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

Author: William Byrne Cogar, DO, MS, MA, FACEP, Medical Director, Emergency Management and Preparedness; Department Head, Department of Emergency Medicine, Naval Medical Center, Portsmouth, VA
Coauthor(s): Lanny F Littlejohn, MD,, Resident and Medical Director for Tactical Combat Casualty Care, Department of Emergency Medicine, Naval Medical Center, Portsmouth, Virginia
Contributor Information and Disclosures

Updated: Apr 28, 2009

Introduction

Background

Although most smokes used for obscuring purposes are not concentrated enough to be hazardous, any smoke can be hazardous to health if the concentration is sufficient or if the exposure is long enough. The smoke itself can be directly toxic, or it may carry, adsorbed to the particulate surface, any of a variety of toxic gaseous substances that interact with mucosa, skin, or any surfaces of the airway. Smokes consist of particles of various sizes, sedimentation rate, and impact rate. Therefore, smoke inhalation has a complex distribution pattern at various levels in the airway.

This article reviews the pathophysiology and toxic effects of lung and airway injury caused by different smokes: the oxides of nitrogen (NOx), zinc oxide (HC), red phosphorus (RP), sulfur trioxide (FS), titanium tetrachloride (FM), standard gas fuel-2 (ie, fog oil [SGF2]), and pyrolysis of Teflon.

Oxides of nitrogen

NOx are components of photochemical smog, usually approximately 0.053 ppm. Nitrogen dioxide exists as a mixture of nitrogen dioxide, a reddish brown gas, and nitrogen tetroxide, a colorless gas. Other forms of nitrogen oxide include nitrous oxide, which is a common anesthetic or (when given without oxygen) asphyxiant, and nitric oxide, which quickly decomposes to nitrogen dioxide in the presence of moisture.

Zinc oxide

HC smoke, also termed "white smoke," is a mixture of equal amounts of hexachloroethane, zinc oxide, and approximately 7% grained aluminum or aluminum powder. Upon combustion, the pyrotechnic mixture of zinc chloride and hexachloroethane rapidly absorbs moisture from the air to form a grayish white smoke. More humid air results in thicker smoke. Other chemicals also are released in the combustion process, such as chlorinated hydrocarbons (eg, phosgene and carbon tetrachloride), chlorine gas, carbon monoxide, and several other compounds.

HC smoke resulted from the French and US Chemical Warfare Service, which, after World War I, sought an obscurant that was not fraught with as many difficulties as white phosphorus. HC has a sweetish acrid odor, even at moderate concentrations. Although HC can irritate the upper airway mucous membranes, it probably is studied most for its role in fume fever.

Red phosphorus

After World War II, RP smoke was developed as an attempt to avoid the toxicity associated with the manufacturing of white phosphorus. RP is 95% phosphorus in a 5% butyl rubber base and provides an adequate tank screen on the battlefield. When RP is oxidized, it forms a mixture of phosphorus acids. When these acids are exposed to water vapor, they in turn form polyphosphoric acids, which may be responsible for the toxic injuries to the upper airways. Most of these injuries are mild irritations. No human deaths have been reported from exposure to either white phosphorus or RP smokes.

Sulfur trioxide

FS, also known as sulfuric oxide, chlorosulfonic acid, or sulfuric anhydride, is typically a colorless liquid, which can exist as ice, fiberlike crystals, or gas. When it is exposed to air, it rapidly takes up water and forms white fumes. The smoke consists of 50% sulfur trioxide and 50% chlorosulfonic acid. It usually is dispersed by spray atomization. The sulfur trioxide evaporates from spray particles, reacts with surrounding moisture, and forms sulfur acid. The sulfur acid condenses into droplets that produce a dense white cloud. FS is extremely corrosive, which led to its disuse in the army.

Titanium tetrachloride

FM is a colorless – to – pale yellow liquid that has fumes with a strong odor. Once it comes in contact with water, it rapidly forms hydrochloric acid and titanium compounds. It is used to make titanium metal, white pigment in paints, and other products. It breaks down rapidly in the environment.

FM readily hydrolyzes in the presence of water or moist air via an exothermic reaction that occurs in 2 stages. First, FM reacts to form a highly dispersed particulate smoke. This smoke reacts with more moisture in the air to form hydrolytic products of FM such as hydrochloric acid, titanium oxychlorides, and titanium dioxide. Generation of the smoke has been used as screens in military operations. The formation of hydrochloric acid makes it irritating and corrosive.

