- Identify the difference between civilian and firefighter smoke exposure.
- Recognize the effects different types of smoke have on the body.
- Learn how to assess and treat victims of smoke inhalation.
- Carcinogen: A substance that can cause the growth of cancer.
- Hydrogen cyanide: A colorless, toxic, volatile liquid or gas with the aroma of bitter almonds.
- Hypoxemia: An abnormal deficiency in the concentration of oxygen in arterial blood.
- Ultrafine particles: Nano-sized particles that are the result of combustion or friction processes or natural processes in the air or water.
What’s the biggest danger in a structure fire for citizens and firefighters? The National Fire Protection Association report “Fatal Effects of Fire” estimates that victims trapped in a structure fire are twice as likely to die of smoke inhalation when compared to burns.1 In fact, victims are rarely found in the fire room—more often, they’re found in nearby unburned rooms, possibly exposed to heavy smoke loads. The smoke may be hot or mixed with steam, and capable of causing hypoxemia and damage to every portion of the respiratory tree.
Even though firefighters are typically exposed to smoke at every fire, those exposures account for less than 2.5% of all line-of-duty injuries.2
The difference between civilian and firefighter exposures is easy to identify. The smoke civilians are exposed to during fire development and suppression is thick, hot and very toxic, while the smoke firefighters experience after the fire is lighter and more likely to be laden with fine particulates and carcinogens. Exposure to heavy smoke conditions will create very different signs and symptoms when compared to longer exposures to light smoke.
Smoke exposure and CO can injure the victim immediately or over a cumulative time period.
The composition of the gaseous mixture “fire smoke” varies according to the fuel and conditions. A well-oxygenated, outdoor wood fire may produce a very light smoke with relatively few chemicals. Although there are particulates in wood smoke capable of causing low-level inflammation, this type of exposure rarely requires medical attention. Toxic fire smoke, however, is the result of a fire when the fuel load is more complex (e.g., plastics, artificial fabrics) or the oxygen supply is limited. Structure fires are usually the primary concern when we consider smoke inhalation, but toxic fire smoke is also created at trash bin/dumpster and automobile fires. Wildfire smoke can also be toxic if the burning area was recently sprayed with chemicals.
The composition of fire smoke has changed over the past 50 years. The homes of our grandparents and great-grandparents were largely furnished with wood, cotton and wool since these were the common materials used in manufacturing in the 1940s and 1950s. Advancing technology and changing manufacturing practices resulted in a shift away from natural materials to polymer-based composite materials and manufactured wood (e.g., particle board). These materials release toxic gasses and particulates when burned. (See Table 1.) Chemicals are released from incomplete combustion and from the off-gassing of glues used in the manufacturing process.
Also contained within fire smoke are small inhalable particles known as fines and ultrafines. These particles (less than 0.00001 mm in diameter) are less well-known to the public safety services but can be very damaging to health. Ultrafine particle concentration can be very high after fire suppression, even when there doesn’t appear to be a significant amount of smoke in the room.3
Acute vs. Chronic Effects
Smoke exposure can injure the victim immediately (acute onset) or over a longer period of time (chronic/delayed onset). Victims trapped near the fire source may be exposed to hot and dense smoke with off-gassing chemicals including carbon monoxide (CO) and cyanide.
Often, these chemicals cause bronchospasm, sloughing of the epithelial lining of the airway, mucus secretion, inflammation and surfactant inactivation. How quickly these symptoms manifest depends on the chemicals within the smoke and the intensity and duration of the exposure. Smoke inhalation victims may also suffer from thermal burns that require immediate care and transport to the nearest appropriate hospital.
In contrast, firefighters working at the scene after the fire has been extinguished can be exposed to lower levels of these same chemicals and particulates. Some firefighters may leave the scene with elevated but subclinical doses of CO or hydrogen cyanide (HCN). The cumulative exposure to chemicals and particulates over years of service can result in respiratory conditions, heart disease or cancer. The exact particulate exposure required to cause health issues isn’t known, but studies in other occupations have shown that ultrafine particles cause cardiac toxicity. Tollbooth workers and boilermakers are routinely exposed to ultrafine particles and suffer worse forms of cardiac disease and arrhythmia when compared to other occupations.
