Occupational Metal Exposures and the Risk of Parkinson’s Disease

Abstract

Occupational exposure to specific metals (manganese, copper, lead, iron, mercury, zinc, aluminum and others) appears to be a risk factor for Parkinson’s disease (PD) in some, but not all, case-control studies. These epidemiological studies are reviewed. Several methodological issues that may account for the lack of unanimity of findings are discussed, and suggestions for improved case-control methodology are offered. The study of the neurological disease outcome of workers who have had long-term, well-defined occupational exposure to one or more metals is also urged, with collaborative work including industrial hygienists, occupational toxicologists, neurologists, epidemiologists and biostatisticians. Such efforts, employing state-of-the-art case and control ascertainment and enrollment from suitable population bases, neurological diagnostic rigor and exposure assessment, will help to further define the potentially important roles played by metals in PD and other neurodegenerative disorders.

Manganese Stimulation and Stereospecificity of the Dopa (3,4-Dihydroxyphenylalanine)/Tyrosine-sulfating Activity of Human Monoamine-form Phenol Sulfotransferase

“…If this indeed results in a rise in the cytosolic levels of Mn 2ϩ in such cells, the activation of M-form PST may help to detoxify the dopamine and possibly other toxic substances (as discussed below) that could be released by such dying cells. In this connection, it may be pertinent to note that manganese poisoning (or manganism) is known to result in symptoms resembling Parkinson's disease (42,43). One reason could be because the activation of M-form PST in dopaminergic cells by the excess Mn 2ϩ results in mis-guided "detoxification" of dopamine in these cells and consequently parkinsonian symptoms.…”

Mitochondrial-dependent manganese neurotoxicity in rat primary astrocyte cultures

“…In vivo, intrastriatal Mn injections result in the loss of dopaminergic neurons, resembling toxicity caused by mitochondrial poisons, such as aminooxyacetic acid and l-methyl-4-phenyl-pyridinium (MPP + ) (Brouillet EP et al, 1993). Excess brain Mn represents a risk factor for idiopathic Parkinson's disease (IPD) (Gorell et al, 1999a;1999b;Kim et al, 1999;Racette et al, 2001). The strongest correlation between any type of environmental exposure and increased susceptibility to PD is observed in Mn-exposed populations (Gorell et al, 1999a;1999b;Hudnell, 1999).…”

“…Excess brain Mn represents a risk factor for idiopathic Parkinson's disease (IPD) (Gorell et al, 1999a;1999b;Kim et al, 1999;Racette et al, 2001). The strongest correlation between any type of environmental exposure and increased susceptibility to PD is observed in Mn-exposed populations (Gorell et al, 1999a;1999b;Hudnell, 1999). Occupational exposure to Mn for >20 years or combined long-term exposures to Mn and Al (>30 years) are associated with the increased prevalence of PD (Gorell et al, 1999a;Normandin et al, 2002).…”

Amalgam dolguların insan dokuları üzerindeki etkileri

“…[36] Epidemiyolojik çal›flmalar, a¤›r metallerin ancak çok uzun bir süre sonra Parkinson Hastal›¤›na (PH) yol aça-bildi¤ini göstermifltir. [37] Elementer c›vaya ba¤l› bir PH olgusu flelatör uygulamas› ile düzelmifl, 5 y›ll›k gözlem sonras›nda de¤iflme izlenmemifltir. [38] Bir baflka çal›flmada, 14 PH hastas›n›n 13'ünde kan c›va düzeyi anlaml› derecede yüksek bulunmufltur.…”