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.

Neurotoxin Exposure Treatment Parkinson's Research Program

Soldiers may be at risk for neurodegenerative diseases from occupational exposures to psychological stress, toxic industrial and agricultural chemicals, chemical threat agents, head injury, and even radiofrequency radiation. Parkinson.s Disease (PD), as a particularly relevant disorder induced by a variety of environmental exposures, is a central focus of the research program.

Basic research on mechanisms of neurodegeneration will lead to better diagnosis, treatment, and prevention. The NETRP was funded by a total of $70M special congressional appropriations to study neurodegenerative mechanisms and treatments, with a special emphasis on Parkinson's Disease.There are currently 63 discrete research projects in the program.

Parkinson.s Disease (PD) affects nearly one million Americans. Recent evidence that genetic transmission is a minor component of this disorder confirms the importance of environmental factors, some of which are known, such as exposures to specific toxins. Military occupational exposures may be risks for neurodegenerative disease, including some Parkinson.s symptoms. Fundamental mechanisms underlying the development of PD may also be pertinent to other neurodegenerative diseases.

In PD there is a loss of brain cells in the substantia nigra that contain the neurotransmitter dopamine. Insufficient dopamine neurotransmission underlies many of the symptoms of PD. New technologies such as neuroimaging and genetic knockout models, and recent advances in neurobiology such as new drugs and growth factors (e.g., GDNF) are being exploited to advance
this research. This program directly contributes to common objectives in psychological stress and toxicology research in the core-funded basic research program and Gulf War Illnesses/ Force Health Protection research program.

Early Detection

Valid and reliable biological markers of neurodegeneration (e.g., cognitive testing, neuroimaging, specific biochemical markers) are an important technological hurdle. One study tests changes in the ability to manipulate aspects of language to determine if these precede motor dysfunction, as a test for early PD-associated degeneration in the cortical dopaminergic system. A separate
study will develop imaging markers diagnostic for early PD and clarify the relationship between striatal dopamine integrity and cortical activation during motor and memory tasks. Several other projects study biomarkers to detect and monitor neuronal degeneration: a marker of dopamine terminal integrity which may directly evaluate the rate of degeneration and will also be used to study the neurotoxicity of L-dopa. Another study creates a genomic database to identify unique molecular markers associated with progressive decrease in striatal dopamine integrity and consequent impaired motor and cognitive performance in inbred and knockout mouse models of PD.

Pathogenesis Oxidative Damage: A large number of studies focus on oxidative damage as a common mechanism of neurotoxicity. The brain is particularly susceptible to oxidative damage for several reasons: in addition to receiving a high percentage of the body's total oxygen, the brain is relatively deficient in catalase which protects against reactive oxygen species (ROS) damage; it's most important defense mechanism against ROS damage, the glutathione system, is easily saturated; it has a high concentration of polyunsaturated lipids, easily peroxidized by free-radicals; and regions such as the substantia nigra have high concentrations of iron which catalyzes the conversion of H2O2 to OH., allowing production of excess quantities of ROS.

Excitotoxic Damage: Increased action of excitatory amino acid transmitters such as glutamate (Glu) and aspartate may initiate or prolong depolarization of neurons, with subsequent clinical signs (e.g. seizures) or neuronal exhaustion and cellular degeneration.The ionotropic glutamate receptors (iGluR) have a primary role in fast neuronal excitation, including the excitotoxic actions of Glu. The prominent role of the NMDA-preferring class of iGluR in the pathophysiology of excitotoxic neurodegeneration is being studied to develop potentially neuroprotective agents.

Apoptosis: Many studies in the program specifically investigate aspects of apoptosis, a process in which developmental cues and environmental stimuli initiate a genetically established cascade that results in cellular degeneration and cell death. Several studies concentrate on interactions of apoptotic cascade events while others focus on mitochondrial intervention points.

Accumulation of Intracellular Aggregates and Other Cell Damage: Mechanisms of cellular disruption are being studied in four cellular protein systems (alpha-synuclein, tissue plasminogen activator, p38 protein kinase family, and neurotoxic esterase). Studies of the alpha-synuclein gene family will investigate expression/cell distribution, mutations, and over-expression on neurodegeneration. Another study tests the hypothesis that gene expression and functional up-regulation of specific neural sodium channels are contributors to neuronal cell death after cerebral ischemia.

