A Fatal Fire Investigation: The Medical Perspective


According to the United States Fire Administration, the United States has one of the highest fire death rates in the world.1 The National Fire Protection Association has reported that between 3,145 and 3,720 people per year died in the 14-year period preceding 2003. In 2003, there were 3,385 civilian deaths in structure fires; 305 of those civilians, or 9 percent, died in fires that were ruled to be intentionally set.2

Based on these disturbing figures, every fire investigator should be prepared to examine a fire scene in which there has been a loss of life. To complicate this matter, research suggests that arson is the leading cause of fire in the United States;3 therefore, the fatal fire must be viewed as an investigation for the criminal acts of arson and homicide. The investigator must take due care and caution to ensure that the various investigatory steps are taken to reach the appropriate legal conclusion. Although the topic of legal action in the course of the investigation deserves discussion, we are not going to discuss those investigatory procedures here.

It is essential that the fire investigator have a basic understanding of how fire and its by-products (combustion products) affect the human body and what these effects can reveal about the fire. In this sense, the investigator, while maintaining the reverence and respect that must be shown for the deceased, has to examine the body in place and view it in reference to the fuel load of the structure.

A literature search would reveal that numerous articles, papers, and chapters in books have been written about “fatal fire investigation,” but most deal with just that-the investigation surrounding the events of a fatal fire. Here, fatal fires are explored from a medical perspective so that fire investigators develop a better understanding of the nature of thermal burns and the effects of the products of combustion on the human body.


Injuries sustained in a fire caused by the body’s exposure to heat or flames are known as thermal injuries. Although there is a tendency to focus on thermal injuries because they are very dramatic and easily observable, a majority of injuries and fatalities occur as the result of smoke inhalation, a condition that may not be as easily identified but may present a significant risk to the victim. Research has indicated that smoke inhalation, or the inhalation of the toxic by-products of combustion, is the leading cause of death in fires.4

The injuries sustained in a fire come from a wide variety of sources and exposures to a myriad of dangers and, therefore, cannot be considered in isolation-the overall scenario must be examined. As an example, if a victim were brought to a hospital with a broken leg that resulted from falling down a set of stairs in a burning house, the emergency room staff could not treat the broken leg without considering the possible effects of exposure to the products of combustion. Other injuries may occur from trauma, such as the individual’s falling down a flight of stairs as a result of smoke obscuration, the debilitating effects of smoke inhalation, or being hit by a falling object. The victim may also suffer from a preexisting medical condition that was worsened by exposure to the products of combustion or the stress associated with the event.

We propose a new classification of fire injuries based on the injury hazards associated with the fire scene: primary (10), secondary (20), tertiary (30), and quaternary injuries (40). Primary injuries are those associated with the effects of the victim’s direct exposure to the flame, heat, and smoke associated with a fire. They include thermal injuries as well as smoke inhalation. Secondary injuries occur from trauma that results from the victim’s exposure to the products of combustion or from the obscuration from smoke. An example of this would be a victim who fell down the stairs because of decreased awareness caused by smoke inhalation or the victim’s being unable to see the hazard because of the limited visibility resulting from the smoke. Tertiary injuries are caused by trauma resulting from debris or other objects falling on the victim.

Quaternary injuries are medical emergencies (i.e., heart attack) caused by the victim’s exposure to the fire or fire scene. Such injuries generally involve preexisting or acute medical conditions (those that happen quickly and without warning, such as a heart attack or a stroke). The question becomes, what came first? Was the heart attack or stroke (to use only two examples of thousands that could exist) the result of the fire or the cause of the fire? Consider these things when examining the scene and interviewing family and witnesses.

Since most fire-related fatalities are not the direct result of the flames but the effects of the toxic by-products of the fire (4), it is important for fire investigators be familiar with the types of burns and the effects these burns have on the human body.


Burns are classified by the agent that produced the burn-namely thermal, chemical, electrical, and radiological. Thermal burns may be caused by flame; radiation; or excessive heat from fire, steam, hot liquids, and hot objects.

