By LARRY FELKER, Belimo Americas, Reno NV
Smoke kills—that is well-known. Far less understood is the reason why. We know we cannot inhale smoke because of its noxious effects. We know it smells bad, but that is about it.
In addition to being chemically toxic, hot smoke can be damaging to the skin, eyes, and lungs and lead to disablement. Further, it can obscure vision, hindering escape. Explosion or flashover can occur if the concentration of smoke particles is sufficient and the particles have been heated to their ignition temperature.
Composition of Smoke
When a building and its contents start to combust—smolder or flame—smoke is generated. Typically, this smoke is composed of a large number of various molecules and particles that form an aerosol. All common fuel sources from building structure to furnishings contain carbon and hydrogen, while most modern materials (plastics and polymers) also contain sulfur and nitrogen. Recycled materials can contain other potentially harmful compounds. The nitrogen and sulfur compounds produced in a fire are highly toxic. Among the products of combustion are hydrogen sulfide, sulfur dioxide, hydrogen chloride, ammonia, and various organic products. Black soot forms from incompletely burned carbon. More than a hundred known toxins are generated.1,2
CO and HCN
In a typical non-hazardous-occupancy fire, carbon monoxide (CO) and hydrogen cyanide (HCN) are the two most dangerous compounds.3,4,5
The mechanisms of action of CO and HCN are different. CO attaches very tightly to the hemoglobin in blood and prevents oxygen from being delivered and carbon dioxide (CO2) from being removed. The result is asphyxiation. HCN acts on the mitochondria of cells, particularly in the nervous system.6 Its mechanism of action is more complex, but essentially stops the production of adenosine triphosphate (ATP), the biochemical that drives functioning of almost all of the processes in a cell. With the recycling of ATP 10 times a second, HCN is more destructive than CO because it acts almost immediately and shuts down cell functions.
At high temperatures, CO2 commonly is produced. At low temperatures, incomplete combustion occurs, and CO is produced instead. HCN is produced at higher rates at lower temperatures.
During the early stages of combustion, as fire spreads, CO and HCN production begins. Oxidation of HCN leads to formation of other toxic compounds and more CO. Where present, sprinklers limit 88 percent of fires until firefighters arrive.7 When water cools a fire, formation of HCN is promoted. In a like manner, restricting oxygen promotes formation of CO instead of CO2. The best practice is to completely extinguish a fire and douse the embers,8 but this takes time.
Long-Term Effects of Smoke Inhalation
Less well-known than the immediate dangers of smoke are the effects of long-term exposure. CO attaches to other molecules, particularly myoglobin and mitochondrial cytochrome oxidase. This leads to significant damage to the heart and nervous system. Cyanide kills brain cells by reducing their energy-production capability.9,10 The heart attacks of many firefighters are suspected to be caused by cyanide poisoning.11 The higher the concentration of cyanide, the quicker the death.
Among the mid- to long-term symptoms of smoke inhalation are hoarseness (vocal-cord damage), coughing, breathlessness, worsening of asthma symptoms, and impairment of pulmonary function.12,13,14,15 The most exhaustive reference on the subject is a study on health impacts on 9/11 responders.16 Smoke can cause or contribute to the formation of cancer, autoimmune diseases, sleep apnea, and sarcoidosis.
Summary
Smoke from building and furnishing fires contains more than 100 toxins, with CO and HCN the most dangerous in general. While the immediate effects of smoke inhalation can be death or permanent damage, the long-term effects also are serious. Efforts to control smoke protect the long-term health of occupants and firefighters alike.
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Based in Nevada, the author is a specialist in fire and smoke dampers and actuators, and manager of fire and smoke products for Belimo Americas. Felker is also vice chair of the Air Movement and Control Association International’s Fire and Smoke Damper Task Force. He is a member of the International Code Council, the National Fire Protection Association, and the Society of Fire Protection Engineers, as well as a life member in ASHRAE. He co-authored the book “Dampers and Airflow Control,” published by ASHRAE Special Publications in 2010.
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References
1) Alarie, Y. (2002). Toxicity of fire smoke. Critical Reviews in Toxicology, 32, 259-289.
2) Gann, R.G. (2001, March 14). Toxic hazard of building products and furnishings. Retrieved from National Institute of Standards and Technology Website: http://bit.ly/Gann_Paper
3) Stamyr, K., Thelander, G., Ernstgård, L., Ahlner, J., & Johanson, G. (2012). Swedish forensic data 1992-2009 suggest hydrogen cyanide as an important cause of death in fire victims. Inhalation Toxicology, 24, 194-199.
4) Hall, A.H., & Schnepp, R. (2011, December). Cyanide: Fire smoke’s other “toxic twin.” Fire Engineering. Retrieved from the Fire Engineering Website: http://bit.ly/Cyanide_1211
5)Formation of hydrogen cyanide in fires. (n.d.). Retrieved from the RISE Research Institutes of Sweden Website: http://bit.ly/Hydrogen_Cyanide
6) NIOSH. (n.d.). Hydrogen cyanide (AC): Systemic agent. Retrieved from the Centers for Disease Control and Prevention Website: http://bit.ly/Hydrogen-Cyanide
7) NFPA. (2017, July). Sprinklers in reported U.S. fires during 2010 to 2014. Retrieved from the National Fire Protection Association Website: http://bit.ly/Sprinklers_2010-2014
8) National Center for Biotechnology Information. (2004). Hydrogen cyanide. Retrieved from National Center for Biotechnology Information Website: http://bit.ly/HydrogenCyanide
9) Pettersen, J.C., & Cohen, S.D. (1993). The effects of cyanide on brain mitochondrial cytochrome oxidase and respiratory activities. Journal of Applied Toxicology, 13, 9-14.
10) Nůsková, H., Vrbacký, M., Drahota, Z., & Houštěk, J. (2010). Cyanide inhibition and pyruvate-induced recovery of cytochrome c oxidase. Journal of Bioenergetics and Biomembranes, 42, 395-403.
11) Burke, R. (2006, December 31). Hydrogen cyanide: The real killer among fire gases. Firehouse. Retrieved from the Firehouse Website: http://bit.ly/Burke_1206
12) Tobe, E. (2012, August 9). Progressive neuropsychiatric and brain abnormalities after smoke inhalation. BMJ Case Reports.
13) Fogarty, P.W., George, P.J., Solomon, M., Spiro, S.G., & Armstrong, R.F. (1991). Long term effects of smoke inhalation in survivors of the King’s Cross underground station fire. Thorax, 46, 914-918.
14) Cha, S.I., et al. (2007). Isolated smoke inhalation injuries: Acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns, 33, 200-208.
15) Gupta, K., Mehrotra, M., Kumar, P., Gogia, A.R., Prasad, A., & Fisher, J.A. (2018). Smoke inhalation injury: Etiopathogenesis, diagnosis, and management. Indian Journal of Critical Care Medicine, 22, 180-188.
16) Webber, M.P., et al. (n.d.). Health impacts on FDNY rescue/recovery workers 15 years: 2001 to 2016. Retrieved from City of New York Website: http://bit.ly/FDNY_Workers