Etiologies

Stress: Early markers of neurodegeneration, such as hippocampal changes and memory impairment, are being studied in a social mouse model of combat stress. Regional susceptibility of the nigrostriatal system to damage after prolonged periods of stress is being studied in 6-OHDA lesioned rats. Another study investigates beneficial short-term and deleterious long-term actions of acetylcholinesterase (AChE) in animals subjected to acute psychological stress or anticholinesterases. Stress, AChE inhibitors (chloropyrifos), and fuel additives (which may synergistically promote degeneration in structures such as the hippocampus) are being investigated for changes in behavior and CNS excitability.

Other studies include the construction of a tetracycline-inducible vector system in which either an anti-sense message for the AChE or a ribozyme directed against the AChE will be expressed via a plasmid injected into the hippocampus.

Toxins: Insecticides (permethrin and chloropyrifos), in combination with MPTP, will be studied to clarify whether insecticide exposure can intensify development of PD and will provide a full
dose-effect curve useful in extrapolating animal data to man for risk assessment. Mechanisms by which mustard chemical warfare agents induce neuronal cell death (a model for neurotoxic DNA damage) are being studied using mice deficient in DNA repair mechanisms. Another study examines synergistic effects of excitotoxicity, free radicals, and a depleted bioenergetic state in causing dopaminergic cell death. A sample of men who have been well characterized by serial neurologic examinations over a 26-year period, will be used to correlate environmental and occupational risk (including pesticide residues in brain tissue) for development of PD and related neurodegenerative disease.

Trauma: Mechanisms of cell death due to traumatic brain injury will be studied and may lead to identification of optimal brain region targets for calpain inhibitors to prevent further neurodegeneration in already damaged brain tissue.

Viral: Animals infected with Venezuelan equine encephalitis virus (VEE) variants will be studied for gradations of neurotoxicity resulting from glial cell activation, including assessment of alterations in production of cytokines and reactive nitrogen intermediates that influence neuronal degeneration in VEE infection.

Therapeutic Strategies

Interventions Targeting Specific Mechanisms of Damage: Several studies test treatments for excitotoxic damage (including neuroprotective effects provided by a metabotropic GluR (mGluR) agonist); neuroprotectant combinations of vitamin E, Co-enzyme Q, melatonin, FK506, and benzamide; Huperzine A analogs to shield glutamate ionotropic receptors in cultured neuronal cells; and efficacy of NMDA receptor agonist drugs to mitigate excitotoxic neuronal damage (from retinal laser irradiation). The mechanisms by which transforming growth factors protect neurons against excitotoxic damage and induce motor axon growth using gene transfer of GDNF or Bcl-2 into nigral neurons in animal models of PD are also being studied in a comparison of gene delivery methods: encapsulated BHK cells genetically modified to secrete GDNF and intrastriatal infusion of an adenovirus GDNF transgene vector in aged monkeys. One project investigates mechanisms by which some neuronal cell lines resist ROS damage following exposure to the neurotoxins nitrogen mustard and arsenite.

Neuroprotectants: Potential neuroprotective effects of progesterone, based on recent evidence that progesterone decreases excitotoxicity leading to neuronal cell loss, will be explored to determine if the effects are direct or involve neurosteroid metabolites acting on GABA receptors. Another project investigates the effects of glycosphingolipids (GSL) using two unique insect model systems that permit structure-function studies of GSLs on growth and repair of nerve cells. A study investigating liposome delivery systems for a recombinant enzyme (OPAA-2) may greatly increase neuroprotection against alkyl-phosphate chemicals, and the protective actions of various anti-inflammatory drugs, anticonvulsants, and glutaminergic potentiator agents (ampakines) will be studied to identify neuroprotectant drugs which will not block other important receptors or signal transduction systems.

Restoration of Dopaminergic Secretory Capabilities: Replacement graft strategies have suffered from poor survival, insufficient axonal outgrowth from surviving neurons, poor functional recovery provided by the procedure, and disabling side effects such as dyskinesia; however, functional recovery associated with surviving grafts encourages further work. Several studies attempt new approaches to improve transplant survival including use of caspase inhibitors, regulation of Bcl-2 and GDNF to improve survival of transplanted neural cells, and identification of neurotrophic factors in other types of brain cells (O2-A cells). A study of differentiation of mesencephalic progenitor cells will attempt to create new dopaminergic neurons induced by hematopoietic cytokines such as IL-1.

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.

Research on Toxins 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.

Neurotoxic Chemical Effects

The mission: To provide the highest quality clinical and forensic services for the evaluation and diagnosis of neurobehavioral, neuropsychological and neurotoxic illness from chemicals, injuries and drugs.

Evaluating neurobehavioral function and the effects of toxic chemicals, drugs and substances (neurotoxic agents) on the nervous system;

Symptoms of neurotoxicity: Toxic chemicals can damage the nervous system and brain. Such chemicals are neurotoxic. A person may or may not be aware of neurotoxic damage when it occurs.