Chemical burns are associated with various acids, bases, and caustics. Electrical burns come from the transfer of heat energy as the electrical current passes through the tissues of the body (electrical burns may also be caused by arcing or from direct exposure to the heat given off from the electrical source). Radiation burns are caused by the exposure to some type of nuclear source; ultraviolet light is a source of such energy and can cause burns if exposure of the skin is prolonged. Cancer therapies and other medical procedures may also cause burning of the skin secondary to the application of radiation therapies.

After determining the cause of the burn, you must measure the severity of the burn. Multiple factors affect the severity of a burn, including the rate at which heat is transferred from a given object to the skin. This rate is further dependent on various temperatures (including the temperature of the object), the duration of contact, the temperature of local tissues, and a variable known as “the heat transfer coefficient.” This transfer coefficient varies according to the composition of the substance through which the heat must be transferred to contact the skin.

Heat transfer occurs between regions at different temperatures, moving thermal energy from an area of higher temperature to an area of lower temperature. Heat is transferred between objects or to the surrounding environment by conduction, convection, or radiation. Certain materials, depending on their composition, thickness, surface properties, and other qualities, transfer heat better and more efficiently than others.

Another important property of a material is its thermal conductivity, a measure of how well the material conducts heat. The fire investigator should consider the position of the body in terms of its proximity to a good conductor of heat and the burn damage to the body. The presence of protected areas underneath the body or the amount and type of debris found on top of the body may help the fire investigator determine at what point in the fire the victim became incapacitated or perished.

Heat flux causes objects to get hot, become damaged, or become ignited. As a benchmark, the radiant heat flux from the sun at the earth’s surface is nearly 1.0 kW/m2 at the most. Minimum values of heat flux that cause damage under fire conditions are as follows: pain to bare skin, 1.0 kW/m2; burn to bare skin, 4.0 kW/m2; and ignition of objects, 10 to 20 kW/m2. 5

Suffice it to say that a relationship exists between temperature and distance and the degree of injury to the skin. It can be assumed that as the exposure time to heat increases, the severity of a burn increases. This also depends on many variables-for example, wet heat or a scalding type injury travels through the skin much more rapidly than dry heat or flame.6 Liquids heated to temperatures of 160°F to 180°F will cause an almost instantaneous burn.7

Burns can be described using several evaluation systems. An older system still used in many textbooks and commonly recognized by many includes first-, second-, third-, and fourth-degree burns. First-degree burns reflect a superficial injury that involves only the epidermis, or outer layer of the skin, and are characterized by a reddening of the skin and perhaps some swelling. A second-degree burn occurs when the epidermis is burned through and the second layer of the skin (dermis) is damaged, but the burn does not pass through to the underlying fat and muscle tissue. There may be deep intense pain, intense reddening, blisters, and a spotted or mottled appearance to the affected skin. Third-degree burns are full-thickness burns with all of the layers of the skin damaged. The skin usually appears black (charred) or dry and white. In fourth-degree burns, all the layers of the skin have been burned and the damage has reached the underlying structures of the muscles and, in some cases, bone.

This evaluation system for the most part has been replaced with the terms “full-thickness” and “partial-thickness” burns. First- and second-degree burns are now typically referred to as “partial-thickness” burns and third- and fourth-degree burns as “full-thickness” burns. Full-thickness burns destroy the epidermis and dermis as well as the structures contained therein, such as blood vessels and nerves. Generally speaking, unless a body has been completely incinerated, concentric areas of burn exist on the body. This means that areas of full-thickness burns (or third-degree burns) are surrounded by areas of lesser damage, or partial-thickness burns.

