Firehouse.com Article: New Indiana Law Recognizes Parkinson's Disease as Line-of-Duty Disability

Firehouse.com Article: New Indiana Law Recognizes Parkinson's Disease as Line-of-Duty Disability

Firefighting and Toxic Exposures

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.

Firefighting and Occupational Exposures

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.

Research on Toxic Exposure and Parkinson's Disease

Research Findings and New Directions

During the past five years, researchers have made substantial advances in our understanding of the biological factors involved in PD. They are beginning to decipher the roles environmental factors in PD and to learn how the interplay of these factors can lead to the disease.

Environmental Factors

Many researchers believe that environmental exposures also increase a person's risk of developing the disease. As with many familial cases, exposure to toxins or other environmental factors may influence when symptoms of the disease appear and/or how the disease progresses.

One of the primary pieces of evidence that environmental factors play a role in the development of PD is that the relative risk of the disease is higher in industrialized countries than in less industrialized ones. In addition, studies have found that farmers and other workers who work in fields that are exposed to toxic chemicals have an increased risk of developing PD. Taken together, these studies suggest that toxic chemicals or exposure to other environmental factors present in industrial and agricultural areas might increase the risk of PD.

Another piece of evidence comes from observations of people who have been accidentally poisoned with the toxin MPTP (1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine). MPTP is structurally similar to some pesticides and other toxic chemicals. A breakdown product of MPTP, called MPP+, is toxic to substantia nigra neurons — the neurons that are affected in PD. MPTP produces a severe, permanent parkinsonian syndrome in affected people, and is now used to create animal models of PD. This discovery demonstrated that a toxic substance can damage the brain and produce parkinsonian symptoms.

A study of people in the World War II Veteran Twins Registry has suggested that genetic factors do not play a major role in causing sporadic Parkinson's Disease. A number of other twin studies have found similar results. The chance that two siblings will both have PD is similar for fraternal and identical twins, suggesting that environmental exposures are more important than genetics in determining who will get the disease. Other studies have found that fraternal and identical twins of people with PD often have significant loss of dopamine neurons even when they don't experience any symptoms.

Viruses are another possible environmental trigger for PD. People who developed encephalopathy after a 1918 influenza epidemic were later stricken with severe, progressive Parkinson's-like symptoms. However, these cases showed that viruses can sometimes affect the region of the brain damaged in PD. Other studies have found evidence of activated immune cells and the accumulation of inflammation-associated proteins in PD. These changes might be triggered by viruses in some cases. Firefighters and Emergency Medical personnel are constantly exposed to viruses during medical responses, which is 78% of their work load.

Scientists are continuing to study environmental toxins, supported by the National Institute of Environmental Health Sciences, has shown that other agricultural compounds also can produce abnormalities in cells that are similar to those seen in PD. This research is supported through a program called the Collaborative Centers for Parkinson's Disease Environmental Research (CCPDER) Consortium. This program sponsors a variety of projects to examine how occupational exposure to toxins and use of caffeine and other substances may affect risk, and whether inherited genetic mutations may predispose certain people to developing PD after exposure to certain chemicals.