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| Fact No | Subject | Verb | Object | Weight | |
|---|---|---|---|---|---|
| 1 | brain | damage | from chemical injury | 6 | |
| 2 | brain | is | more susceptible | 4 | |
| 3 | chemical breakdown products | called | free radicals | 1 | |
| 4 | It | has | high proportion of polyunsaturated forming myelin | 1 | |
| 5 | brain | has | special vulnerability to toxic damage, due to the following factors | 7 | |
| 6 | brain function | verified | by testing | 4 | |
| 7 | petrochemical compounds | have been shown | to cause chronic changes in brain function | 5 | |
| 8 | Lipid soluble chemicals | enter | brain | 4 | |
| 9 | Lipid soluble chemicals | pass | blood brain barrier easily10 | 4 | |
| 10 | Brain changes | are accompanied | by persisting chronic symptoms including headache, fatigue, weakness, balance disturbance, impaired coordination, reduced memory, attention span and concentration and mood and personality changes | 5 | |
| 11 | Even low-level exposure to volatile organic compounds | can cause | changes in brain function | 7 | |
| 12 | intermittent repeated exposures | have been documented | dependent sensitization | 1 | |
| 13 | This study | was | study of the acute short-term effects | 1 | |
| 14 | Brain damage | can occur | even following relatively short-term exposure to hydrocarbon/petrochemical compounds, which can also induce cacosmia | 9 | |
| 15 | Toxic induced brain damage | can induce | chemical intolerance | 8 | |
| 16 | Other studies | document | brain changes with low level chronic exposure | 6 | |
| 17 | Further exposure | causes | further damage | 5 | |
| 18 | Individuals with toxic encephalopathy | have | long-term or permanent brain damage, which creates severe impairment in their ability to function | 6 | |
| 19 | Toxic exposure | leads | to the formation of antibodies to the brain/nervous system | 2 | |
| 20 | Toxic exposure | leads | to changes in the neuromuscular function | 3 | |
| 21 | Long term exposure to organic solvents | can induce | toxic encephalopathy with chronic persisting symptoms of fatigue | 2 | |
| 22 | various chemical compounds | cause | chronic brain effects | 6 | |
| 23 | nerve cell membranes and energy metabolism | causing | disturbances in the detoxification system | 2 | |
| 24 | nerve cell membranes and energy metabolism | creating | toxic metabolites | 1 | |
| 25 | means | include | solubility in fatty tissue which is highly prevalent in the brain, the high rate of blood flow in the brain, and the ability of solvents and other petrochemicals to attack | 5 | |
| 26 | Petrochemical substances | being lipid | soluble | 1 | |
| 27 | Petrochemical substances | are taken up | into the brain and concentrate in the lipid part of the brain including but not limited to the brain stem | 5 | |
| 28 | Toxic chemical compounds | are | also capable of entering the brain directly through the nose | 6 | |
| 29 | SPECT brain scans on adults with chronic symptoms following a history of toxic exposure to mixed petrochemical solvents compared to healthy controls | showed | reduced ability to take up the tracer substance in the early phase of injection | 7 | |
| 30 | Increased tracer | was found | in the late phase of injection, consistent with impaired detoxification ability and/or reduced blood flow | 2 | |
| 31 | Changes | were seen | in frontal, temporal and limbic brain areas | 4 | |
| 32 | PET scans | associated | with chemical intolerance | 2 | |
| 33 | limbic hypermetabolism | documented | on PET scans | 1 | |
| 34 | Persons with toxic encephalopathy | can develop | limbic hypermetabolism | 1 | |
| 35 | exposures | causing | brain damage in this study | 7 | |
| 36 | Types of exposures | included | industrial exposures and accidents, "tight" sick office building exposure and environmental overexposure | 3 | |
| 37 | SPECT scans | show | reduced blood flow to the brain in toxic encephalopathy | 5 | |
| 38 | high blood flow and oxygen | reduced | flow easily damages their function | 2 | |
| 39 | high blood flow and oxygen | needs | 10 | 1 | |
| 40 | brain cells | are | readily damaged by reduced energy metabolism,10 a common finding in chemically injured patients | 5 | |
| 41 | Chemicals | breathed | in enter the limbic system,1,10 which then affects the hypothalamus and pituitary, and through pituitary control, adrenal, thyroid and reproductive function | 1 | |
| 42 | Persisting brain damage | can be caused | by symptomatic exposure | 8 | |
| 43 | Persisting brain damage | can be caused | combustion products, pesticides, solvents, volatile organic compounds | 8 | |
| 44 | not | limited | to environmental controls to reduce future exposure | 2 | |
| 45 | chemicals | interfering | with brain function | 4 | |
| 46 | Chronic toxic encephalopathy | is | long lasting brain structural damage or brain dysfunction secondary to an exposure from a chemical or mixture of chemicals | 10 | |
| 47 | International Classification of Disease (ICD) code for toxic encephalopathy | is | 349.82 | 1 | |
| 48 | Toxic petrochemicals | are excreted | using Phase I and II detoxification | 1 | |
| 49 | Phase II detoxification | requires | causing significant further fatigue | 1 | |
| 50 | Phase II detoxification | requires | lot of energy from the body's energy stores,38 thus | 2 | |
| 51 | Phase II detoxification | requires | nutritional cofactors, which must be replaced | 1 | |
| 52 | Petrochemical toxins | generate | increased free radicals in Phase I, which damage the energy generating mitochondria , thus leading to less energy for Phase II and increased tissue damage from Phase I free radicals which cannot be detoxified adequately in Phase II | 5 | |
| 53 | Nutrients necessary for energy production | include | adequate thiamine | 1 | |
| 54 | Nutrients | needed | to help protect from free radical damage | 3 | |
| 55 | not | limited | to vitamins C, E, Zinc, Selenium and Copper | 1 | |
| 56 | I | include | adequate antioxidants and other detoxification cofactors, including but not | 1 | |
| 57 | Nutrients necessary for Phase II detoxification | include | cobalamine | 1 | |
| 58 | Brain ischemia | can lead | to increased free radicals, death of brain cells and neurodegenerative disease | 8 | |
| 59 | Increased free radicals | cause | increased risk of neurodegenerative disease such as Parkinson's, AML, Altzeimers and increased brain aging | 4 | |
| 60 | Accelerated neurodegenerative disease | occurs | from increased oxidative stress41 such as from chemical exposure | 4 | |
| 61 | Increased lipid peroxides | is | indicator of brain and cellular membrane lipid damage | 8 | |
| 62 | cellular and other body membranes | resulting | in reduced polyunsaturated lipids | 1 | |
| 63 | cellular and other body membranes | resulting | making membranes less flexible | 1 | |
| 64 | membranes | makes | them more permeable to undesired amounts of substances | 1 | |
| 65 | Free radicals from chemicals | damage | cellular and other body membranes | 1 | |
| 66 | energy-generating structures | called | mitochondria | 1 | |
| 67 | transport minerals and other vital nutrients and proteins | needed | for body repair | 1 | |
| 68 | Free radicals | attack | proteins | 1 | |
| 69 | Free radicals | attack | including but not limited to body enzymes, proteins | 1 | |
| 70 | Free radicals | damage | producing more damaged DNA products such as 8-oxo-2'-deoxyguanosine | 1 | |
| 71 | Free radicals | damage | DNA and RNA | 1 |
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| Name: | 23 Toxic Encephalopathy.doc source |
|---|---|
| Language: | English |
| Words: | 1089 |
| Sentences: | 49 |
| Size: | 4.36 standard page(s)* |
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