According to statistics published by the National Funeral Directors Association, complete cremation of an adult requires temperatures in the range of 1,400°F to 1,800°F (760°C to 982°C) for two to two and a half hours.8 Even after this exposure, identifiable portions of the skull, pelvic bones, and teeth will survive. It is unlikely that a normally ventilated and fueled fire could completely destroy the remains of an adult; the skeletal remains of children, because of their size and density, are far more prone to destruction.9 Since it is generally accepted that common structure fires rarely sustain temperatures greater than 1,900°F (1,040°C) for long periods of time [National Fire Protection Association 921, (NFPA) Guide for Fire and Explosion Investigations], fire investigators rarely would investigate a fire that had the intensity and the time to completely destroy the human body.

When investigating a fire, thoroughly examine the body at the scene before it is moved. It is important to attempt to determine if the damage to the body is consistent with the fuel load at hand. The examination may also aid in determining the spread of fire or the path of fire travel. More significant burning to one side of the body than the other may be helpful in determining the direction of fire travel. This finding is subject to the location of the body in reference to objects with significant heat flux, areas of ventilation, areas of significant fuel, and the movement of the body post-mortem. It is also important to document the presence and composition of fire debris found on top of and underneath the body because it may help in determining the stage at which the victim became incapacitated.


On occasion, the fire investigator will observe long splits in the skin and muscle of a badly burned body that resemble lacerations and can be mistaken for an ante-mortem injury. These splits may occur when the fat and grease of the fatty tissue inside the body burn. As the fatty tissue inside the body heats, it liberates various gases, and the pressure within the body rises. As the pressure increases, it exerts force against the skin and overlying structures, eventually splitting the overlying structures and tearing the skin.

This increase in pressure is an acute medical condition referred to as “compartment syndrome,” in which swelling and an increase in pressure within a limited space (a compartment) press on and compromise blood vessels, nerves, or tendons that run through that compartment.10

One type of injury historically reported in the fire victim is the “blowout” of the skull. This blowout, or open fracture, is the result of a buildup of pressure from the off-gassing of brain tissue inside the closed compartment of the rigid skull. When this syndrome occurs, the pressure inside the skull usually is released through the area of least resistance-in this case, the base of the brain or at the suture lines near the temporal area of the skull. (When a fracture at the base of the brain occurs, it will not generally be apparent to the observer and is usually detected at autopsy.)

A buildup of fluid inside the skull may result in a victim’s brain being forced downward through the base of the skull and the patient’s dying prior to the skull’s fracturing. This phenomenon, known as herniation, is also observed in someone who experiences severe head trauma in which blood accumulates in the skull from some type of wound and pushes the brain out of the base of the skull and down the neck. This is a fatal event and would be noted on autopsy.

Bones of deceased victims can be fractured during a severe fire. These fractures may be the result of fire penetration or muscle spasms or contractions during a fire. The fractures usually occur to the long bones of the arms and legs. Bones may also shrink when exposed to fire. The services of a forensic anthropologist are often needed to determine whether a fracture was caused by the fire or was the result of a prefire injury.

The pugilistic position many bodies assume in a fire was once thought to be the victims’ attempt of self-defense. This position is the result of the contraction of the large muscles from the heat of the fire but may be absent if the fire is short-lived or not intensely hot. (9) The absence of this position in a burned body should be viewed as suspicious and warranting further investigation, because this position will not be present if rigor mortis had developed prior to the fire (meaning that the death occurred prior to the fire).

Not all fire fatalities are immediate. The victim may die hours, days, or months after the event. Because of this fact, treat fire scenes with severe injuries as fatal fire investigations. The risk of death from a burn depends on the depth of the burn and total body surface area involved as well as comorbidity, the cumulative effects of all other diseases from which the victim may suffer.

A widely accepted principle in medicine is, in general, that the age of the patient plus the percent of total body surface area (TBSA) burned equals the risk of death. Three risk factors for death following a burn injury have been identified: an age greater than 60 years, greater than 40 percent of TBSA burned, and some type of inhalation injury.11 When confronted with a victim that fits into one or all three of these risk factor categories, consider that the possibility of death increases and that the investigation may become a fatal fire investigation. Keep in mind that a victim’s stay in a burn unit may last weeks to months and that there are constant and persistent dangers from infection (sepsis) and other evolving conditions that may be life threatening and may ultimately cause the victim to die weeks to months after admission.


