More than 15,000 people are treated annually in hospital emergency rooms for carbon monoxide gassing, and approximately 500 people a year die from the poisoning. Carbon monoxide is the leading cause of accidental poisoning deaths in the United States. Its danger is heightened by the fact that it is a colorless and odorless gas and, therefore, may not be detected by its victims. More than half of the carbon monoxide deaths involve faulty heating systems and 71% of the deaths are caused by consumer products occurred in the home.
Robert Schuster has been at the leading edge of carbon monoxide case prosecution. He has represented victims of carbon monoxide gassing from North Carolina, Wyoming, Virginia, Tennessee, Texas, New Mexico, California, Arizona, Kansas, Mississippi, Illinois, and Georgia.
WILLIAMS V. VAIL RESORTS
Two hotel guests were gassed by carbon monoxide at the Snake River Lodge & Spa in Teton Village, Wyoming, a hotel that Vail Resorts owned and managed through its subsidiary corporations. The guests — Dr. and Mrs. Randall Williams — were attending a medical conference at the resort. Dr. Williams, a urologist from Columbus, North Carolina, was killed and his wife, a cardiac surgery nurse, suffered permanent brain injury from the poisoning. The hot water for the hotel was supplied by a propane-fired boiler, which was equipped with a safety shutdown switch to prevent dangerous levels of carbon monoxide from being produced. The hotel had located a dryer vent too close to the air intake for the boiler. Lint from the dryer vents was sucked into the boiler’s air intake, clogged the burner screen, and thereby starved the boiler of needed oxygen. With insufficient oxygen, combustion of the propane was incomplete, and carbon monoxide was produced as a byproduct of the incomplete burning. Under those circumstances, the safety shutdown switch would activate and turn off the boiler so that carbon monoxide would not be produced.
When the safety switch was triggered, it caused the boiler to shut down, which then resulted in complaints from guests that their showers were cold. The hotel’s response was to place a jumper, or electrical bypass, across the safety switch (thereby disabling it) so that the boiler would not turn off. Hot showers were preserved, but guest safety was dangerously sacrificed. A perfectly safe hot water boiler had been converted into a deadly carbon monoxide generator. When Dr. and Mrs. Williams checked into the hotel, they were assigned to a room directly above the exhaust for the boiler, which had a safety shutdown switch that had been jumpered for more than four months. The carbon monoxide, a colorless, odorless gas, was sucked into their room through the air conditioning ducts, and they were asphyxiated.
Bob Schuster—together with the Murdock Law Firm, P.C.—represented Mrs. Williams for her personal injury case and the family of Dr. Williams for the wrongful death case. Both cases were consolidated for trial in the United States District Court for the District of Wyoming, and the jury returned a verdict of $17.5 million—the largest personal injury verdict in Wyoming’s history.
CARBON MONOXIDE FACTS
Carbon monoxide is a potentially lethal — yet colorless and odorless — gas that can cause devastating and permanent injuries due to the multiple mechanisms by which it damages brain, cardiac, and other vital structures. For decades, it has been known that carbon monoxide causes hypoxic (lack of oxygen) damage to brain structures as a consequence of elevated carboxyhemoglobin levels in the blood stream. But medical research undertaken in the past fifteen (15) years has demonstrated the even greater pervasiveness of carbon monoxide’s damage potential.
While hypoxic injury is clearly an element of the systemic damage, scientists have found that carbon monoxide is a neurotoxin and—due to a cascade of complex biochemical events—it creates a marked increase in oxidative injury that can directly damage perivascular (the area surrounding a blood vessel or lymphatic vessel) and neuronal (relating to a nerve cell or neuron) structures. Those same biochemical cascades can also result in injury to the cardiovascular and pulmonary systems.
Victims of carbon monoxide poisoning, then, are at risk for a range of injuries, including to the brain, the central nervous system, the cardiovascular system, and the pulmonary system. The manifestations of those injuries can be devastating, including cognitive damage, impairment of executive functioning, memory loss, damage to learning processes, headaches, reduced capacity to multi-task or to contend with multiple environmental inputs, impaired emotional control, irritability and frustration and confusion, tinnitus (ear ringing) and hearing loss, vision disturbances, anxiety and depression, fatigue, reduced stamina and pulmonary functioning, motor weakness, peripheral neuropathies including tics and movement disorders, cardiac damage with possible increased risk of cardiac-related death, and accelerated development of dementia, premature cognitive decline, and Parkinson’s-like syndromes.