When FM liquid is exposed to the air, it produces white fumes. These white fumes can come into contact with skin, where a mild epithelial irritation results and usually subsides within 24 hours. When it is mixed with water, it generates a vigorous exothermic reaction that produces both heat and hydrochloric acid, which can work synergistically to produce deep thermal burns.

Oil fog

SGF2 is one type of chemical smoke obscurant used in the military. SGF2 is generated by injecting a light petroleum-based lubricating oil onto a heated engine exhaust manifold, causing the oil to vaporize and eventually recondense in the atmosphere. Any industry that generates an oil mist also may produce similar exposures. Petroleum oil smokes are the least toxic smokes. They seldom produce ill effects even after prolonged or multiple exposures.

Teflon (polytetrafluoroethylene [PTFE]) is used widely in a variety of industrial and commercial settings such as lubricants and fabric treatments. Its lubricity, high dielectric constant, and chemical inertness make it a desirable component in military vehicles such as tanks and aircraft. Closed-space fires in such settings have prompted studies of the toxicity of exposure to the by-products created from incinerated organofluorines. Pyrolysis of PTFE produces a particulate smoke, which, if inhaled, produces a constellation of symptoms termed polymer fume fever (PFF).

Pathophysiology

Oxides of nitrogen

Inhalation of nitric oxide causes the formation of methemoglobin. Inhalation of nitrogen dioxide results in the formation of nitrite, which leads to a fall in blood pressure, production of methemoglobin, and cellular hypoxia. Inhalation of high concentrations causes rapid death without the formation of pulmonary edema. Milder yet still severe exposures may result in death with production of yellow frothy fluid in the nasal passages, mouth, and trachea and marked pulmonary edema. The symptoms following the inhalation of NOx are mostly due to nitrogen dioxide.

Zinc oxide

HC is probably the most acutely toxic of the military smokes and obscurants. HC's toxicity mainly is attributed to the irritating effects of zinc chloride. Most likely, carbon monoxide, phosgene, hexachloroethane, and other products contribute to the observed respiratory effects. While upper respiratory tract damage can occur from zinc chloride, the mean diameter of the primary smoke particles is approximately 0.1 micrometers, allowing them to reach the alveoli.

Studies have demonstrated that HC exposure can produce a gradual decrease in total lung capacity, vital capacity, and diffusion capacity of carbon monoxide (DLCO). It also is associated with the presence of pulmonary edema, increased airway resistance, and decreased compliance. When these episodic exposures were stopped, the changes were reversible.

Lung injury comes primarily from the zinc chloride product of HC combustion. In a retrospective cohort study of 20 patients, Hsu et al correlated findings on high-resolution CT with pulmonary function tests (PFTs) performed within 3-21 days following acute exposure.¹ CT findings were predominantly diffuse ground-glass opacities in the lung parenchyma. PFTs showed a restrictive functional impairment with significant reduction in forced vital capacity (FVC), forced expiratory volume in 1 second (FEV₁), total lung capacity (TLC), and diffusing capacity of lung for carbon monoxide (D_LCO) without impairment of FEV₁/FVC ratio. Follow up in 1-2 months showed significant improvement with mild-to-moderate exposures. Severe exposures led to interstitial fibrosis and continued functional limitation. 
 
In a study by Conner et al performed with guinea pigs, exposure to ultrafine HC particles (0.05 µm) in increasing degrees was associated with a dose-response elevation in protein, neutrophils, and angiotensin-converting enzyme found in lavage fluid.² A direct relationship also was observed with alkaline phosphatase, acid phosphatase, and lactate dehydrogenase in lavage fluid. Centriacinar inflammation was seen histologically, indicating evidence of pulmonary damage.

An interesting study by Marrs et al involving mice, rats, and guinea pigs demonstrated a positive association of alveologenic carcinoma in a dose-response trend to HC smoke as well as a variety of inflammatory changes.³ The article states that hexachloroethane and zinc, as well as carbon tetrachloride (which may be present in HC smoke), may be animal carcinogens in certain circumstances. This raises the suspicion of HC as a potential carcinogen.