Carbon Monoxide & Hydrogen Cyanide
CO and HCN are both chemical asphyxiates commonly found in fire smoke, and exposure should be considered in every case of smoke inhalation.
CO is produced when a carbon-containing material, such as wood, is burned and there isn’t enough oxygen present to completely transform into carbon dioxide (CO2). It’s also commonly found near burning hydrocarbon fuels (e.g., gasoline and diesel). Although the fire smoke or fuel fumes are easy to identify, CO itself is colorless, odorless, tasteless and initially nonirritating. Hemoglobin has a high affinity for CO and once bound, the new molecule (carboxyhemoglobin [COHb]) is no longer capable of binding oxygen. Since oxygen dissolves poorly in blood plasma, high COHb levels result in poor oxygen-carrying capacity and hypoxemia.
HCN is a by-product of the combustion of materials such as green wood, tobacco, cotton, paper, wool and silk. When burned, these materials release nitrogen gas into the air. Hot fires in enclosed spaces can convert the nitrogen gas to small amounts of cyanide. Unlike CO that alters the blood capacity to transport oxygen, cyanide binds to the cytochrome c oxidase protein in mitochondria and limits cells’ ability to use oxygen. Without functioning mitochondria, cells can’t efficiently produce adenosine triphosphate and rely on anaerobic metabolism. Ultimately, the cell accumulates lactic acid and the intracellular pH drops.
You should assume that both CO and HCN are present in fire smoke and that fire victims have been poisoned by both, resulting in both oxygen transport and utilization issues. The immediate danger to life and health toxicity for cyanide is much lower (50 ppm) when compared to CO (1200 ppm), so firefighters should be extremely cautious about working in a smoky environment unless wearing self-contained breathing apparatus (SCBA).
Strutcture fires are usually the primary source of smoke inhalation victims.
Victims of smoke inhalation should be assessed with three particular injury patterns in mind: thermal burns to the airway, chemical damage to the trachea and bronchi and systemic poisoning from CO and/or HCN.
The critical first step in assessing smoke inhalation is examining the airway and lung sounds. Look for soot deposited in the nares and oropharynx. Examine the mouth for swelling or blistering that might indicate thermal damage. Are there signs of burns to the face and neck? Any of these might indicate a need for aggressive air-way management.
Listen closely for abnormal lung sounds. Thermal damage to the upper airway can induce stridor or hoarseness. Chemical damage to the trachea and bronchi can create wheezing or rhonchi and deep inhalation into the alveoli can cause pulmonary edema.
Understanding the circumstances of the exposure will provide important information to support your assessment of the patient’s airway, breathing and circulation. Was your patient rescued from the fire room or another room in the structure? Greater distance between a patient and the fire origin decreases the chance of thermal injury. Longer exposures increase the chance of significant systemic poisoning.
Is the victim a civilian or a firefighter? Firefighters will rarely be symptomatic from smoke exposure at the scene unless the SCBA wasn’t worn or the mask was dislodged or failed during fire suppression. In these cases, a firefighter may have been exposed to very dense, hot smoke and have a combination of thermal and chemical injuries.
Was the victim exposed to steam during fire suppression? Although fire suppression tactics avoid using steam conversion, it can occur. Inhaling steam is particularly damaging to the lungs since the low-density vapor is easily inhaled into the alveoli, causing atelectasis and pulmonary edema.
The common systemic endpoint for inhalation injury is hypoxia. The hypoxia can be the result of poor ventilation through damaged airways, reduced oxygen carrying capacity of hemoglobin after CO exposure, or reduced oxygen utilization from HCN. Assess the patient for agitation, anxiety, stupor and other signs of hypoxia. Cyanosis may be present if the inhalation exposure caused an impairment of ventilation or a mismatch between pulmonary ventilation and perfusion. If the victim’s condition is primarily the result of CO poisoning, then cyanosis may be absent since CO2 removal isn’t effected by the creation of COHb.
The threshold for symptoms varies among individuals. Although charts relating COHb levels to symptoms appear commonly in medical texts, they’re guidelines. Individuals who regularly smoke cigarettes have a higher tolerance for COHb and aren’t symptomatic at low levels. Others are very sensitive and may become tachycardic with relatively low COHb levels.