1. Damage Mechanism: Hypoxia
Carbon monoxide’s destructive potential arises—in part—because it prevents oxygen from being delivered to brain cells and other vital organs of the body. If the cells do not have a rich supply of oxygen, delivered by the hemoglobin that is a constituent part of our red blood cells, the cells will die. Carbon monoxide molecules are 200 times more likely to bind to hemoglobin than are oxygen molecules.
Thus, when carbon monoxide is inhaled, it enters the bloodstream, binds to hemoglobin, and crowds out the oxygen molecules, thus depriving the cells of the oxygen needed to maintain their vitality. Moreover, the iron atoms which are embedded in the hemoglobin molecule (and which normally bind oxygen to the hemoglobin) will hold onto any residual oxygen more tightly if carbon monoxide is present—resulting in even less oxygen being delivered to the cells and tissue. The cells die, and, for the brain, the cells cannot regenerate.
The brain is extraordinarily dependent upon a constant supply of oxygen and is, accordingly, extraordinarily vulnerable to permanent damage when deprived of oxygen. Areas of the brain that can be damaged by carbon monoxide poisoning include the deep white matter structures (particularly in the periventricular white matter regions) and deep gray matter structures such as the basal ganglia (particularly the globus pallidus and putamen, which are located within the basal ganglia). These structures are found at the “end” of the vascular “watershed” — the intricate elaboration of arterial vessels through which hemoglobin transports oxygen to the cells — and are especially susceptible to damage from a lack of oxygen. The hippocampus — another “watershed” structure of the brain — can atrophy as a result of carbon monoxide exposure, and this damage may not develop for weeks or longer following the exposure.
Those areas of the brain — the white matter, the basal ganglia (including the globus pallidus and the putamen), and the hippocampus — are critical structures for the regulation of learning, memory, cognitive functioning, emotional functioning, and movement.
2. Damage Mechanism: Cardiac Injury
The hypoxic insult resulting from the increase of carboxyhemoglobin levels in the bloodstream can damage structures in addition to the brain, including the heart. It also is composed of cells that require oxygen for survival—and that will die when deprived. But cardiac injury can then magnify the hypoxic injury to the brain in that reduced cardiac efficiency will reduce perfusion of the blood to the brain, thereby exacerbating the hypoxic impact of the increased carboxyhemoglobin levels. Less oxygen is delivered by the hemoglobin molecule—but less blood is also being delivered.
3. Damage Mechanism: Oxidative Destruction
The injury potential of carbon monoxide also arises from oxidative damage, and associated complex biochemical processes that can directly injure perivascular, neuronal, cardiovascular, and other structures and organs. Understanding this mechanism of injury begins with a discussion of the concept of oxidative destruction.
Oxidative damage is a destructive process. It occurs at the atomic or molecular level and involves an imbalance in the electrical charge of the atom or molecule. An oxidant, for instance, can have an unbalanced charge, such as an extra electron which would impel it to seek a balancing proton. Atoms can be oxidized if they lose their balanced charge equilibrium—or a molecule can be biologically oxidized, for instance, by the removal of hydrogen atoms which would alter the charge balance of the molecule. When the atom or molecule has an unbalanced charge, it actively seeks out molecules from which it can gain a balancing charge—for instance, another proton—and in doing so, will alter that molecule…or oxidize it. The cascading alterations also release oxidative by-products. The destructive potential of an oxidant such as an oxygen radical is enhanced within the human body because the radical—due to its unbalanced charge—can readily move through membranes and tissue.
Related: Brain Injury Legal Case News
Examples are instructive. Iron can be oxidized and the consequence is rust. Fire is the oxidization of fuel—and the result is flames and by-products of combustion (which, in the case of petroleum-based fuels, can be carbon monoxide if the burning or combustion is incomplete). Oxidizing agents include caustics, such as Drano used to eat away clogs in pipes, or hydrogen peroxide. Rust or fire can usually be monitored or controlled. But when brain cells or tissue—or cardiac structures—are oxidized, the consequence (both in regard to the alteration of the molecular structure as well as the by-products that are generated) can be very serious and damaging.
