Firefighting and Parkinson's Disease

Carbon Monoxide Exposure

Carbon monoxide is the most common cause of poisoning in industrialized countries, including the United States. Fire department (FD) personnel are often the first to encounter victims of carbon monoxide poisoning. In addition, because of the nature of the profession, firefighters are at increased risk of occupational exposure to carbon monoxide.

In this presentation we will review the chemistry, incidence, pathophysiology, detection, long-term effects, and treatment of carbon monoxide poisoning. There will be an emphasis on new technologies that now allow the diagnosis and monitoring of patients exposed to carbon monoxide in the prehospital setting. In addition, we will investigate the incidence and significance of combination poisonings with cyanide and carbon monoxide.

Exogenous Sources

Certainly, most CO exposure is related to exogenous causes. Among these are house fires, automobile exhaust fumes, fumes from propane-powered vehicles (e.g., forklifts), heaters, indoor stoves, camp stoves, boat exhaust fumes, gas-powered electrical generators, cigarette smoke, and smoke from charcoal-fired cook stoves and ovens. Essentially, any combustible item should be considered a possible source of CO. Methylene chloride is an organic hydrocarbon consisting of two hydrogen atoms and two chloride atoms bound to a carbon atom. It is often used as an industrial solvent, particularly as a paint remover and adhesive remover. Methylene chloride is converted to CO in the liver after inhalation. Persons exposed to high levels of methylene chloride can develop carboxyhemoglobinemia and the signs and symptoms of CO toxicity.

Typically, following CO exposure, there will be a phase of decreased oxygen levels in the blood (hypoxemia). This is usually followed by a period of re-oxygenation when the victim is removed from the toxic environment and oxygen administered. It also occurs when carboxyhemoglobin is broken down and replaced with normal hemoglobin. The effects of CO-mediated hypoxemia are dependent upon any underlying disease that might be present (such as emphysema or heart disease). These periods of hypoxemia often result in the formation of dangerous chemicals called free radicals. Free radicals are highly reactive chemical compounds and can cause significant damage to the cells of the body. An increase in free radical compounds results in what is known as oxidative stress. Oxidative stress can injure cells, tissues, or organs and is associated with the development of many diseases including atherosclerosis, Parkinson’s disease, Alzheimer’s disease, and several other chronic disease processes. Thus, oxidative stress can cause injury to oxygensensitive tissues, such as the brain and the heart, beyond those caused by the initial hypoxemic insult.

A phenomenon called delayed neurologic syndrome (DNS) has been identified as a complicationof acute and chronic CO poisoning. In DNS, recovery from the initial CO poisoning is seemingly apparent only to have the victim develop behavioral and neurological deterioration anywhere from 2–40 days later. The true prevalence of DNS is uncertain with estimates ranging from 1–47% after CO poisoning. It is clear that patients who have more CO poisoning-related symptoms initially appear more apt to develop DNS. In addition, DNS is more common when there is a loss of consciousness in the acute poisoning. DNS has also been reported in children. Scientific studies are mixed as to whether hyperbaric oxygen therapy prevents DNS. Other neurologic complications, such as Parkinsonism, have been reported with DNS.

Information Provide by the International Association of Firefighters