Exposure to heavy smoke conditions will create very different signs and symptoms when compared to longer exposures to light smoke.
The first priority of managing smoke inhalation victims is assuring the airway remains patent. Apneic and near-apneic patients should be ventilated with 100% oxygen by bag-valve mask and the appropriate airway adjuncts. Smoke inhalation victims with a patent airway should be treated with high-flow oxygen administered with a tight-fitting mask. For most EMS systems, the best mask available is the standard non-rebreather mask, but a double-sealing silicone mask will deliver higher fraction of inspired oxygen.
Continually reassess the airway and lung sounds during transport. Providers should carefully watch the patient for worsening signs and symptoms of hypoxia. Neither CO nor HCN can be detected by a standard pulse oximeter. Oxygen-carrying capacity can be greatly reduced by CO even though the SpO2 reads in the high 90s or even 100%.
The best initial treatment for CO poisoning is to provide the highest fraction of inspired oxygen possible. The half-life of CO bound to hemoglobin while breathing air is approximately 5.5 hours, but breathing 100% oxygen reduces the half-life to 80 min.4 Most cases of mild CO poisoning respond well to this therapy alone.
IV access should be established during transport. It may become necessary to administer medications if the patient’s condition continues to deteriorate or if the patient becomes pulseless. There are multiple antidotes available for HCN poisoning but the drug hydroxycobalamin has become most common. This drug is a precursor to vitamin B12 and is marketed as Cyanokit for cyanide poisoning. The standard adult dose is 5 g given intravenously over 15 minutes. However, the drug is expensive and not routinely available to prehospital providers in the United States. Because of its deep red color, hydroxocobalamin may interfere with colorimetric determination of certain laboratory parameters, which may limit the physician’s ability to diagnose other issues related to the exposure for 24 to 36 hours.
Hospital victims of significant smoke inhalation can decompensate quickly and should be rapidly transported to an appropriate hospital. Even mild cases of smoke inhalation should be treated with high-flow oxygen and assessed by a physician.
Severe cases of CO poisoning may be treated with hyperbaric oxygen. Patients are placed in a hyperbaric chamber and exposed to oxygen at pressures higher than those experienced at sea level. Hyperbaric oxygen delivered at three atmosphere’s absolute pressure (equivalent to scuba diving to 66 feet) decreases the half-life of CO to 23 minutes.4 The high pressures cause oxygen to dissolve into the blood plasma, allowing the tissues to oxygenate while the CO is being removed from hemoglobin. Not every hospital will have a hyperbaric facility and not all physicians support hyperbaric oxygen therapy.
It’s important to know your local protocols for hyperbaric oxygen indications and the hospitals capable of delivering that therapy. The most common indications for hyperbaric oxygen therapy to treat CO poisoning are:
- Carboxyhemoglobin > 25%;
- Pregnant women with symptomatic CO poisoning;
- Chest pain;
- ECG changes; and
- Altered mental status.
Inhalation burns are more likely in victims rescued close to the fire origin, in industrial settings and among firefighters when the SCBA mask becomes dislodged or fails under extreme heat.
Since the oropharynx is lined with moist mucous membranes, heat transfer is very efficient and most thermal burns caused by hot smoke occur above the glottis. Exceptions to this rule are exceedingly dense smoke, long exposures and steam. Steam and superheated steam (steam heated beyond the vaporization of the water content) are inhaled more deeply into the lungs before transferring their heat to the tissues, resulting in alveolar damage, pulmonary edema and ultimately a ventilation perfusion mismatch. These are difficult burns to treat and require the provider to aggressively capture the airway and supply high concentrations of oxygen.
Thermal exposure may cause swelling of the oropharynx and laryngopharynx. Airway swelling may worsen during transport, so signs of upper airway edema or blistering should result in endotracheal (ET) intubation. If intubation is delayed, continued airway swelling may obscure important landmarks for successfully placing an ET tube. (Indications for ET intubation are listed in Table 2.)
