Neurological Degenerative Disease related to Occupational Exposures for Firefighters.

BACKGROUND FACTS & HISTORY

Fire Fighters face a wide variety of hazards while carrying out the occupational requirement of saving lives and reducing property damage.Fire Fighters are regularly exposed to burning chemicals and other toxins. There are 70,000 toxic substances on file with the Environmental Protection Agency (EPA) in the United States. In reality, when these substances burn together, there are 70 million possible combinations that are created in a fire. Fire Fighters routinely endure exposure to these burning toxins in the course of protecting the lives and property of their fellow citizens.

It is fact that even with the best respiratory practices and protective equipment the exposures will continue to occur due to absorption through the skin once a fire fighter has become soaked during fire suppression activities. Furthermore, the concentration of chemicals in today’s materials is much higher than in the past due to the increased use of composite materials.Many studies have revealed an increased rate of disease in the Fire Fighter population versus the general population. A 1990 study of Houston fire fighters indicated that Parkinsonism was significantly more common in fire fighters than in the general population. This was demonstrated by a finding of 3-4 cases per 1,000 in the general population compared to 30 Parkinson's cases per 1,000 firefighters.

Identify potential occupational risk factors, this study examined the occupational occurrence of various neurodegenerative diseases.

METHODS: Death certificates from 27 states in the National Occupational Mortality Surveillance System were evaluated for 1982 to 1991. Proportionate mortality ratios were calculated by occupation for presenile dementia, Alzheimer's disease, Parkinson's disease, and motor neuron disease.

RESULTS: Excess mortality was observed for all four categories in the following occupational categories: Early death from motor neuron disease was found for firefighters and military Personnel.

CONCLUSIONS: Neurodegenerative disease occurs more frequently in some occupations than in others, and this distribution, which may indicate occupational risk factors, should be further investigated.

Minerbo GM, Jankovic J. Prevalence of Parkinson's disease among firefighters. Presented at the 42nd Annual Meeting of the AAN, Miami, 5/4/90, Neurology (Suppl. 1) 1990;40:348.

Firefighting Exposures 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

New National Standard for CO Screening by Pulse CO-OximetryTM 2008 NFPA 1584 establishes the routine use of Pulse CO-Oximetry

as a way to protect the lives of the nation’s firefighters from the dangers of CO Poisoning Irvine, California – February 14, 2008 – Masimo (NASDAQ: MASI), the inventor of Pulse COOximetry and Measure-Through Motion and Low Perfusion pulse oximetry, announced today that the National Fire Protection Association (NFPA) has made Carbon Monoxide (CO) screening by Pulse COOximetry a new national healthcare standard for firefighters potentially exposed to Carbon Monoxide poisoning. NFPA’s consensus codes and standards serve as the worldwide authoritative source on fire prevention and public safety—with virtually every building, process, service, design, and installation in society today is affected by NFPA documents.

The new standard, which became effective December 31, 2007 and was published on January 31, 2008, establishes that “any firefighter exposed to CO or presenting with headache, nausea, shortness of breath, or gastrointestinal symptoms” must be measured for CO poisoning by Pulse CO-Oximetry or other available methods. It also requires every fire department to establish Standard Operating Guidelines (SOGs) that outline uniform rehabilitation procedures for firefighters at incident scenes and training exercises.

Too often, even the most skilled first responders miss the chance to treat carbon monoxide poisoning early because, until Masimo invented Masimo Rainbow SET Pulse CO-Oximetry in 2005, there wasn’t a noninvasive way to detect elevated levels of CO in the blood. With the Masimo Rad-57 Pulse COOximeter, fire fighters, EMS professionals and ER clinicians can easily detect carbon monoxide poisoning by applying a noninvasive LED-based sensor on the victims or themselves, allowing for prompt and possibly life-saving treatment that can also limit the likelihood of long-tern cardiac and neurological damage.

Studies have shown that even a single high level exposure, or prolonged exposure to low levels of CO, has the potential to cause long-term heart, brain and organ damage. Long-term effects of CO include: cardiac arrests, Parkinson-syndromes affecting motor skills and speech, dementia, cortical blindness, acute renal failure, and muscle cell death.