Chapter 23 Smoke Inhalation
Smoke inhalation is the leading cause of death from fires for both humans and animals. More than 80% of fire-related deaths are the result of smoke inhalation and not from surface burns.1 Smoke itself is the complex mixture of vapors, gases, fumes, heated air and particulate matter, and liquid and solid aerosols produced by thermal decomposition. Thermal decomposition can result from flaming combustion or from pyrolysis, which is the application of intense heat. These thermal decompositions can result in the rapid oxidation of a substance by heat. Pyrolysis occurring with high heat and relatively low oxygen concentration is known as smoldering. Although flaming combustion generates light (flame), heat, and smoke, smoke can be produced in the absence of flames. Thus flames are not a prerequisite for smoke production, and furthermore, the gaseous product of combustion (smoke) is not always visible.
Combustion products are difficult to predict in fires. Even within the same fire, the concentration of the smoke may vary.2 Temperature, oxygen concentration, and the chemical composition of the burning material determine the combustion products.
In recent years, the use of newer synthetic building materials and furnishings has led to an increase in inhalational injuries caused by fires.3 Although more rigorous building codes make new structures less likely to burn, the materials used to make them have become more dangerous when they do catch fire through their production of more toxic smoke. At about the time of the World War II, differences were noted between natural materials and synthetics in terms of their combustion products and relative toxicity when burning. It is now recognized that compared with natural materials (e.g., cotton, wood, wool) plastics generate more heat more swiftly, spread flames faster, generate larger amounts of denser visible smoke, and release more toxic and greater concentrations of invisible products of thermal decomposition. Despite testimonials to the contrary, plastics are neither nonburning nor self-extinguishing and, like many other synthetic substances, burn hotter and smokier than wood or other natural substances. Some of the more common and more toxic combustion products are listed in Tables 23-1 and 23-2, and Box 23-1.
|Wood, paper, cotton||Carbon monoxide, acetaldehyde, formaldehyde, acetic acid, formic acid, methane|
|Silk||Ammonia, cyanide, hydrogen sulfide, sulfur dioxide|
|Wool||Phosgene, cyanide, hydrogen chloride, chlorine|
|Rubber||Hydrogen sulfide, sulfur dioxide|
|Plastics||Ammonia, aldehydes, cyanide, phosgene chlorine, hydrogen chloride|
|Polyvinyl chloride||Carbon monoxide, phosgene, chlorine, hydrogen chloride|
|Fluorinated resin||Hydrogen fluoride|
|Sulfur-containing material||Sulfur dioxide|
|Nitrogen-containing material||Cyanide, isocyanates|
|Fire-retardants||Hydrogen bromide, hydrogen chloride|
|Petroleum products||Carbon monoxide, acetic acid, formic acid|
|Acrylic||Carbon monoxide, hydrogen chloride, acrolein|
|Heat/flame||Flaming combustion||Burns, laryngotracheitis|
|Soot||Organic material||Airway obstruction|
|Steam||Water heated to boiling||Laryngotracheitis, bronchitis, alveolitis|
|Oxygen depletion||Combustion/pyrolysis||Burns, laryngotracheitis|
|Trauma||Explosions, collapsing structures||Burns|
|Acrolein||Cotton, paper, wood, acrylics, polystyrene||Respiratory tract irritation|
|Aldehydes||Acrylonitrile-butadiene styrene (ABS), polyester (alkyds) phenolics||Respiratory tract irritation|
|Carbon monoxide||Incomplete combustion of organic material||Functional anemia, cellular asphyxia|
|Carbon dioxide||Complete combustion of organic material||Simple asphyxia, narcosis|
|Halogen acids, such as hydrochloric, hydrobromic, and hydrofluoric acid||Acrylics, vinyl (polyvinyl chloride), film, resins, fire retardants||Respiratory tract irritation|
|Cyanide||Paper, silk, wool, urethane acrylonitriles||Cellular asphyxia|
|Isocyanates||Urethane (foam)||Respiratory tract irritation|
|Organic acids||Cotton, paper, wool, wood||Respiratory tract irritation|
|Nitrogen oxide||Paper, petroleum products, wood||Respiratory tract irritation|
|Phosgene||Fire retardants, vinyls, polyvinyl chloride||Respiratory tract irritation|
|Styrene||ABS, polystyrene||Respiratory tract irritation|
|Sulfur oxides||Rubber, fur, hair, hide, wool, petroleum||Respiratory tract irritation|
Box 23-1 Toxic Combustion Products
Every 12 seconds a fire department responds to a fire alarm in the United States.4 When compared with other countries, the United States has one of the highest numbers of fire-related deaths in the world. The majority of fires in the United States (more than 70%) occur in residential homes. Carelessness with cigarettes, heating devices, matches, flammable liquids, and malfunctioning electrical appliances is overwhelmingly the most common initiatory cause of fires. Every year there are nearly 3600 human deaths in the United States. Deaths in companion animals as a consequence of fire are harder to quantify, but certainly thousands of animals suffer fire-related injuries and smoke inhalation each year.
