Parkinsonism due to Manganism in a Welder

Sadek, Ahmed; Rauch, Ronald A.; Schulz, Paul E.

doi:10.1080/713936672

Cited by 16 publications

(15 citation statements)

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“…Neuroepidemiological findings, albeit limited, suggest a potential relationship between welding and parkinsonism (9,10). While welding is considered a high-risk occupation for the development of manganism (52)(53)(54), it is also implicated as a potential risk factor for PD (9,14). Moreover, concerns remain that welding might enhance the risk of PD, particu- larly with early-onset forms (10,55).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction and loss of Parkinson's disease-linked proteins contribute to neurotoxicity of manganese-containing welding fumes

et al. 2010

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Welding generates complex metal aerosols, inhalation of which is linked to adverse health effects among welders. An important health concern of welding fume (WF) exposure is neurological dysfunction akin to Parkinson's disease (PD), thought to be mediated by manganese (Mn) in the fumes. Also, there is a proposition that welding might accelerate the onset of PD. Our recent findings link the presence of Mn in the WF with dopaminergic neurotoxicity seen in rats exposed to manual metal arc-hard surfacing (MMA-HS) or gas metal arc-mild steel (GMA-MS) fumes. To elucidate the molecular mechanisms further, we investigated the association of PD-linked (Park) genes and mitochondrial function in causing dopaminergic abnormality. Repeated instillations of the two fumes at doses that mimic ∼1 to 5 yr of worker exposure resulted in selective brain accumulation of Mn. This accumulation caused impairment of mitochondrial function and loss of tyrosine hydroxylase (TH) protein, indicative of dopaminergic injury. A fascinating finding was the altered expression of Parkin (Park2), Uchl1 (Park5), and Dj1 (Park7) proteins in dopaminergic brain areas. A similar regimen of manganese chloride (MnCl(2)) also caused extensive loss of striatal TH, mitochondrial electron transport components, and Park proteins. As mutations in PARK genes have been linked to early-onset PD in humans, and because welding is implicated as a risk factor for parkinsonism, PARK genes might play a critical role in WF-mediated dopaminergic dysfunction. Whether these molecular alterations culminate in neurobehavioral and neuropathological deficits reminiscent of PD remains to be ascertained.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction and loss of Parkinson's disease-linked proteins contribute to neurotoxicity of manganese-containing welding fumes

et al. 2010

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“…However, the Mn-related hyperintensities in the brains of patients with Mn intoxication disappear within about 6 months following cessation of exposure [Ejima et al, 1992;Nelson et al, 1993]. So, this biomarker of Mn exposure cannot be used long after exposure has ceased and the usefulness of MRI as a diagnostic tool for exposure assessment is limited [Sadek et al, 2003]. Moreover, at present T1-weighted MRI images have been used as a qualitative and not as a quantitative marker of Mn exposure, although a study in non-human primates showed that manganese concentrations can be calculated from actual T1-values [Bock et al, 2009] and such an approach may one-day be feasible in humans.…”

Section: Introductionmentioning

confidence: 99%

Bone manganese as a biomarker of manganese exposure: A feasibility study

Pejović‐Milić

Aslam

Chettle

et al. 2009

American J Industrial Med

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“…Hyperthyroidism may induce tremor, as well as high levels of toxic agents, such as medications (see Chapter 4), metals (manganese, lead, methylmercury, copper, iron overload), etc. (Sadek et al, 2003). Copper overload is associated with Wilson's disease (characterized by corneal deposits, overload of copper in liver, low ceruplasmine level in blood, and increased 24-h cupruria) (Benito-León and .…”

Section: Blood Studiesmentioning

confidence: 99%