Toxic Exposures and Parkinsons: the Mercury Connection

Bernard Windham(Ed.)- Chemical Engineer



I. Introduction.

There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last 2 decades(574). The increase in Parkinson’s and other motor neuron disease has been over 50%. The primary cause appears to be increased exposures to toxic pollutants(574).

Amalgam fillings are the largest source of mercury in most people with daily exposures documented to commonly be above government health guidelines (49,79,183,199,506,600,217). This is due to continuous vaporization of mercury from amalgam in the mouth, along with galvanic currents from mixed metals in the mouth that deposit the mercury in the gums and oral cavity(605). Due to the high daily mercury exposure and excretion into home and business sewers of those with amalgam, dental amalgam is also the largest source of the high levels of mercury found in all sewers and sewer sludge, and thus according to government studies a significant source of mercury in rivers, lakes, bays, fish, and crops(603). People also get significant exposure from vaccinations, fish, and dental office vapor(600).

When amalgam was placed into teeth of monkeys and rats, within one year mercury was found to have accumulated in the brain, trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormone glands, and lymph glands(20). People also commonly get exposures to mercury and other toxic metals such as lead, arsenic, nickel, and aluminum from food, water, and other sources(601). All of these are highly neurotoxic and are documented to cause neurological damage which can result in chronic neurological conditions over time, as well as ADHD, mood, and behavioral disorders (601,602). A study found that those with occupational exposure to lead, arsenic, or copper have more than double the incidence of Parkinson’s than normal(560).

Mercury is one of the most toxic substances in existence and is known to bioaccumulate in the body of people and animals that have chronic exposure(600). Mercury exposure is cumulative and comes primarily from 4 main sources: silver(mercury) dental fillings, food(mainly fish), vaccinations, and occupational exposure. Whereas mercury exposure from fish is primarily methyl mercury and mercury from vaccinations is thimerosal(ethyl mercury), mercury from occupational exposure and dental fillings is primarily from elemental mercury vapor. Developmental and neurological conditions occur at lower levels of exposure from mercury vapor than from inorganic mercury or methyl mercury(606). Mercury in amalgam fillings, because of its high vapor pressure and galvanic action with other metals in the mouth, has been found to be continuously vaporized and released into the body, and has been found to be the directly correlated to the number of amalgam surfaces and the largest source of mercury in the majority of people (49,183,199,209,79,99,600), typically between 60 and 90% of the total. The level of daily exposure of those with several amalgam fillings commonly exceeds the U.S. EPA health guideline for daily mercury exposure of 0.1 ug/kg body weight/day, and the oral mercury level commonly exceeds the mercury MRL of the U.S.ATSDR of 0.2 ug/ cubic meter of air(217,600). When amalgam fillings are replaced, levels of mercury in the blood, urine, saliva, and feces typically rise temporarily but decline between 60 to 90% within 6 to 9 months (79,600.).

The main factors determining whether chronic conditions are induced by metals appear to be exposure and genetic susceptibility, which determines individuals immune sensitivity and ability to detoxify metals(405). Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals, or have an inability to detoxify metals due to such as deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals

II. Mechanisms by which mercury causes neurological conditions found in Parkinson’s and neurodegenerative diseases.



Programmed cell death(apoptosis) is documented to be a major factor in degenerative neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc. Some of the factors documented to be involved in apoptosis of neurons and immune cells include inducement of the inflamatory cytokine Tumor Necrosis Factor-alpha(TNFa) (126), reactive oxygen species and oxidative stress(13,43a,56a,296b,495), reduced glutathione levels(56,126a,111a), liver enzyme effects and inhibition of protein kinase C and cytochrome P450(43,84,260), nitric oxide and peroxynitrite toxicity (43a,521,524), excitotoxicity and lipid peroxidation(490,496), excess free cysteine levels (56d,111a,33,330),excess glutamate toxicity(13b, 416), excess dopamine toxicity (56d,13a), beta-amyloid generation(462), increased calcium influx toxicity (296b,333,416,432,462c,507) and DNA fragmentation(296,42,114,142) and mitochondrial membrane dysfunction (56de, 416). The mechanisms by which mercury causes(often synergistically along with other toxic exposures) all of these conditions and neuronal apoptosis will be documented.

TNFa(tumor necrosis factor-alpha) is a cytokine that controls a wide range of immune cell response in mammals, including cell death(apoptosis) in neuronal and immune cells. This process is involved in inflamatory and degenerative neurological conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc. Cell signaling mechanisms like sphingolipids are part of the control mechansim for the TNFa apoptosis mechanism(126a). Gluthathione is an amino acid that is a normal cellular mechanism for controlling apoptosis. When glutathione is depleted in the brain, reactive oxidative species increased, and CNS and cell signaling mechinsisms are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results and neurological damage. Mercury has been shown to induce TNFa and deplete glutathione, causing inflamatory effects and cellular apoptosis in neuronal and immune cells(126b,126c).

PD link
continued

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