There is no standard toxic or lethal dose for smoke inhalation in animals. The composition of smoke can vary tremendously even from the same fire. Combustion products and their concentrations are difficult to predict, and the relative toxicity of smoke produced depends upon the composition of the substance burning, amount of oxygen available, the temperature of the fire, the length of exposure, and the size of the animal involved. In addition, the incredible variety of materials currently used in an animal’s environment and their wide spectrum of toxic combustion products ensure that there is no such thing as “typical” smoke.
If burns are present and respiratory tract tissue displays burn edema, the episode becomes much more serious and much more likely to be life threatening. Increased vascular permeability of burned, edematous respiratory tissue greatly enhances the toxic effects of smoke inhalation. In one study in humans, mortality as a result of smoke inhalation alone was 12%; where smoke inhalation was also associated with burns, 61% were fatal.5 Thus mortality from smoke inhalation is dramatically increased in animals with concomitant thermal burns.
The pathophysiology of smoke inhalation can be traced to the mechanism of action of the individual toxins involved, their subsequent physiological effects, and the cause of clinical toxicity after exposure. Toxic combustion products are classified as simple asphyxiants, irritant toxins, and chemical asphyxiants. These categories and their production products are included in Box 23-1.
Simple asphyxiants are space occupying and fill enclosed spaces at the expense of oxygen. In addition to this effect, combustion uses oxygen and creates an oxygen-deprived environment. The net effect is less oxygen available to the animal.
Irritant toxins are chemically reactive substances. They produce local effects on the tissue or the respiratory tract. Ammonia is produced by burning wool, silk, nylon, and synthetic resins.6 Ammonia has high water solubility and dissolves in moist membranes of the upper respiratory tract, resulting in nasopharyngeal, laryngeal, and tracheal inflammation. Acrolein is lipid soluble and penetrates cell membranes. It denatures nucleic acid and intracellular proteins and results in cell death. Acrolein is a very common irritant gas generated by combustion. Sulfur dioxide is found in more than 50% of smoke from fires.7 Sulfur dioxide reacts with the moist respiratory membrane mucosa, producing the potent caustic, sulfurous acid. Polyvinyl chloride is ubiquitously found in floor coverings, office and home furniture, electrical insulation, and clothing. The resultant combustion products phosgene, chlorine, and hydrogen chloride are produced in many residential fires.8 Together with water in the mucosa, chlorine produces hydrogen chloride free oxygen radicals and is very damaging to tissue. Phosgene descends and produces more delayed alveolar injuries. Isocyanates are produced from burning and smoldering upholstery, and intense irritation of both upper and lower respiratory tissue results.
Organic material produces finely divided carbonaceous particulate matter upon combustion. This particulate matter or soot is suspended in the gases and hot air of smoke. Not only just carbon, soot has aldehydes, acids, and reactive radicals that adhere to its surface.6 The inhalation of soot and associated aerosols heightens the effect of other irritant toxins. Soot binds with respiratory mucosal surfaces, allowing other irritant chemicals to adhere and react with adjacent tissue. The penetrance and deposition of these particles within the respiratory tract is dependent on size. Small particles (1 to 3 μm) reach the alveoli. In various animals, lung injury is decreased when smoke is filtered to remove particulate matter. Sulfur dioxide shows a high propensity to adhere to soot. In addition, polyvinyl chloride combustion produces a large amount of soot-containing smoke coated with its particular combustion products phosgene, chloride, and hydrogen chloride. In addition to soot and related particles, irritant gases, acids, and other combustion products can also adhere to aerosol droplets.
The most important determining factor in predicting the level of respiratory injury is the water solubility of the toxin. Water-soluble chemicals injure the mucosa of upper respiratory airways by releasing the mediators of inflammation and deleterious free radicals. This type of inflammation increases microvascular membrane permeability and results in a net influx of fluid from intravascular spaces into the upper respiratory tissue. The underlying tissue of the supraglottic larynx may become terrifically swollen and edematous. This edematous reaction can result in minutes to hours postexposure, continue to progress, and close off upper airways completely.
Low water-soluble molecules react with the lung parenchyma. They react more slowly and produce delayed toxic effects. Concentration of the toxic element inhaled, particle size, duration of exposure, respiratory rate, absence of protective reflexes, preexisting disease, and size and age of the animal also contribute to the level and degree of respiratory injury in addition to the water solubility of toxic products.