It’s important to understand singed nasal hair alone isn’t sufficient justification for ET intubation. In cases of thermal burns to the airway, many burn surgeons prefer ET intubation over blind insertion techniques, but supraglottic airways are acceptable if intubation isn’t available or can’t be established quickly. Inhalation injuries complicated by thermal burns should be treated at a burn center unless the patient has associated trauma that’s more appropriately treated at a trauma center.
Delayed Signs & Symptoms
Even when treated appropriately, long-term consequences of smoke exposure can be seen in both civilian victims and firefighters. A notable long-term issue for CO exposures is neurological problems developing weeks after recovery from acute CO poisoning.5 These late neurological sequelae include intellectual deterioration, memory impairment and deterioration of personality.6
Among firefighters, symptoms of smoke exposure may not appear for hours. The subclinical exposures incurred at one incident may create symptoms later if the firefighter is exposed again at a second fire.
In 2006, a firefighter from the Providence (R.I.) Fire Department experienced symptoms including headache, dizziness, difficulty breathing and a cough after working at a residential structure fire. Crewmembers reported that at times he was talking incoherently. The firefighter was transported to Rhode Island Hospital and diagnosed with cyanide poisoning.
Additional firefighters, from three different fires within the 24-hour period, became symptomatic. In total, 27 firefighters were tested for cyanide poisoning and eight were found to have elevated cyanide levels. Only two of the firefighters were symptomatic at the scene, demonstrating that it’s possible to leave the incident with a subclinical exposure that may worsen later in the shift or at a second fire.
It’s likely that the same situation occurs among firefighters with regards to CO exposure. Breathing apparatus is rarely worn after fire suppression when the structure is being overhauled. Although it’s becoming more common for firefighters to be screened for elevated COHb during emergency incident rehabilitation, routinely monitoring the structure during overhaul for high CO levels with a four-gas meter could reduce the exposures.
Lastly, many chemicals in fire smoke are known carcinogens. A recent study examined mortality patterns and cancer incidence in a group of 29,993 U.S. career firefighters.7 This large study concluded that several cancers were more common among firefighters including malignant mesothelioma, a type of lung cancer caused by asbestos exposure. Another study reported that there are chemicals deposited on fire gear during fire suppression that have been associated with reproductive cancers.3 Collectively, these studies indicate the smoke is never innocuous. Exposures that don’t cause signs or symptoms at the scene can still harm individuals hours and possibly years later.
Rapid recognition of acute smoke inhalation and inhalation burns should lead to immediate and aggressive airway management, high-flow oxygen therapy and rapid transport to an appropriate hospital. It’s equally important to recognize the hazards of smoke exposure after the fire has been extinguished. The cumulative exposures suffered over a career by firefighters and EMS personnel during overhaul may lead to significant chronic health problems.
1. Hall JR. (March 2011.) Fatal effects of fire. National Fire Protection Association. Retrieved June 30, 2014, from www.nfpa.org/research/reports-and-statistics/demographics-and-victim-patterns/fatal-effects-of-fire.
2. Karter MJ Jr, Molis JL. (October 2013.) Firefighter injuries in the United States. National Fire Protection Association. Retrieved June 30, 2014, from www.nfpa.org/research/reports-and-statistics/the-fire-service/fatalities-and-injuries/firefighter-injuries-in-the-united-states.
3. Baxter CS, Ross CS, Fabian T, et al. Ultrafine particle exposure during fire suppression—Is it an important contributory factor for coronary heart disease in firefighters? J Occup Environ Med. 2010;52(8):791–796.
4. Myers RAM, Snyder SK, Emhoff TA. Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med. 1985;14(12):1163–1167.
5. Meredith T, Vale A. Carbon monoxide poisoning. Br Med J (Clin Res Ed). 1988;296(6615):77–79.
6. Raub JA, Mathieu-Nolf M, Hampson NB, et al. (2000) Carbon monoxide poisoning—A public health perspective. Toxicology. 2000;145(1):1–14.
7. Daniels RD, Kubale TL, Yiin JH, et al. Mortality and cancer incidence in a pooled cohort of U.S. firefighters from San Francisco, Chicago and Philadelphia (1950–2009). Occup Environ Med. 2014;71(6):388–397.