"The mine cases are persuasive, but they suffer from the defect that many of the symptoms of manganese intoxication are also associated with the aging process and/or other disease conditions. A case study that is free from such objections is entitled 'Manganese Intoxication: the cause of an inexplicable epileptic syndrome in a 3 year old child.' In that case a 3 year old child with epileptic syndromes was found to have elevated blood manganese levels. Chelation therapy with CA NA (2) EDTA promptly succeeded in reversing all epileptic syndromes and his EEG and blood manganese levels returned to normal."

"Currently, the American Conference of Governmental Industrial Hygienist Threshold Limit Value (ACGIH TLV) for airborne manganese is (0.2 mg/m.). If airborne manganese were not neurotoxic, there would be no need for the ACGIH TLV regulations and no need for the mine owners to keep manganese levels below that number. The ACGIH TLV limits are comparable to the limits set in the majority of states regulating airborne manganese levels."

"Included in the material that was provided to me are two articles marked as discovery exhibits in the case of Ronald Pressler vs LEC Cause No. 23472*BH03. If this material were offered to suggest that exposure to toxic levels of manganese may not pose a danger to welders, I find it unpersuasive. In the study of 1423 welders entitled, 'Prevalence of parkinsonism and relationship to exposure in a large sample of Alabama welders' the author found that the prevalence of 'Parkinsonism' was higher among the welders than in the general population but drew no conclusions or inferences. A second article entitled, 'Welding-related parkinsonism: Clinical features, treatment and pathology' with the same first author concluded that though welding may be risk factor, the data cannot exclude a genetic contribution. These articles are totally irrelevant to the case at hand. Exposure to toxic levels of manganese causes manganism not Parkinsonism. The Alabama welders could have both Parkinsonism and manganism. For purposes of legal liability, the question is whether Alabama welders have more Parkinson-like symptoms than the general public."

"The liver maintains manganese homeostasis. Liver disease causes manganese levels to rise and Parkinson-like symptoms to appear. Most of the manganese accumulated after high exposure is excreted in the bile by the liver. Liver disease is therefore an increased risk factor for the accumulation of manganese in the brain. It may reasonably be assumed that the limits on manganese exposure, referred to above, reflect the maximum capacity of a healthy liver to prevent the accumulation of toxic amounts of manganese and that regulations on manganese exposure like the ACGIH TLV regulations reflect the manganese-removing limits of the average healthy human liver."

"Apart from the liability issue, the case raises serious issues as to the measure of damages. In varying degrees, many of the symptoms of manganism abate without medical intervention upon removal from the exposure to the toxic levels of manganese. Both short-term and long-term manganese removal by the liver has been evaluated. In a study of the short-term effect of high dose manganese exposure on learning defects in rats withdrawal of manganese exposure produced a compete remission of learning impairment within 15 days. The effects of long term exposure at 1 mg/mn/M3 (5 times the recommended maximum exposure level (ACGIH TLV of 0.2 mg/mn/m3) for 5.5 years depended on the value of what one study called the 'MNT' (the total Manganese dust exposure). The results also varied according to which of the several standards were being measured (eye-hand coordination, simple visual reaction time or hand steadiness). Although the workers did suffer demonstrable neurological damages in no way could the damages be described as disabling."

"Part of the discovery that I received included a document entitled, 'Litigation'. It was apparently prepared by HSBC. In it they project potential damages as high as 35 to 70 billion dollars. I disagree. Apart from prolonged muscle contractions, decreased muscle movement, rigidity and muscle tremors, many of the symptoms associated with manganism are also associated with normal healthy aging and unhealthy aging. These would include compulsive or violent behavior, emotional instability, hallucinations, fatigue, headache, diminished libido, loss of appetite, apathy, and insomnia. Unhealthy aging means alcoholism, smoking, poor diet, high blood pressure, lack of exercise and even lack of mental stimulation."

"The common route that this damage takes is through the mechanism of cerebral atrophy. Cerebral atrophy is an inevitable part of aging. The loss of brain tissue is roughly 0.45% per year after age 30 and diseases like mild Alzheimer's disease can double that amount. Chronic alcohol consumption also significantly increases the loss of brain tissue. Most of the neurological symptoms associated with manganism including compulsive or violent behavior, hallucinations, fatigue, headache,apathy, and insomnia are also associated with age-related cerebral atrophy. I see great difficulty in proving which damages are ascribable to the exposure to welding fumes and which are ascribable to normal aging and the patient's life style."

"I see this case as one of mistaken assumptions. Manganese is toxic at high exposure levels but it does not cause Parkinsonism. Parkinson is a degenerative disease and it can eventually cause the type of damages that the plaintiffs are claiming. Cessation of the manganese exposure would not change the damage picture and chelation therapy would have no effect."

"Manganism is totally different than Parkinsonism. In manganism, manganese accumulates in the globus pallidus, a different area of the brain from that which is affected by Parkinsonism. The globus pallidus is not the movement center of the brain. It is a sort of relay station that moderates input from other areas of the brain that control motion. The manganese accumulation alters the signals coming from the globus pallidus, thus causing the movement disorders. Removal by the liver and/or by chelation stops the symptoms."

"The residual damages after cessation come from the fact that manganese also accumulates in other brain cells. It then slows the cellular metabolic rate 33 and causes oxidative damage. This weakens these brain cells and many of them die through a process call apoptosis. Apoptosis is a process that is designed to get rid of unhealthy cells to prevent them from becoming cancerous or spilling their toxic contents into the intracellular spaces. This sort of damage is permanent and cannot be reversed by the liver or by chelation. The best way to describe this damage is that it is accelerated brain atrophy. It causes the age-related problems that are also associated with the aging process, but it does not cause the severe movement disorders that are associated with Parkinsonism."