When you google manganism, this is one of the first links to come up.
Manganism or Manganese Poisoning
At first glance it appears to be an informative website on the hazards of welding fumes, but then if you look in the upper left corner of the page notice the logo shows that the website is setup by a law office.
Reading that website scares the sh** out of me knowing I've been welding for 7 years without knowing the risk for developing parkinson disease.
The thing is if you google rare diseases, for example bacterial meningitis, you will find many stories of people who experienced the disease. When I google manganism there are no first hand stories from patients. It just does not seem as common as the propaganda websites make it seem.
Do any of you long time welders know coworkers who developed manganism or parkinsons disease?
Reguardless, I'm heading to the welding supply store to pickup a 3m 7502 respirator with 2091 cartridges and will wear is for welding and grinding.
Neurotoxins:
Neurotoxins may affect neurons, axons, or glial cells. They may cause metabolic imbalance that can secondarily affect the central nervous system (CNS). Some neurotoxins like manganese and MPTP have typical regional predilections. The following is a concise review of selected commonly encountered neurotoxins.
Metals
Metals have been known to be neurotoxic for centuries.
Contamination of groundwater with arsenic has been associated with epidemics of arsenic poisoning in some parts of south Asia.[4]
Increased awareness of lead toxicity over the past decades and regulations regarding the use of lead-based paints has decreased the incidence of lead toxicity.
Manganism was described as recently as 1989 in Taiwan.
Metals
Most reports of acute and chronic arsenic toxicity result from arsenic trioxide. In the United States, the drinking water standard for arsenic is 100 ppb.
Lead exists in 3 forms: metallic, inorganic, and organic. Lead is absorbed through the gastrointestinal tract or lungs. Approximately 99% of lead is in erythrocytes, and 1% is in plasma and serum. Lipid-rich tissue of the CNS is particularly sensitive to the organic form of lead. Leadç—´ ability to interfere with regulatory effects of calcium in cell systems may lead to its effect on voltage-gated channels and synaptic transmission.
Manganese is an essential trace element widely distributed in the environment. Most cases of manganese toxicity result from chronic inhalation of manganese dioxide.
Metals
Arsenic affects both motor and sensory peripheral nerves. Lead affects the motor nerves of upper and lower extremity. Acute lead poisoning can affect the CNS. Manganese can accumulate in globus pallidus and cause toxicity.
Metals
Arsenic causes a gastrointestinal disease characterized by vomiting and diarrhea, which may be followed by an encephalopathy with confusion, seizure, and coma. Chronic arsenic toxicity is a multisystem disease, characterized by sensorimotor polyneuropathy, skin changes, and alopecia.
The major target of lead toxicity is the peripheral nervous system in adults and CNS in children.[20] Intense toxicity may lead to an acute illness characterized by encephalopathy or an acute abdomen. Chronic lead exposure leads to predominantly motor neuropathy, affecting the upper extremity more than the lower. The minimum blood concentration needed is 10 ï½µg/dL in children and 40 ï½µg/dL in adults.
Initial signs and symptoms of manganese toxicity are nonspecific: headache, asthenia, somnolence, anorexia, and/or loss of sexual drive. Manganese causes an extrapyramidal syndrome characterized by progressive parkinsonism, dystonia, and neuropsychiatric symptoms (Manganese madness).[21] MRI shows a hyperintense T1 signal in the pallidum
Metals
Sural nerve biopsy in patients with arsenic poisoning shows axonal degeneration involving myelinated axons of all sizes with relative sparing of unmyelinated axons. Nerve biopsy in lead poisoning shows both axonal degeneration and segmental demyelination with prominent endoneural edema. Manganese encephalopathy is characterized by selective neuronal loss and gliosis in globus pallidus with relative sparing of the substantia nigra. There is also some involvement of the subthalamic nucleus and mamillary bodies.
Background
Some debate exists as to exactly what constitutes a "heavy metal" and which elements should properly be classified as such. Some authors have based the definition on atomic weight, others point to those metals with a specific gravity of greater than 4.0, or greater than 5.0. The actinides may or may not be included. Most recently, the term "heavy metal" has been used as a general term for those metals and semimetals with potential human or environmental toxicity.[1, 2] {{RE This definition includes a broad section of the periodic table under the rubric of interest.
Regardless of how one chooses to define the category, heavy metal toxicity is an uncommon diagnosis. With the possible exceptions of acute iron toxicity from intentional or unintentional ingestion and suspected lead exposure, emergency physicians will rarely be alerted to the possibility of metal exposure. Yet, if unrecognized or inappropriately treated, heavy metal exposure can result in significant morbidity and mortality. This article provides a brief overview of general principles in the diagnosis and management of metal toxicity. The Table reviews the typical presentation of the most commonly encountered metals and their treatment in summary form. It is not intended to guide clinical decision-making in specific cases.
Many of the elements that can be considered heavy metals have no known benefit for human physiology. Lead, mercury, and cadmium are prime examples of such "toxic metals." Yet, other metals are essential to human biochemical processes. For example, zinc is an important cofactor for several enzymatic reactions in the human body, vitamin B-12 has a cobalt atom at its core, and hemoglobin contains iron. Likewise, copper, manganese, selenium, chromium, and molybdenum are all trace elements, which are important in the human diet. Another subset of metals includes those used therapeutically in medicine; aluminum, bismuth, gold, gallium, lithium, and silver are all part of the medical armamentarium. Any of these elements may have pernicious effects if taken in quantity or if the usual mechanisms of elimination are impaired.
Exposure to metals may occur through the diet, from medications, from the environment, or in the course of work or play. Where heavy metal toxicity is suspected, time taken to perform a thorough dietary, occupational, and recreational history is time well spent, since identification and removal of the source of exposure is frequently the only therapy required.
A full dietary and lifestyle history may reveal hidden sources of metal exposure. Metals may be contaminants in dietary supplements, or they may leech into food and drink stores in metal containers like lead decanters. Persons intentionally taking colloidal metals for their purported health benefits may ultimately develop toxicity. Metal toxicity may complicate some forms of drug abuse. Beer drinkerç—´ cardiomyopathy was diagnosed in alcoholics in Quebec, and later Minnesota, during a brief period in the 1970s when cobalt was added to beer on tap to stabilize the head. More recently, a parkinsonian syndrome among Latvian injection drug users of methcathinone has been linked to manganese toxicity.
Manganese- acute exposure to fumes causes MFF, Chronic Exposure causes a Parkinson-like syndrome, with respiratory and neuropsychiatric impairments.
Nearly all organ systems are involved in heavy metal toxicity; however, the most commonly involved organ systems include the CNS, PNS, GI, hematopoietic, renal, and cardiovascular (CV). To a lesser extent, lead toxicity involves the musculoskeletal and reproductive systems. The organ systems affected and the severity of the toxicity vary with the particular heavy metal involved, the chronicity and extent of the exposure, and the age of the individual.
Parkinsonism-Dementia-ALS Complex
Parkinsonism – dementia – amyotrophic lateral sclerosis complex (PDALS) is a condition well described on the island of Guam and is known there as Lytico-Bodig disease. The latter term is derived from the local Guamanian dialect, with lytico referring to the paralysis caused by the ALS component and with bodig referring to the "laziness" that describes the parkinsonian component.
Extensive genetic and environmental research has been performed on this disorder in the last 50 years. The incidence of PDALS peaked in the 1950s and has declined since then. Dietary toxins in native flour were once considered the source of a potential neurotoxin. However, this hypothesis has been ruled out. The flour is obtained from the seeds of the cycad tree. Because the seed contains a potent hepatotoxin, the flour must be washed many times before consumption. Cycasin and beta-N -methyl-amino-L-alanine (BMAA) are putative neurotoxins in the seed. If the seeds are repeatedly washed, ingestion of an estimated 70 kg of flour is required to receive a toxic dose; therefore, this hypothesis is unlikely. Toxic effects of manganese and aluminum are also being considered.
That is all I could find re:manganese and parkinson's, and it does obviously suggest that ventilation is a key way to avoid metal toxicity.