Aerobic cells in our body—by definition—are those cells that require oxygen in order to produce energy, to function, and to live. It is a necessary fuel for the cell’s energy-generating “engine”—the mitochondria, a cell component found in the cytoplasm. As oxygen is used or metabolized in the mitochondria—and as energy is produced—a certain type of molecule is naturally produced that is known as “reactive oxygen species.” The presence of carbon monoxide in the bloodstream—carried by the hemoglobin—triggers the extra, and dangerous, production of the reactive oxygen species (ROS) molecules, both directly as the carbon monoxide is carried through the body and the brain as well as by triggering their production in other cells and structures (primarily platelets and neutrophils) that are fellow-travelers in the bloodstream. The resulting proliferation of new ROS molecules overwhelms the body’s natural defense mechanisms to neutralize their destructive potential. They commence a destructive assault that kills cells, that damages the intricate vasculature upon which the brain is dependent, and that attacks the protective sheathing around nerve fibers in the brain, disrupting the ability of the nerves to transmit their signals and thereby causing brain damage and neurological compromise.
There are different kinds of reactive oxygen species (ROS) molecules, and they include free radicals, reactive nitric oxide-associated species, superoxide, peroxynitrite, and hydrogen peroxide—all of which can be damaging to cell membranes, essential proteins, and DNA. The key is to keep ROS molecules in check. The cells accomplish that task through “repair” enzymes—known as antioxidants—that inactivate the ROS molecules as they are generated. It is a balancing act—trying to assure that, as the ROS molecules get produced, they are removed or their damage repaired at the same rate by the antioxidants. If the balance is not maintained and the ROS molecules predominate, the “steady state” of cell health is lost, oxidative destruction or “stress” results, and cell damage ensues.
Carbon monoxide molecules enter the blood stream, having been breathed into the victim’s lungs and then attached to hemoglobin as the blood bathes the alveoli sacs of the lungs in its quest for oxygen. Once in the bloodstream, it becomes a toxin that can interact with other constituents in the blood. Of particular relevance to its role in causing oxidative destruction are the processes that are triggered that transform and damage platelets and neutrophils. Platelets are disc shaped, colorless structures that are abundant in the bloodstream, being of primary importance to clotting. Although lacking a nucleus, platelets have a structure and constituent materials within their walls. Neutrophils (sometimes referred to as leukocytes) are mature white blood cells and are the most plentiful of all of the white blood cell population. Like the proverbial Hatfields and McCoys, platelets and neutrophils exist in close proximity but they keep their distance—and if they happen to get together, bad things can happen.
Initial Platelet-Neutrophil Reaction
Carbon monoxide—an unnatural stranger in the bloodstream—triggers the platelets to discharge nitric oxide (an oxidant) into the bloodstream. Superoxide is released from neutrophils—in part as a reaction to nitric oxide oxidants and in part as a direct reaction to the presence of carbon monoxide in the blood stream. The two compounds (nitric oxide and superoxide) interact, producing reactive nitric oxide-associated species molecules (ROS molecules), including peroxynitrite, in their biochemical clash. Peroxynitrite is the most oxidizing substance to be found in mammalian systems.
An unfortunate characteristic of this species of molecule (reactive nitric oxides, including peroxynitrites which in turn can produce nitrotyrosine) is that it causes platelets and neutrophils to adhere or aggregate (a process called heterotypic aggregation) rather than keeping their safe Hatfield-McCoy distance. Nitrotyrosine is a culprit in this “stickiness” or adherence. It gets produced from the series of interactions kicked off by carbon monoxide—initiating the discharge of nitric oxide from platelets, the triggering of superoxide release into the bloodstream from the neutrophils, then a reaction between nitric oxide and superoxide to generate peroxynitrite, and finally the emergence of nitrotyrosine.
Once the platelets and neutrophils are physically linked, two things happen:
- Cascade of ROS Molecules. The neutrophils experience an oxidative burst. While a neutrophil will safely package or contain oxygen radicals (oxidants) until they are needed to attack an organism (such as a bacteria when we are sick), the oxidative burst releases them prematurely and they attack healthy cells pathologically. Thus, additional reactive nitric oxide-associated species molecules are formed. So the production of even larger numbers of ROS molecules (which includes the reactive nitric oxide species) within the bloodstream is enhanced—a cascading effect.
