Manganese produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this Parkinsonism-like disease. The Lewy bodies typical to PD are not seen in Mn-induced parkinsonism. Animal experiments have given the opportunity to examine the consequences of manganese overexposure under controlled conditions.
Manganese natural gas provides the heat (needs to be at least 850 °C) and the reducing agent (carbon monoxide). This reduces all of the manganese ore to manganese oxide (MnO), which is a leachable form. The ore then travels through a grinding circuit to reduce the particle size of the ore to between 150–250 μm, increasing the surface area to aid leaching. The ore is then added to a leach tank of sulfuric acid and ferrous iron (Fe) in a 1.6:1 ratio. The iron reacts with the manganese dioxide to form iron hydroxide and elemental manganese. This process yields approximately 92%