Evidence exists of a link between exposure to pesticides and herbicides and PD; a two-fold increase in risk was seen with paraquat or maneb/mancozeb exposure.[15]
Chronic manganese (Mn) exposure has been shown to produce a parkinsonism-like illness characterized by movement abnormalities.[16] 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.[16] Manganese may accumulate in the basal ganglia, leading to the abnormal movements.[17] 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.[18] The Lewy bodies typical to PD are not seen in Mn-induced parkinsonism.[17]
Agent Orange may be a cause of parkinsonism, although evidence is inconclusive and further research is needed.[19]
Other toxins that have been associated with parkinsonism are:
In the United States, the 2021 National Defense Authorization Act (NDAA) added parkinsonism to the list of presumptive conditions associated with Agent Orange exposure, enabling affected service members to receive Veterans Affairs disability benefits.[33]
^ abcAminoff MJ, Greenberg DA, Simon RP (2005). "Chapter 7: Movement disorders". Clinical Neurology (6th ed.). Lange: McGraw-Hill Medical. pp. 241–45. ISBN978-0-07-142360-1.
^ abOgawa T, Fujii S, Kuya K, Kitao SI, Shinohara Y, Ishibashi M, Tanabe Y (September 2018). "Role of neuroimaging on differentiation of Parkinson's disease and its related diseases". Yonago Acta Med (Review). 61 (3): 145–55. doi:10.33160/yam.2018.09.001. PMC6158357. PMID30275744. Parkinsonian syndromes are a group of movement disorders characterized by classical motor symptoms such as tremors, bradykinesia, and rigidity. They are most frequently due to primary neurodegenerative disease, resulting in the loss of dopaminergic nerve terminals along the nigrostriatal pathway, similar to idiopathic PD, MSA, PSP, CBD, and DLB.
^Christine CW, Aminoff MJ (September 2004). "Clinical differentiation of parkinsonian syndromes: prognostic and therapeutic relevance". The American Journal of Medicine. 117 (6): 412–9. doi:10.1016/j.amjmed.2004.03.032. PMID15380498.
^ abcdefghijklmnopqrstuvwxyzaaabacadaeafagJankovic J, Lang AE (2004). "Diagnosis and Assessment". In Bradley, Walter George (ed.). Neurology in Clinical Practice: Principles of diagnosis and management. Vol. 1. Taylor & Francis. pp. 295–96. ISBN9789997625885.
^Fabrizi, Monaco, Dalla Libera (2004). "Parkinsonian syndrome following MDMA (Ecstasy) addiction". Movement Disorders. 19: S73–S74.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^Maltête D, Guyant-Maréchal L, Mihout B, Hannequin D (March 2006). "Movement disorders and Creutzfeldt-Jakob disease: a review". Parkinsonism & Related Disorders. 12 (2): 65–71. doi:10.1016/j.parkreldis.2005.10.004. PMID16364674.
^Tse W, Cersosimo MG, Gracies JM, Morgello S, Olanow CW, Koller W (August 2004). "Movement disorders and AIDS: a review". Parkinsonism & Related Disorders. 10 (6): 323–34. doi:10.1016/j.parkreldis.2004.03.001. PMID15261874.
^Carod-Artal FJ (2003). "[Neurological syndromes linked with the intake of plants and fungi containing a toxic component (I). Neurotoxic syndromes caused by the ingestion of plants, seeds and fruits]". Revista de Neurología (Review) (in Spanish). 36 (9): 860–71. PMID12717675.