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Source: Racette BA, et al. Welding-related parkinsonism: clinical features, treatment and pathophysiology. Neurology. 2001;56:8-13.
A variety of toxins can produce acute parkinsonism, including MPTP, organophosphate pesticides, carbon monoxide, carbon disulfide, cyanide, and methanol. Although all of these agents induce a parkinsonian state, MPTP produces an illness that is clinically indistinguishable from Parkinson’s disease (PD). Patients with MPTP-induced parkinsonism are similar to PD in their response to levodopa and their propensity to develop motor fluctuations and dyskinesias. However, MPTP-induced parkinsonism differs from PD in several important ways. First, the parkinsonism is acute, evolving over hours to days to produce a typically severe akinetic-rigid state. Second, the pathology of MPTP parkinsonism is different from PD, as there are no Lewy bodies in the nigra. While the discovery of MPTP produced an explosion of interest in possible environmental triggers of PD, MPTP is clearly not responsible for sporadic PD. The search for environmental agents that are responsible for PD has been unsuccessful, until this report.
In their seminal paper, Racette and colleagues report 15 career welders who developed a parkinsonian state indistinguishable from PD. In their professional life, welders are exposed to particulate fumes and gases with high concentrations of F, Mn, Zn, Pb, As, S, Cr, Ni, CO, CO2, F, and HF. All 15 welders in this series were men, with an average occupational exposure of 47,144 welding hours. They developed symptoms of parkinsonism at an average age of 46 years, and were evaluated 8.5 years into the course of their illness.
Parkinsonian welders were clinically indistinguishable from patients with sporadic PD. The incidence of asymmetry, bradykinesia, tremor, rigidity, and postural instability were the same. Thirteen of 15 welders treated with levodopa improved, and younger patients developed motor fluctuations and dyskinesias. Two patients underwent 18-fluro-dopa PET scanning, which measures the nigro-striatal dopaminergic projection. The scans showed selective reductions of dopaminergic innervation in the posterior putamen, a pattern indistinguishable from that seen in idiopathic PD.
Racette et al compared the clinical features of their 15 welders to a group of 100 sequential patients diagnosed with idiopathic PD, and to 6 patients that were age- and gender-matched to each welder. There were no differences between the welders and PD patients in any clinical features, with the exception that welders developed their first symptoms of parkinsonism an average of 17 years before sporadic PD patients.
This is the first report to directly link an environmental exposure to an illness that is indistinguishable with PD. What is the likely mechanism to explain the development of parkinsonism in welders? Racette et al speculate that a certain population of welders may be at higher risk for the development of PD. Given an adequate exposure to inhaled welding gases, a certain proportion of welders will likely develop PD. This report adds strong support to the argument that sporadic PD may result from exposure to low levels of environmental toxins in susceptible patients.
It is not known which element in welding vapor is responsible for the development of parkinsonism, although manganese is a likely culprit. Occupational exposure to manganese produces a syndrome called manganism, characterized by extrapyramidal signs of parkinsonism and dystonia. However, the response of manganism to levodopa is only partial and often transient, and such patients often have neuropsychiatric features that were not seen in PD welders. Nevertheless, the possibility exists that long-term, low-level manganese exposure in a susceptible patient population produces a syndrome that is indistinguishable from sporadic PD. —Steven Frucht