Year : 2018 | Volume
: 8 | Issue : 2 | Page : 33--34
Environmental Chemicals and Parkinson’s Disease
Shaaban Abdelfattah1, Mohamed Salama2, Rania Hamed Abdel-Rahman1, Laila El-Zalabany1, Mona El-Harouny1,
1 Clinical Toxicology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
2 Clinical Toxicology Department, Faculty of Medicine, Mansoura University, Mansoura; Medical Experimental Research Center (MERC), Faculty of Medicine, Mansoura University, Mansoura, Egypt
Clinical Toxicology Department, Faculty of Medicine, Mansoura University, Mansoura-35516
|How to cite this article:|
Abdelfattah S, Salama M, Abdel-Rahman RH, El-Zalabany L, El-Harouny M. Environmental Chemicals and Parkinson’s Disease.Int J Nutr Pharmacol Neurol Dis 2018;8:33-34
|How to cite this URL:|
Abdelfattah S, Salama M, Abdel-Rahman RH, El-Zalabany L, El-Harouny M. Environmental Chemicals and Parkinson’s Disease. Int J Nutr Pharmacol Neurol Dis [serial online] 2018 [cited 2019 Dec 7 ];8:33-34
Available from: http://www.ijnpnd.com/text.asp?2018/8/2/33/231272
The interest toward the environmental causes of Parkinson’s disease (PD) was initiated when the chemical 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine “MPTP” was identified as causing manifestations clinically similar to PD. These observations provided proof to the hypothesis that environmental chemicals exposure could cause PD. Environmental chemicals refer to the chemical elements present in air, water, food, soil, or other environmental media, for example pesticides, solvents, metals, and air pollutants.
Pesticides include hundreds of chemicals with widely different structures and effects. Identifying the specific chemicals is important to understand the disease pathogenesis. It was claimed that pesticides exposure is associated with PD. Oxidative stress and neuroinflammation are the potentially involved mechanisms in both PD pathophysiology and pesticide neurotoxicity. Susceptibility to PD due to pesticides exposure may occur through the modification of genes responsible for coding detoxifying enzymes. For example, alterations in the neuronal aldehyde dehydrogenase enzymes are associated with an increased risk of the development of PD in the persons who are exposed to fungicides.
Occupational exposure to chlorinated solvents such as trichloroethylene is associated with an increased risk of PD. Experimental studies showed that trichloroethylene causes parkinsonism in rats, producing degeneration of dopaminergic neurons, reactive microglia, mitochondrial complex I inhibition, oxidative stress, and alpha-synuclein aggregation.
There is an increased risk of PD when people are exposed to various metals including manganese (Mn), iron, and copper. Chronic manganese exposure results in its accumulation in brain, causing brain dysfunctions and extrapyramidal manifestations similar to PD known as Mn-induced parkinsonism or manganism, and this can be explained by the oxidative stress and mitochondrial dysfunction caused by Mn. It was also found that iron and copper chronic exposure can be a risk of PD through the production of free radicals that cause lipid, protein, and deoxyribonucleic acid (DNA) oxidation, potentially resulting in dopamine neuron cell death.
Some epidemiological studies linked ambient air pollutants to the PD incidence. Air pollutants such as nitrogen dioxide may affect the brain either directly through the transport of pollutants from the olfactory bulb or through the systemic inflammation that contributes to the neurodegenerative process.
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