THE WELDING FUME LITIGATION FROM A MEDICOLEGAL PERSPECTIVE - by By Robert Eli, JD

APRIL NEWSLETTER -------------------------------------------------------------------------------- THE WELDING FUME LITIGATION FROM A MEDICOLEGAL PERSPECTIVE 10 April 2006 By Robert Eli, JD INTRODUCTION This short medicolegal brief is an attempt to answer three questions: 1) If the exposure to welding fumes containing manganese is potentially toxic, why has liability been so difficult to prove in a court of law? 2) What can be done to provide a medical treatment rather than a legal remedy for the damages that are claimed? 3) What factors relating to neurological damage from the exposure to welding fumes containing manganese might confound the issues of proximate cause and the evaluation of damages? WHY IT IS SO DIFFICULT TO PROVE THAT THE EXPOSURE TO WELDING RODS CONTAINING MANGANESE CAUSE NEUROLOGICAL DAMAGE Proof that the exposure to welding rods containing manganese causes neurological damages a court of law is particularly difficult for two reasons: 1) For ethical reasons there cannot be a controlled scientific human study of the neurodegenerative effects of high level exposure to welding fumes containing manganese; and, 2) There are so many other factors that can cause neurodegeneration that the normal control group needed for such a scientific study would be difficult to assemble. We only know that manganese exposure causes neurological damage in humans from the many case studies that have reported it. The same is true for all other metals at high exposure rates. There are no controlled scientific human studies proving that lead, mercury or antimony is neurotoxic in humans. Yet, no one would seriously claim that these metals could not be neurotoxic at high levels in humans. There is no plausible scientific basis for arguing that manganese is an exception. Case studies in humans are generally not considered persuasive evidence because of wide differences in the patient population. For this reason, they are rarely cited as references in the literature; and, if used in a court of law, they are subject to the objection of their limited probative value. But the connection between excessive manganese exposure and neurological damage has definitely been demonstrated in controlled scientific studies using rats. These studies have used oral or injected manganese. Arguably they have no relevance to whether the exposure to welding fumes containing manganese would produce similar results. However, a study of the affect of welding fumes containing manganese could be constructed using young rats, to minimize the influence of confounding factors. The Parkinson-like symptoms that result from the uncontrolled exposure to welding fumes containing manganese is properly designated as an issue of toxicology. For obvious reasons toxological studies are always done with rats. THE MEDICAL ASPECTS OF NEUROLOGICAL DAMAGE ASSOCIATED WITH THE EXPOSURE TO WELDING FUMES CONTAINING MANGANESE Manganese deficiency is associated with a number of pathological conditions. The liver maintains manganese homeostasis. Liver disease causes manganese levels to rise and Parkinson-like symptoms to appear. The rate of removal has been calculated in animal studies and it is fairly rapid. Thus, a welder who either stops welding or starts welding with adequate ventilation may suffer only minor damages where the exposure has been limited in terms of time and degree. Manganese deficiency is associated with a number of pathological conditions. The liver maintains manganese homeostasis. Liver disease causes manganese levels to rise and Parkinson-like symptoms to appear. The rate of removal has been calculated in animal studies and it is fairly rapid. Thus, a welder who either stops welding or starts welding with adequate ventilation may suffer only minor damages where the exposure has been limited in terms of time and degree. Certain degenerative factors associated with the aging process inevitably contribute to the same neurodegenerative processes as those that are associated with the exposure to welding fumes containing manganese. The net effect of these factors causes a loss of brain tissue even in the normal otherwise healthy aging population. The normal healthy aging population means that portion of the population who are not obese; don't smoke or drink alcohol in excess; do not have diabetes or other degenerative diseases; and, are not totally sedentary. These other factors significantly aggravate the neurodegeneration otherwise seen in the normal healthy aging population. Of all the factors that might cause symptoms that duplicate or augment the same type of neurological damage as that caused by exposure to welding fumes containing manganese, excessive alcohol use is by far the most important one. Alcohol can cause liver cirrhosis, thus preventing the liver from removing manganese from the body. The effect is the same as that of excessive exposure to welding fumes containing manganese. Chronic alcoholism could rise to the level of proximate cause. It could also significantly increase the damages from the exposure to welding fumes containing manganese. Liver cirrhosis is easy to test for and the scientific proof of both causation and damage is very persuasive. Besides alcohol, aging and the other factors enumerated above cause far more damage than the uncontrolled exposure to welding fumes containing manganese. The damage includes both reduced mortality and deterioration in the quality of life. These other factors are both easy to test for and easy to quantify. Unlike the symptoms induced by the uncontrolled exposure to welding fumes containing manganese, chelation therapy has little or no effect. Also, unlike the neurodegeneration caused by the uncontrolled exposure to welding fumes containing manganese, the neurodegeneration caused by these factors does not abate over time.