- Vascular Damage and Destruction of Lipids and Myelin Sheath. The physical association of platelets and neutrophils precipitates neutrophil degranulation—releasing myeloperoxidase (MPO), an enzyme that resides in the granules. Granules are typically located within the cell’s cytoplasm and those tiny structures will safely confine products, including myeloperoxidase, that would be toxic if allowed to escape. With “degranulation,” the granules move to the neutrophil’s cell surface, a portal opens to release the products within the granules, and the cell membrane then closes—but only after the MPO has escaped the confines of the granules and cell structure. Once poured into the bloodstream, three destructive biochemical processes are initiated by the myeloperoxidase (MPO):
- Accelerated MPO Release. Some of the released MPO adheres to the outer surface of the neutrophils, triggering additional neutrophil activation, additional degranualtion, and additional release of more MPO from the neutrophil’s cell membrane. It is an “outside-in” neutrophil activation.
- Lipid Destruction and Vascular Damage. The MPO molecules deposit along the vascular lining of the blood vessels (the endothelium)—the interior lumen surface—and interact with nitrotyrosine, the culprit in causing the platelets and neutrophils to stick together. In a series of biochemical reactions, the interaction results in the destruction of the constituents in cells used for fuel, the lipids, and thus the destruction of the cells themselves within the endothelium of the blood vessels, most particularly the blood vessels of the brain but also in the lungs and the cardiovascular system. It is a process known as lipid peroxidation—where the perivascular cells are damaged by oxidative destruction. The damage to lipids is not limited to their fuel function, however. A lipid is a fatty structure and—in addition to be used as a source for cellular energy—is an important constituent for membranes and cell structure and can be used as a fuel, a barrier, and an insulator. The myelin sheath surrounding axons, for instance, is composed of lipids. Thus, the oxidative destruction of lipids has consequences beyond the destruction of a cell’s fuel source.
- The MPO-nitrotyrosine interaction also activates the endothelial cells—and their adherent or attraction characteristics—which causes the neutrophils themselves to adhere to the perivascular lining. When the neutrophils adhere, they are more likely to release damaging substances such as myeloperoxidase, cytokines, thromboxanes, and oxygen radicals.
- The damage to the endothelium—whether from lipid peroxidation or from the adherence of neutrophils—kicks off yet another destructive cycle. Platelets are designed to respond to damage because of their clotting properties. Platelets, then, will adhere to the damaged endothelium and activate, releasing nitric oxide, and triggering (through the processes described earlier with the initial platelet-neutrophil interaction) the production of peroxynitrite, the most oxidizing substance found in mammalian systems. The platelet adherence—in activating the clotting process—can also cause fibrin to be deposited, which can disrupt local blood and nutrient flow.
- Destruction of Myelin Sheath. The release of MPO has resulted, then, in the destruction of lipids and the cells they are to fuel through lipid peroxidation—as well as lipids that are the constituents of membranes. But that process also has a second—and entirely separate—level of damage because byproducts are generated in the degradation of the lipids that have their own dangerous properties: lipid peroxides. They attack the myelin sheath, the protective and insulating sheath that surrounds the axon of nerve cells. That sheath’s primary structure is composed of myelin basic protein (MBP). Through peroxidation, the byproducts attack the MBP (and, thus, the integrity of the protective sheathing for the nerves), damaging it in two ways—damaging its three dimensional structure and altering its charge pattern. An inflammatory process—also called an immunological response—is initiated: the alteration gets “perceived” by inflammatory cells as a foreign body and there is an influx of the inflammatory cells to attack the MBP. This damage is critical because the axons are the “wires” or pathways over which the nucleus of a nerve “fires” its signal. Destruction of the myelin sheath around the axon—and there are billions of them in the brain alone—disrupts the transmission capacity of nerve cells and can cause profound neurological damage. The inflammatory process also causes the release of yet more by-products that damage adjacent tissue.
- The biochemical interactions resulting from carbon monoxide poisoning, then, can be profound. Separate and apart from the hypoxic damage, carbon monoxide is a neurotoxin, triggering biochemical processes that will kill cells, that accelerates apotosis (programmed cell death), and that damages significant neuronal structures, including the protective sheathing around axons. It is believed that the presence of carbon monoxide can also cause iron release in molecules. Iron is highly reactive and can trigger its own inflammatory processes. The different biochemical processes, moreover, do not reach a quick conclusion. They occur over a period of time, thereby accounting for damage that can be developing over a period of weeks or more after the exposure.