A study of the relationships between Parkinson's disease and markers of traffic-derived and environmental manganese air pollution in two Canadian cities

There is concern that industrial emissions of manganese (Mn) and the use of Mn-containing compounds as fuel additives might increase the population risk of Parkinson's disease (PD)-like disorders. We investigated associations between the diagnosis and treatment of PD and markers of exposure to...

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Bibliographic Details
Published in:Environmental research 2007-07, Vol.104 (3), p.420-432
Main Authors: Finkelstein, Murray M., Jerrett, Michael
Format: Article
Language:English
Subjects:
Adult
Aged
Air
Air Pollutants - analysis
Air Pollutants - toxicity
Air pollution
Antiparkinson Agents - therapeutic use
Biological and medical sciences
Canada - epidemiology
Case-Control Studies
Chemical and industrial products toxicology. Toxic occupational diseases
Cities
Cohort Studies
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Environmental pollutants toxicology
Humans
Levodopa - therapeutic use
Manganese
Manganese - analysis
Manganese - toxicity
Medical sciences
Metals and various inorganic compounds
Middle Aged
MMT
Nervous system (semeiology, syndromes)
Nervous system as a whole
Neurology
Parkinson Disease - drug therapy
Parkinson Disease - epidemiology
Parkinson Disease - etiology
Parkinson Disease - pathology
Parkinson's disease
Toxicology
Traffic
Vehicle Emissions - analysis
Vehicle Emissions - toxicity
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Summary:There is concern that industrial emissions of manganese (Mn) and the use of Mn-containing compounds as fuel additives might increase the population risk of Parkinson's disease (PD)-like disorders. We investigated associations between the diagnosis and treatment of PD and markers of exposure to vehicle exhaust and industrial emissions of Mn within a cohort of 110,000 subjects in the cities of Toronto and Hamilton, Canada. Methylcyclopentadienyl manganese tricarbonyl (MMT) has been added to Canadian gasoline since 1976 and steelmaking in Hamilton emits Mn to the air. Using residential postal codes, subjects were mapped to: (1) residence locations close to traffic and to neighbourhood levels of NO 2, as markers of traffic-generated air pollution (TGAP); and, (2) neighbourhood levels of ambient Mn in Hamilton, as measured by the Mn fraction of total suspended particulate. Subjects were linked to Ministry of Health administrative databases, 1992–1999, to identify physicians’ diagnoses of PD and prescriptions for l-Dopa containing medications. In Toronto, we found no association between PD and the markers of TGAP. In Hamilton, the odds ratio for a physician's diagnosis of PD was 1.034 (1.00–1.07) per 10 ng/m 3 increase in Mn in TSP. The estimate of the “doubling exposure” for physician-diagnosed PD was about 150 ng/m 3 Mn in TSP. Examination of prevalence curves suggested that exposure to ambient Mn advances the age of diagnosis of PD, consistent with the theory that exposure to Mn adds to the natural loss of neurons attributable to the aging process.
ISSN:0013-9351
1096-0953
DOI:10.1016/j.envres.2007.03.002