A majority of fire victims perish from inhalation injuries, not burn injuries. J.R. Hall of the NFPA Fire Analysis and Research Division,12 for instance, reports that most victims who perish in fires do so as the result of their exposure to smoke and toxic gases instead of burns. According to the Children’s Hospital of Boston, 75 percent of fire deaths are the result of smoke inhalation. (4)

NFPA 921 defines smoke as an airborne particulate product of incomplete combustion suspended in gases, vapors, or solid and liquid aerosols. The materials in smoke can be separated into three basic classes: asphyxiants, irritants, and other toxic materials.

Asphyxiants are toxicants capable of causing central nervous system depression, loss of consciousness, and ultimately death. The effects of asphyxiants depend on concentration and exposure time. Many asphyxiants are produced during a fire; however, only carbon monoxide (CO) and hydrogen cyanide (HCN) have been measured in sufficient concentrations in fire gases to cause significant acute toxic effects.13 Other asphyxiants are hydrogen sulfide, methylene chloride, argon, carbon dioxide, ethane, helium, hydrogen, methane, nitrogen, and organophosphates. Asphyxiants cause death by displacing oxygen from hemoglobin in the body, depriving the body of oxygen (this topic is discussed in more detail below).

Irritants are generally classified as two types: sensory, which irritate the eyes and upper respiratory tract, and pulmonary, which affect the lungs. Fire victims experience airway swelling as a result of direct thermal injury. Air itself has a very low heat capacity; therefore, it typically does not produce lower airway injury.

Numerous studies have shown that in most modern-day structure fires a diverse array of toxic chemicals is produced and is present in smoke. One of the better known studies, by the Bureau of Alcohol, Tobacco, Firearms and Explosives (ATF)/National Institute for Occupational Safety and Health (NIOSH) study,14 identified the presence of aldehydes (formaldehyde, acetaldehyde, and acrolein), hydrogen cyanide, inorganic acids (sulfuric acid), volatile organic compounds (VOCs), and polynuclear aromatic hydrocarbons (PAHs) in varying levels. All of these chemicals would exhibit both short- and long-term effects in the body.

Of these three classes, asphyxiants cause the greatest number of fire deaths. (9) The asphyxiant carbon monoxide (CO) is the most abundant, although not the most toxic, gas found in smoke. Its abundance makes it a major threat in most fires. CO affects the transfer of oxygen from the lungs to the bloodstream. Normally, oxygen leaves the alveoli of the lung and enters the bloodstream, where it reversibly binds with the iron contained within the hemoglobin molecule of the red blood cell. Each hemoglobin molecule is capable of binding with four oxygen molecules. This complex, the hemoglobin-oxygen complex, is then transported in the red blood cell to the tissues of the body. As the red blood cell travels through the tissues of the body, oxygen “jumps” off the hemoglobin molecule and enters the tissue bed, where it can be used by the cells. In the tissue bed, carbon dioxide, liberated as a by-product of cellular metabolism, leaves the tissue and enters the bloodstream, where it also combines with the hemoglobin and is then transported to the lungs for elimination from the body.

CO also has the ability to bind with hemoglobin and form a complex known as carboxyhemoglobin (COHb), which is approximately 200 to 300 times as stable as the oxygen-hemoglobin complex and, therefore, is much harder for the body to eliminate. Since the CO is bound to the hemoglobin, those hemoglobin “binding sites” are taken up and are not available to bind with oxygen, starving the cells of oxygen and causing internal suffocation, or cellular hypoxia.

