The medical literature is repleat with studies and individual cases showing the link between manganism (manganese poisoning) and parkinsonism. Many welders have elevated Manganese levels from the welding rod fumes.
For example, an abstract from Department of Neurology, Chang Gung Memorial Hospital and Medical College, Taipei, Taiwan in 1998 showed that the mean scores of the King's College Hospital Rating Scale for Parkinson's disease increased from 15.0 +/- 4.2 in 1987 to 28.3 +/- 6.70 in 1991 and then to 38.1 +/- 12.9 in 1995. This study is one of many that documents the close link between manganism and Parkinsonism. They studied the long-term clinical course of five patients with chronic manganese intoxication. They found significant deterioration in gait, rigidity, speed of foot tapping, and writing. The data indicate that clinical progression in patients with manganese parkinsonism continues even 10 years after cessation of exposure.
Another study showing Parkinsonism due to manganism in a welders. This study, was of a 33-ycan ear-old right-handed male who presented complaining of a 2-year history of progressive cognitive slowing, rigidity, tremors, slowing of movements, and gait instability leading to falls. On examination, he had a Mini-Mental Status Examination (MMSE) score of 29, slowed saccadic eye pursuit, hypomimia, cogwheel rigidity, a 3- to 4-Hz tremor, and a "cock-walk" gait. His symptoms and signs were similar to idiopathic Parkinson's disease; however, he was young, inattention and forgetfulness occurred early in the course of the disorder, levodopa was unhelpful, and his gait was atypical. His work up for secondary causes of parkinsonism was negative, except for increased signal intensity on T1-weighted magnetic resonance image (MRI) in the bilateral basal ganglia. Typical etiologies for that finding were ruled-out, which led to further inquiries into the patient's lifestyle. He was a welder, and discussion with his employer revealed that he used a steel-manganese alloy, he often worked in a confined ship's hold, and he did not use a respiratory mask. Because manganese toxicity can produce increased T1-weighted signal intensities in the basal ganglia, the authors tested his serum and urine manganese, and both were elevated. This patient emphasizes the importance of a careful occupational history in persons presenting with atypical manifestations of a neurodegenerative disorder. It also lends support to the hypothesis that welding can produce enough exposure to manganese to produce neurologic impairment. This study was conducted by the Department of Neurology, Baylor College of Medicine, Houston, Texas.
One year before the Baylor case, a case was reported with Secondary progressive chronic manganism associated with markedly decreased striatal D2 receptor density, which supports the hypothesis that manganese intoxication may trigger a neurodegenerative disease process.
Manganism is of great concern because of the severe injury - parkinsonism. The manganese does damage over a long period of time, since it has a long half life (the amount of time it takes the body to reduce its manganese load by half). Thus, manganese remains in the central nervous system for a long time, and the effects of mangansim are seen later in life (onset of the disease typically is between the ages of 45 and 65). Levy describes three stages that are differentiated in manganism, including behavioral changes, parkinsonian features, and dystonia and gait disturbances. The onset of manganism includes: