{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T08:01:22Z","timestamp":1784793682476,"version":"3.55.0"},"reference-count":97,"publisher":"Korean Society of Occupational & Environmental Medicine","content-domain":{"domain":["aoemj.org"],"crossmark-restriction":true},"short-container-title":["Ann Occup Environ Med"],"abstract":"<jats:p>In Korea, welders diagnosed with \u201cidiopathic Parkinson's disease (iPD)\u201d often face denial of workers\u2019 compensation, as \u201cidiopathic\u201d is interpreted as excluding occupational contribution. This narrative review examines whether a categorical distinction between iPD and \u201ctoxic parkinsonism\u201d is defensible on diagnostic, pathological, neuroimaging, epidemiological, causal-inference, and legal grounds. The 2024 NSD-ISS (Neuronal \u03b1-synuclein disease Integrated Staging System) and SynNeurGe (Synuclein-Neurodegeneration-Gene) frameworks challenge categorical use of the \u201cidiopathic\u201d label by defining Parkinson's disease (PD)\u2013related disease biologically, irrespective of etiology. Nonhuman primate studies show that chronic low-dose manganese exposure can produce nigrostriatal deficits and \u03b1-synuclein aggregation overlapping with PD biology. Dichotomous use of FP-CIT dopamine transporter imaging or levodopa responsiveness to separate manganese poisoning from iPD is therefore scientifically unsound, as chronic welding exposure can induce presynaptic dysfunction and treatment responses indistinguishable from PD. Epidemiological findings diverge methodologically: direct clinical examination has reported elevated parkinsonism prevalence among welders, whereas administrative cohorts have generally found no increased PD risk. This divergence is plausibly explained by differences in case ascertainment, exposure assessment, healthy-worker-survivor selection, and disease latency. Bradford Hill and Rothman frameworks support a causal interpretation, although validated biomarkers and dose-response thresholds remain undefined. Under Korea\u2019s Industrial Accident Compensation Insurance Act, causation is evaluated as a \u201cproximate causal relationship\u201d rather than strict scientific proof. A multi-hit model integrating genetic predisposition, aging, and cumulative environmental exposure supports recognition under this standard, and compensation eligibility should not depend on whether the diagnosis label is \u2018PD\u2019 or \u2018parkinsonism.\u2019 When parkinsonian symptoms occur in welders with at least approximately 20,000 exposure-weighted welding hours, or with substantial high-intensity exposure such as confined-space welding, inadequate ventilation, or flux-cored arc welding, occupational contribution should be considered under a weight-of-evidence approach. This criterion is sufficient for recognition but is not a necessary condition.<\/jats:p>","DOI":"10.35371\/aoem.2026.38.e20","type":"journal-article","created":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T07:02:09Z","timestamp":1784790129000},"page":"e20","update-policy":"https:\/\/doi.org\/10.35371\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Reframing welders\u2019 parkinsonism: from the \u201cidiopathic\u201d label to biological causation and legal recognition"],"prefix":"10.35371","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7017-2623","authenticated-orcid":true,"given":"Chul 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