Fresh air or oxygen may help the patient to improve. In more severe cases, the CO must be forcefully driven off the hemoglobin through aggressive ventilatory measures, including hyperbaric oxygenation. As part of a Johns Hopkins University research program, autopsies were performed on 530 fire death victims in Maryland. Sixty percent were found to have more than one-half of the hemoglobin in their blood converted to COHb. Twenty percent of these victims had a lower COHb level but were found to have had a preexisting cardiovascular disease.15 Cardiovascular disease in and of itself makes an individual more susceptible to the harmful effects of CO.

An abnormal form of hemoglobin, methemoglobin, develops when the chemical state of the iron molecule in hemoglobin is altered. Methemoglobin levels can be higher in the presence of certain genetic disorders or when an individual is exposed to certain compounds or chemicals like nitric oxide or nitrogen dioxide. The presence of COHb and the increased production of methemoglobin make fewer binding sites available to transport oxygen. An individual in excellent physical condition may be able to withstand a 40 to 50 percent COHb saturation level without any serious consequence. A CO level that would not have any effect on the well-conditioned individual may kill elderly people with cardiovascular problems. Heavy smokers might have significant baseline blood levels of CO (between five and 10 percent).

Patients with CO poisoning complain of mild to very severe symptoms. Typically, a headache occurs initially with nausea, confusion, seizures, and coma, and, if left uncorrected, may lead to cardiac arrest. Increased CO levels may be responsible for unexplained actions or behavior of a victim during a fire. Long-term consequences of CO include personality disorders and memory loss. These symptoms become significant when the investigator interviews the fire victim, whose memory or perception of the events leading up to the injury is altered or absent. Although an individual with firsthand knowledge of a fire is considered a great witness, this individual may not be able to recall the events because of exposure to CO. Rarely, a patient with CO poisoning may present with a cherry-red appearance; however, this is typically a sign after death has occurred. Patients with excessive methemoglobin levels may have dark blood, commonly referred to as “chocolate blood” in the medical community.

The following are possible outcomes when testing for the CO level. First, the levels may be very high and represent the immediate cause of death. Second, it may be at a moderate level and may have been on the rise, but the victim’s death, either because of the fire or a lack of oxygen, actually stopped the CO level from rising. It may also be quite low but not attributable to the fire (as previously stated, heavy smokers can have a baseline CO level of five to 10 percent). The fourth outcome could be the absence of CO. There are occasions when a fire victim will die from the fire without any CO being present in the blood. This may occur when the victim is hit in the face with extremely hot fire, such as a blast from a flammable liquid explosion or the backfire of a furnace.

During a flash fire, the victim breathes superheated air. With one or two breaths, the trachea will spasm, causing asphyxiation. Inhalation of these gases may also cause swelling of the tongue or pharynx. If this occurs, there will be limited evidence of CO in the blood and little or no soot in the mouth or airway. In these types of cases, the autopsy will reveal that the trachea has a seared appearance.

Soot will often be found in the stomach, nose, throat, larynx, trachea, and bronchi. The absence of soot or thermal injuries in the airway (including nose, mouth, pharynx, larynx, and trachea) along with no CO in the blood is strong circumstantial evidence that the victim was dead before the fire began.

Treatment of CO poisoning involves measuring the COHb level and possibly the methemoglobin level. This is done by taking a sample of a patient’s arterial blood. Newer rapid devices that may eliminate the need to bring every potential patient to the hospital are becoming available. Prior to establishment of the CO level, all patients should be treated with 100-percent oxygen.

The asphyxiant, hydrogen cyanide (HCN), is produced by the burning of combustible materials that contain carbon and nitrogen, such as wood, papers, nylon, acrylonitirile polymers, urea-formaldehyde polymers, and polyurethanes- virtually everything found in the modern day home (from carpeting to furniture to other combustibles) is composed of these materials.