Neurotoxicity is a cause of brain damage. Common symptoms can include problems with memory, concentration, reaction time, sleep, thinking, language, as well as depression, confusion, personality changes, fatigue, and numbness of the hands and feet. Many types of nervous system disorders could be caused by neurotoxicity, including numerous neurologic diseases.

Chemicals that we have researched that can cause neurotoxic illness include: Adhesives, Agent Orange, aspartame, ammonia, arsenic, benzene, carbonless copy paper, carbon monoxide, carpet cleaning agents, CCA (copper-chromium- arsenate), chemical warfare agents, chlorine, combustion products, contaminated or defective products, copper-chromium-arsenate, damp buildings, dioxin, drugs, formaldehyde, gamma butyrolactone, gasoline, glues, heavy metals, herbicides, lacquer sanding sealer, lead, lithium, MDI (methyl diisocyanate), MEK (methyl-ethyl-ketone), manganese, mercury, metals, methylene chloride, mixed toxic waste, mold, municipal sludge, mycotoxins, naphthalene, n-hexane, oil and gas field emissions, opiates, organic metals, paint, paint remover, pesticides (organochlorines, organophosphates, etc.), phenolic resins, pollution (ground, soil, water, air), polychlorinated biphenyl (PCB), radiation injuries, sick buildings, smoke removing agents, solvents, styrene, synthetic carpets, TDI (toluene diisocyanate), toluene, toxic waste, trichloroethane, trichloroethylene, welding fumes, wood preservatives, xylene, etc.

Illnesses that we have studied that can result from neurotoxic chemical poisoning Include: chemical sensitivity syndrome, environmental illness, memory dysfunction, multiple chemical sensitivity, neurologic illnesses due to toxic chemicals (amyotrophic lateral sclerosis, movement disorders, multiple sclerosis, paralysis, , etc.), panic disorder, Parkinson's disease, tremor, etc.

Toxic Chemicals and their Effects

Evidence is building about the effects of our toxic environment on our long-term health and toxins' role in chronic diseases. Although scientists have known for quite some time that pollution and pesticides can adversely affect human health, mounting evidence reveals far more deadly connections between toxic exposure and a variety of diseases. The most disturbing discovery is that chronic exposure to even low levels of common toxins can have negative health effects as the toxins accumulate over time, damaging the neurological, immune, and endocrine systems.

To complicate matters, many governments and health organizations do not seem to be addressing this serious problem. Without accountability and clean-up programs, the toxic exposure overload continues to spiral out of control.

The following are frequently asked questions about toxins.

1. What are toxins?
Toxins are generally defined as anything in our environment with the potential to negatively affect the health and function of the body. These dangerous foreign substances can be consumed through polluted food or water, breathed in through the air, or absorbed through the skin. They may be organic biotoxins or inorganic toxins such as poisonous chemicals and other toxic man-made substances. Ultimately, all toxins take a serious toll on our health and can even cause cancer. The damage can result quickly from exposure to a large or very concentrated dangerous toxin, but more often, it, results from a gradual accumulation of smaller amounts of less-potent toxins from a variety of sources, often referred to as "chronic toxic overload."

2. What are the most common sources of toxins?

Perhaps more troubling than the sources of these toxins is the prevalence of toxins. We now come in contact with more toxins than ever before. It is estimated that we are exposed to more than 100,000 toxins in our environment, a quarter of which are known to cause cancer. In one year alone, the EPA estimated that 1.9 billion pounds of chemicals ended up in our water supplies, and 2.4 billion were released into the atmosphere. Meanwhile, the National Research Council (NRC) recently estimated that a shocking 70,000 commercially-used chemicals have not even been tested for toxic effects.

This constant bombardment puts our body in a state of chronic toxic overload, which puts us at risk for several diseases. The most common types of toxins that may affect our health include:

Dioxins: Notorious for their harmful effects on hormones and the endocrine system, these byproduct pollutants are widespread and linger for years in the environment.

Furans: The result of plastic production, these toxins are considered very toxic to the endocrine system and are believed to have cancer-causing effects.

Heavy metals: There are over twenty toxic heavy metals to which we are commonly exposed. Of greatest concern are mercury, arsenic, lead and cadmium, whose affects range from developmental abnormalities and behavioral disorders to cancer.

Mercury is found in dental amalgam, infant and adult vaccines, many types of fish, thermometers and fluorescent lights to name a few sources. Coal-fired power plants are the number one source of mercury emissions into the air world-wide.

