after accidental exposures in unventilated farm silos, welding in confined spaces, detonating nitrogen-based explosives in enclosed spaces (tanks, ships), handling nitric acid, resurfacing ice arenas, using anesthesia, and in missile fuel oxidizer spills. Any person engaged in associated occupations or environments is at risk.
  • Zinc oxide: Since this smoke can be distributed by grenades, candles, pots, artillery shells, and special air bombs, any personnel engaged in the use or activity of these tools are at risk for HC exposure. Exposure to zinc oxide also is common among welders and those who are engaged in the smelting of zinc.
  • Red phosphorus: Phosphorus smokes are used in military formulations for smoke screens, incendiaries, smoke markers, colored flares, and tracer bullets. People also can be exposed to phosphorus smoke at phosphorus loading plants.
  • Sulfur trioxide: One may become exposed to FS on the job in a chemical or metal plating industry. FS exposure also may occur in the production of detergents, soaps, fertilizers, or lead-acid batteries (car batteries), in printing and publishing, or in photography shops. Since the army does not use FS much anymore, military exposures are less common.
  • Titanium tetrachloride: Because FM smoke breaks down so rapidly in the environment, those who work with it in industry seem to be most at risk. Because titanium tetrachloride is extremely irritating and corrosive in both the liquid formulation and the smoke formulation, its use has diminished.
  • Oil fog: Military personnel can be exposed to fine-particle oil fog when it is used in training or in combat. Industrial settings where oil mists are created may produce similar exposures (eg, metalworking, automobile and textile industries, pressrooms, mining, die and mould lubrication).
  • Teflon particles: As mentioned in Background, exposure to these fumes is common in closed-space fires where Teflon is pyrolyzed. Also, polymer fume fever has been observed in those smoking Teflon-contaminated cigarettes.
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Contributor Information and Disclosures
Author

Lanny F Littlejohn, MD  Staff Emergency Physician and Medical Director for Tactical Combat Casualty Care, Department of Emergency Medicine, Naval Medical Center, Portsmouth, Virginia

Lanny F Littlejohn, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Association, Special Operations Medical Association, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

William Byrne Cogar, DO, FACEP  Medical Director, Emergency Management and Preparedness; Assistant Chair, Department of Emergency Medicine, Naval Medical Center, Portsmouth, VA

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark Keim, MD  Senior Science Advisor, Office of the Director, National Center for Environmental Health, Centers for Disease Control and Prevention

Mark Keim, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert G Darling, MD, FACEP  Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

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