Like CO, HCN exposure leads to cellular hypoxia, but the mechanism is completely different. The body uses an energy molecule, adenosine triphosphate (ATP), produced through a complicated metabolic pathway in a part of the cell known as the mitochondria. This process depends on the presence of oxygen and is referred to as aerobic metabolism. HCN enters this pathway and blocks one of the steps in this process, making the cell unable to use the available oxygen. ATP is still produced without oxygen (anaerobic metabolism), but the alternative pathways are not nearly as efficient and produce much less ATP. The use of the alternate pathways also leads to the buildup of acids, like lactic acid, in the blood and cells. This condition is very harmful to organs that require a great deal of energy such as the brain and heart.

HCN is a very potent and lethal gas. Lee-Cjiong Jr., M.D.,16 reported that exposure to 140 ppm for 60 minutes or 1,500 ppm for three minutes exhibited a mortality rate of 50 percent. Fire victims exhibiting signs and symptoms of smoke inhalation who have a low concentration of CO in the blood, normal to high concentrations of arterial oxygen, and a low blood pH (a condition known as acidosis) should be critically evaluated for exposure to HCN.

HCN can remain present in water-soaked debris for long periods of time. (5) Fire investigators may be exposed to this asphyxiant anytime the fire debris is disturbed, so the fire investigator and any other personnel entering the scene must wear appropriate respiratory protection. (14) HCN is generally characterized as having an odor similar to burnt almond; in the midst of a fire scene, that odor may be undetectable.

Studies have suggested that HCN independently or in combination with CO may be lethal to those trapped inside a structure. It is now recommended that cyanide poisoning be suspected in any victim exposed to smoke in a closed environment.17 Recent studies also suggest that cyanide is off-gassed, or liberated, as carpeting is heated in the initial stages of a fire through the process of “quantitative decomposition.” This decomposition liberates cyanide, which can affect victims as they stay low and attempt to escape from the structure. It has been theorized that the narcotic effects of cyanide may be responsible for the bizarre behavior of some fire victims.18


Among other irritants present in smoke are acrolein, a potent sensory and pulmonary irritant created by the smoldering of cellulosic materials, and hydrogen chloride (HCl), produced when combustibles containing chlorine, like polyvinyl chlorides (PVC), are burned. HCl gas has not been found to be physically incapacitating to nonhuman primates; however, it did cause post-exposure death even at levels that did not incapacitate.

After the scene has been thoroughly examined and the findings of the fire investigative team documented, the office of the medical examiner will generally remove the decedent and perform an autopsy. A member of the fire investigation team should be present at all autopsies of fire victims to ensure that the burn patterns initially observed were accurately documented as well as to answer specific questions that may arise during the autopsy. Photographs should be taken during the autopsy; the photographs should be made part of the investigative record. The physical findings associated with the post-mortem exam will be available immediately, but the toxicological reports may take several weeks to months. At this point in the investigation, verify that the injuries observed during the autopsy are consistent with the findings at the scene. These findings will be in the written report when the medical examiner has concluded the investigation.

If the victim is injured, attempt to interview the victim as soon as possible. If the victim has suffered a serious burn or acute smoke inhalation, it is possible that the victim will be intubated (a process in which a breathing tube is placed into the lungs) and placed on a ventilator; painkillers or analgesics may also be used. Once these events occur, the victim may not be able to be interviewed for some time (weeks or months, in some instances).

• • •

Fire investigators must view the general principles of burn injuries and the physiologic effects of the various gases present in smoke within the context of the many potential life-threatening injuries associated with exposure to fire and assume that the investigation can come to involve a fatality.


1. “Fatal Fires,” U.S. Fire Administration, 5:II, March 2005.

2. Karter, Michael J., “United States Fire Loss for 2003,” NFPA Journal, 2004.

3. “Arson in the United States,” U.S. Fire Administration, 2001.

4. “Fire Safety and Burns: Injury Statistics and Incidence Rates,” Children’s Hospital Boston, http://www.childrenshospital.org/az/Suite903/mainpageS903PO.html, May 4, 2006.