Arsenic is a common contaminant of water, especially near mining activities, and has been for decades, to manufacture "preserved wood" building materials. Lead is common toxin released during mining and petrochemical manufacturing processes.

Cadmium exposure has increased rapidly over the past few decades, with cigarette smoke being a major source. Even low levels may contribute to kidney disease and bone disorders.

PCBs: Polychlorinated biphenyl, a class of toxic aromatic compounds. Although banned in the U.S. in 1976, these industrial chemicals can linger in the environment for decades and have been linked to cancer and disorders of the nervous system.

Pesticides: Although largely banned, pesticides such as organochlorine insecticides, DDT, and others tend to accumulate in the environment and have been linked to adverse reproductive health and cancer. Organophosphate insecticide metabolites are known to be potent nervous system poisons and are found in foods.

Phthalates: Found in several health and beauty products, as well as some children's toys, these toxins were recently banned in Europe and have been known to cause male reproductive birthdefects.

Volatile and semi-volatile organic chemicals: These industrial solvents (also found in gasoline) negatively affect the nervous system and have been linked to cancer.

3. Why are toxins a threat to my health?

The fact that toxins can be dangerous to our health has been known for quite some time, but our understanding of how exactly low-level toxic exposure threatens our health, and to what extent, is only now being discovered. Research on the detrimental health effects of toxins connects even a little exposure over time to chronic and life-threatening diseases. The danger of toxins lies in the fact that they are invisible, so are not easily avoided; likewise, their effects do not surface
immediately, so the damage done does not necessarily deter repeat exposure. But just because a toxin won't cause immediate death or severe organ shutdown doesn't mean it is less dangerous or that the body is any better equipped to deal with it. Basically, when a body's toxic load becomes greater its ability to adapt to it, its health suffers.

Recent research on the long term health effects of what have previously been deemed as “relatively harmless" toxins is more than just a little worrisome. Scientists are discovering that continued exposure to common, "non-lethal" toxins can negatively affect major body systems. In fact, Britain's Environmental Toxins Foundation recently stated that there is "mounting evidence of structural and genetic damage, potentially caused to the human morphology, through the huge influx of chemical agents found in the air, soil and water today."

Consider the following: In a recent study, more than 160 environmental toxins were discovered in the collective blood and urine of test subjects. Of these toxins, over 75 were identified as cancer causing, more than half were known to damage the brain and nervous system.

4. What is toxic overload and what are its symptoms?

The acute effects of toxic exposure can be prominent, but more often, toxic effects build slowly over time. In fact, one recent study found that subjects tested positive for more than 90 pollutants and industrial chemicals after blood and urine tests, even though none of the individuals studied worked or lived near high-risk industrial areas. In another study from the CDC, subjects tested positive for more than 116 chemicals, many of them banned at least two decades prior because of their health risks.

Because chronic toxic overload happens over time, the effects of exposure may be overlooked. In fact, many symptoms of chronic toxic overload are associated with other conditions and so are misdiagnosed. Chronic contact with toxins, even sources that aren't considered dangerous, will eventually take its toll on the body. Immuno-toxicity may surface as asthma, allergies, chronic infections, or cancer, while neuro-toxicity may appear in the form of dementia, decreased cognition, mood disorders, or memory problems. Signs of endocrine toxicity include problems with libido, reproduction, menses, metabolism, insulin resistance, or the body's inability to handle physical and emotional stress.

Symptoms vary from person to person, but in general, symptoms commonly associated with achronic toxic overload state include:

5. What conditions are linked to toxin overload?

Scientific data now shows that recurring exposure to toxins -- even in small doses -- damages the immune system, increases cardiovascular disease and cancer risks, interferes with essential enzyme activity in the body, affects hormone balance and cell growth, and inhibits brain function. Below is a short list of some health conditions (diseases) that are linked to toxin overload:

Ultimately, what researchers are discovering is that by reducing our exposure to pollutants and toxins and eliminating toxic buildup in the body, we lower our risk of developing numerous diseases, which results in more energy, improved overall health, longevity, and-a greater sense of well-being.

6. Is there research that provides definitive proof of toxins' role in causing disease?

The research linking chronic disease to toxins continues to build, and the results of these studies are more than a little unsettling. Lead exposure alone has been linked to cancer, cardiovascular disease, stroke, heart attacks, renal failure, osteoporosis, and macular degeneration.

In a 2005 article published in Alternative Therapies titled "Metals in Medicines” the authors citednumerous examples of how new links between heavy metals and disease are leading the medical community to change its approach to disease and wellness and to increase awareness about these threats.

Research on Environmental Exposures Causing 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.

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.