An intense inflammatory reaction develops secondary to the initial injury to respiratory mucosal cells by toxic combustion products.9 Inhaled soot and toxic gases generate increased airway resistance caused by inspissated secretions, increased mucosal airway edema, and associated bronchospasm. Damaged mucosal cells stimulate copious exudates rich in protein, inflammatory cells, and necrotic debris. If this reaction continues, mucosal sloughing ensues. The degenerative exudates, bronchorrhea, and extensive sloughing produce casts of the airways. In animal victims of smoke inhalation, these casts increase airway resistance by blocking major airways and prevent oxygen passage to the alveoli. In addition, increased vascular permeability of respiratory tissue contributes to airway blockage. Bronchoconstriction and reflexive wheezing follow in response to inflammation and the toxic mucosal injury.
Chemical asphyxiants produce toxic systemic effects at tissue distant from the lung. Carbon monoxide is generated during incomplete combustion and is regarded as the most serious systemic agent to smoke inhalation victims. Carbon monoxide prevents oxygen binding to hemoglobin, thereby producing a functional anemia. Furthermore, carbon monoxide inhibits release of oxygen, thereby shifting the oxyhemoglobin dissociation curve to the left. Carbon monoxide itself has other toxic effects that cause lipid peroxidation and directly damage cellular membranes. Carbon monoxide is invariably present in smoke from fires and is thought to be the cause of most immediate deaths from smoke inhalation.10 Nitrogen-containing products, such as wool, silk, nylon, plastics, paper, rubber, pyroxylin, polyurethanes, and polyacrylonitriles, all produce cyanide upon their combustion. Cyanide has been detected in samples from many other types of fires as well. Together with carbon monoxide, cyanide has at least an additive and perhaps synergistic toxic effect in victims of smoke inhalation. Nitrogen-containing compounds produce oxides of nitrogen on their burning, which are potent respiratory irritants. Other combustion products can cause systemic and local toxicity. Metal oxides, hydrogen fluoride, hydrogen bromide, and various hydrocarbons can all be retrieved from toxic smoke. Benzene can be detected in the smoke of plastic and petroleum fires.11 Antimony, cadmium, chromium, cobalt, gold, iron, lead, and zinc have all been recovered from smoke samples during fires. Natural disasters, accidents at illegal drug labs, transportation accidents, industrial fires, and acts of terrorism are situations where unusual types of toxic smoke combustion products may be encountered. In fact the entire spectrum of potentially toxic combustion products from fires is endless, and we must remain vigilant.
Super-heated air and steam in smoke results in thermal burns to tissue of the respiratory tract. In animals the higher the air temperature and humidity, the greater is the mortality in affected individuals. Exposure to dry air heated to 200° C for 5 minutes or to 125° C for 15 minutes is potentially lethal in mammals.12 Shorter exposure to dry air at temperatures of 350° C to 500° C results in tracheitis in dogs. Exposure to steam alone results in tracheitis, bronchitis, and pulmonary parenchymal damage. Respiratory tract injury secondary to steam or heat alone is relatively uncommon in animals.
Combustion progressively consumes oxygen. This decrease in oxygen concentration produces hypoxic asphyxia. The normal oxygen fraction at sea level is roughly 21%. Acute reductions in ambient oxygen fractions to 15% result in dyspnea. A reduction to 10% produces dyspnea and altered mentation, and fractions from 8% to 6% cause loss of consciousness followed by death in less than 8 minutes.
It is noteworthy to examine the dynamics of smoke dispersal from fires. Spreading smoke initially accumulates and forms a hot layer mainly at the ceiling, which gradually descends to the floor. The main toxic combustion agent threats (e.g., heat, irritants, asphyxiants, noxious gases, and particulate material) are found in this ceiling layer.13 Depending on the size of the enclosed room, the amount of smoke produced, and duration of time, the toxic products will eventually disperse to the floor. Thus at least initially, animals at the floor are breathing cooler and much less contaminated air and are receiving less radiant heat. Because of this pattern of dispersal, the chance for survival exists for limited periods.
Carcinogens are also some of the toxic products of thermal decomposition. All fires produce benzopyrene, the classic initiator of carcinogenesis. Plastic fires, particularly those involving polyvinyl chloride, produce arsenic, benzene, chromium, and acrylonitrile, all of which are suspected human and animal carcinogens. Smoke from wood and plastic produces the potent carcinogen, formaldehyde. Soot, so long known to cause cancer in chimney sweeps and tobacco smokers, is a principal product of most fires. The exact association of smoke inhalation and the development of cancer are unknown for animals at present.
Smoke inhalation causes progressive physiological dysfunction and ultimately can lead to death. Irrespective of cause, asphyxia is the underlying mechanism. This asphyxia may be due to inhibition of cellular respiration, impaired oxygen transport and delivery, central respiratory depression, direct or indirect occlusion of airways, or a decreased supply of oxygen. For smoke inhalation, there is a direct correlation between the duration of exposure and the severity of effects. Finally the greater the exposure the more rapid and pronounced are the effects observed.