5. Quintiere, James G. Principles of Fire Behavior. (Albany, NY: Delmar, 1997), 60-61.

6. Demling, M.D., H. Robert and Leslie Desanti, R.N., “Burn Injury: Initial Assessment and Management,” Burnsurgery.Org, 2006, Brigham and Women’s Hospital Burn Center, Boston, MA, Aug. 15, 2006, http://www.burnsurgery.com/Modules/initial_mgmt/sec_5.htm.

7. “Scalds: a Burning Issue,” American Burn Association, 2000, Aug. 8, 2006, www.ameriburn.org/Preven/2000Prevention/Scald2000PreventionKit.pdf/.

8. “Cremation FAQ,” Cremation Association of North America, 2004. National Funeral Directors Association, May 3, 2006, http://www.nfda.org/page.phy?plD=160/.

9. Dehaan, John D., Ph.D., Kirk’s Fire Investigation, 4th ed. Upper Saddle River: Brady-Prentice Hall, 1997).

10. “Definition of Compartment Syndrome,” MedicineNet.Com, Aug. 15, 2006, http://www.medterms.com/script/main/art.asp?articlekey=11930/.

11. Ryan, Colleen M., M.D.; David A. Schoenfeld, Ph.D.; William P. Thorpe, Ph.D.; et al, “Objective Estimates of the Probability of Death from Burn Injuries: The New England Journal of Medicine, 6th ser. 338 (1998), 362-366.

12. Hall, J.R. Burns. Toxic Gases and Other Hazards Associated with Fires: Deaths and Injuries in Fire and Non-Fire Situations, National Fire Protection Association, Fire Analysis and Research Division, 2001.

13. “Fires in Mass Transit Vehicles: Guide for the Evaluation of Toxic Hazards,” Commission on Engineering and Technical Systems, National Research Council, National Academies Press, 1991.

14. Kinnes, Gregory M. and Gregg A. Hine, Health Hazard Evaluation Report 96-0171-2692, Bureau of Alcohol, Tobacco and Firearms, Cincinnati, NIOSH Publications Office, 1996.

15. “Fire and Smoke: Understanding the Hazards,” Committee on Fire Toxicology, Board on Environmental Studies and Toxicology, National Research Council, National Academies Press, 1986.

16. Lee-Chiong, Jr., M.D., Teofilo L.. “Smoke Inhalation Injury: When to Suspect and How to Treat, Postgraduate Medicine, 1999.”

17. “Identify Cyanide Poisoning in Victims,” Cyanide Poisoning Treatment Coalition, Aug. 16, 2006, http://www.cyanidepoisoning.org/wt/page/identify_poison/.

18. Gagliano, Mike, Casey Phillipps, Phil Jose, and Steve Bernocco, “The Breath from Hell,” Fire Engineering, March 2006, 73-84.

JOHN NICHOLS, MCJ, MICP, is a detective with the Essex County (NJ) Prosecutor’s Office Arson Task Force. He has been in law enforcement for 10 years and a New Jersey-certified paramedic for 19 years. He is an adjunct professor in the paramedic program at Union County College and an instructor for the basic course for arson investigators for the New Jersey Attorney General’s Office. Nichols is a member of the IAAI and has a B.S. from Fairleigh Dickinson University and a master of criminal justice from Boston University.

ROBERT IRWIN, CFI, has been a special agent with the Bureau of Alcohol, Tobacco, Firearms and Explosives (ATF) for more than 14 years and is a supervisory special agent/certified fire investigator. He was a member of the ATF National Response Team and has been involved in fire/arson investigation for more than 12 years. He has taught fire/arson investigation to federal, state, and local fire and law enforcement personnel.

MARK MERLIN, D.O., is a physician/paramedic with 24 years of experience in emergency medical services. He is the EMS medical director at Robert Wood Johnson Hospital, assistant professor of emergency medicine at Robert Wood Johnson Medical School, medical director of the NJ EMS/Disaster Medicine Fellowship, and director of the NJ “MD-1” Physician Response Program. He is the chair of the NJ MICU advisory board for the NJ Department of Health and Senior Services.

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