Metal fume fever (MFF) is a well-documented acute disease induced by intense inhalation of metal oxides. The exact pathology is not well understood but likely involves the deposition of fine metal particulates in the alveoli that results in a self-limited syndrome of fever, myalgias, headache, and nausea 4-12 hours after exposure to metal fumes. MFF is primarily associated with the inhalation of zinc oxide fumes that are produced when zinc-oxide coated steel (galvanized) or zinc containing alloys (eg, brass) are exposed to high temperatures.

Keyes found that 1 in 5 welders has experienced MFF by age 30.⁴  A study by Kuschner et al on human volunteers showed that pulmonary cytokines such as tumor necrosis factor (TNF), interleukin 6 (IL-6), and interleukin 8 (IL-8) may play important initial roles in mediating metal fume fever.⁵  Symptoms of MFF typically last several hours. Severe cases generally resolve in 1-2 days. Observation is usually all that is necessary.

Hepatotoxicity has also been described in humans exposed to HC/ZnO smokes in enclosed spaces during military training.⁶ The toxic effects appear to be primarily due to the chlorinated compounds produced by combustion: tetrachloromethane, tetrachloroethylene, hexachlorobenzene, and carbon tetrachloride. This last compound is well known for its hepatotoxicity. Acute exposure causes elevated liver enzyme levels by day 1 or 2, with a peak around day 18-21. Liver function test results should normalize by 6 weeks. 

Red phosphorus

Most of the pathologic consequences associated with phosphorus are from elemental white phosphorus fumes or vapor. Contact with elemental phosphorus can cause burns to body surfaces. A well-described condition termed phossy jaw is associated with longer-term occupational exposures to airborne phosphorus fumes. This disease is a degenerative condition affecting the entire oral cavity including soft tissue, teeth, and bones. Massive necrosis of teeth, bone, and soft tissue can lead to life-threatening infections. Treatment typically consists of soft tissue and bone debridement, abscess drainage, and reconstructive surgery.

White phosphorus and RP smokes may cause respiratory tract irritation after 2-15 minutes of exposure. This probably is caused by the polyphosphoric acids that react with moist mucosal membranes. Respiratory tract irritation has been observed at concentrations of 187 mg phosphorus pentoxide equivalents per cubic meter for 5 minutes or longer. Intense congestion, edema, and hemorrhages were observed in lung tissue following a 1-hour exposure at varying concentrations in studies using rats, mice, and goats.

Sulfur trioxide

Since FS is an intermediate used to produce sulfuric acid upon its reaction with moisture, the resulting toxicity is that of an acidic irritation to mucosal membranes and even skin. The corrosive effect of acid on mucosa and keratinized skin causes significant irritations and chemical burns.

Titanium tetrachloride

The same pathophysiologic effects that occur with FS smoke occur with FM smoke, since both are associated with the production of corrosive and irritating acids.

Oil fog

Concentrations of oil mists in industrial settings vary over a wide range (0.8-50 mg/m³), with most at 3 mg/m³. The particle sizes also vary more than 1-5 µm in median diameter. They typically have a high molecular weight and are saturated hydrocarbons derived from distilled petroleum. Exposures to such smoke are likely to last for many hours in a single day or repeatedly over consecutive days.

Animal studies have demonstrated, after chronic exposure, that pulmonary function endpoints such as total lung capacity, vital capacity, residual volume, D _LCO , compliance, and end-expiratory volume were unaffected by oil fog. One exception exists; male rats exposed at 1.5 mg/L had decreased end-expiratory volume.

Bronchiolar lavage and histopathology showed changes consistent with a mild inflammatory edema (ie, increased protein content, total cells, polymorphonuclear leukocytes [PMNs], macrophages).

Teflon particles

Pyrolysis of Teflon occurs at approximately 450°C. The mixture of particles that is produced contains a substance called perfluoroisobutylene (PFIB), which appears to be the main cause of toxicity in polymer fume fever. The ultrafine particles initiate a severe inflammatory response at low inhaled particle mass concentrations, which suggests an oxidative injury. PMNs may regulate the inflammatory process with cytokine and antioxidant expression.

PFIB particles cause an extremely rapid toxic effect on pulmonary tissues. Evidence of microscopic perivascular edema is observed within 5 minutes. Less intense exposures are followed by a latent period during which normal physiologic compensatory measures to control developing pulmonary edema ensue. Once these mechanisms are overcome, the time frame of which depends on the degree of exposure, the clinical syndrome of fume fever follows. More intense exposures also may produce a chemical conjunctivitis. Hemorrhagic inflammation of the lungs also can occur.

Clinical

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

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.

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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