How carbon monoxide kills firefighters
Understanding how carbon monoxide attacks the body is the first step in protecting against it
By Bruce Evans
While looking for an SOP on a large metropolitan fire department's website, I stumbled across something unrelated that caught my eye. This SOP was from a fire department I highly respect as leaders in safety and employee health.
To my surprise I noticed an SOP allowing for firefighters to remove their SCBA if the carbon monoxide level is less than 50 ppm in the sampling. It is commendable that a fire agency is addressing the exposure of CO and following OSHA's permissible exposure limit of 50 parts per million over an 8-hour time frame.
Operational SOPs really need to look at the science and at the long-term and chronic exposure issues involving CO.
There has been excellent work done to identify the risk associated with CO from a knock down or acute illness standpoint. Yet some of the finer details are often missed in the attempt to get the message across.
This is due to a lack of surveillance on exposures and patient outcomes by federal agencies. It's especially true when it comes to firefighters, as only a handful of NIOSH and NIST investigators really understand the fire service's challenges with exposures to chemicals and suppression activities.
Many of these findings don't make it into rehab policies. Therefore, the two insidious effects of exposure to carbon monoxide often go unrecognized in the fire service.
The first of these relates to molecular change. Somewhere in EMT training you learned that CO has an affinity for hemoglobin 150 to 200 times higher than oxygen depending on the source.
What escapes a lot of educational programs on this is that when CO binds to hemoglobin, it also changes the geometry of the hemoglobin molecule.
The normal geometry of the hemoglobin molecule carrying oxygen and carbon dioxide is designed to travel swiftly and unobstructed through our blood vessels and capillary beds, even passing around the changes in arteries and veins as they become embedded with plaque.
The geometrical change in hemoglobin caused by carbon monoxide makes it harder to pass swiftly through the blood vessels and lends itself to clumping together, resulting often in a clot or obstruction. And the geometry change tends to make it sticky.
Couple this with someone with underlying heart disease and the other fire gases that can stop cellular activity and trigger low blood pressure, and you have a line of duty death categorized as cardiac when in fact it maybe toxicology related.
There is suspicion the extended time CO stays in the blood stream maybe be a causal factor in day-later deaths.
A radical CO
A second carbon monoxide lurking on the fire scene is known as CO in the radical form. If you have taken a fire chemistry course, one of the principle concepts is the formation of compounds or elements that are called free radicals.
Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can form when oxygen interacts with certain molecules. Fire often provides the environment that uses oxygen to create these free radicals.
Once formed, these highly reactive radicals can start a chain reaction damaging cells, tissue and organs. Free radicals like carbon monoxide like to attack tissue and cells.
A favorite target for the radical CO is the myelin sheath of a nerve cell.
A myelin sheath is like the insulation on a wire; it ensures the electricity or nerve impulse gets to site of where it is used. When a wire's insulation has a hole in it, the electrical signal is interrupted or delayed, often going somewhere it should not.
A University of Pennsylvania School of Medicine and a National Academies of Science Forum identified long-term effects of CO that parallels the disease process in multiple sclerosis.
They identified an autoimmune response triggered by CO that unleashes lymphocytes that attack the main protein that makes up the myelin sheath. A lot of other neuromuscular diseases are attributed to pitting or breaks in the myelin sheath including Parkinson, muscular dystrophies and a host of others.
In considering the entirety of a CO exposure, we need to rethink what is an acceptable exposure and, more likely, sample the environment and the firefighter. CO levels should be less than five in a non-smoker and less than 10 in a smoker. Anything else should be considered abnormal.
Updates to the NFPA 1584 Standard on Rehabilitation Process for Members During Emergency Operations and Training Exercises calls for SpO2 assessment and for the SpO2 monitors to be able to differentiate between carboxyhemoglobin and oxyhemoglobin along with firefighters being assessed for carbon monoxide poisoning.
Since we know this is a common toxic substance, whether you're compliant or not with NFPA, conduct screening while the firefighters are in the rehab area.
Recording exposures could provide support for firefighters who later become stricken with what appears to be a growing number of issues associated with the long-term CO exposure. This recording may even prevent those illnesses.
There is so much more to CO. Two good resources are the CO Headquarters and the book "Carbon Monoxide Toxicity" by Dr. David Penney.
About the author
Chief Evans is the fire chief and a paramedic at the Upper Pine River Fire Protection District in Bayfield, Colo. He is on the board of directors at the National Association of EMT's, a National Fire Academy instructor and sits on the National Academy of Science's Institute of Medicine's Preparedness Committee. He has a master's degree in public administration and bachelor's degree in science from the University of Nevada, Las Vegas. You can reach him at Bruce.Evans@FireRescue1.com.