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Whole-Body Lifetime Occupational Lead Exposure and Risk of Parkinson’s Disease
Abstract
Background: Several epidemiologic studies have suggested an association between Parkinson’s disease (PD) and exposure to heavy metals using subjective exposure measurements. Objectives: We investigated the association between objective chronic occupational lead exposure and the risk of PD. Methods: We enrolled 121 PD patients and 414 age-, sex-, and race-, frequency-matched controls in a case–control study. As an indicator of chronic Pb exposure, we measured concentrations of tibial and calcaneal bone Pb stores using 109Cadmium excited K-series X-ray fluorescence. As an indicator of recent exposure, we measured blood Pb concentration. We collected occupational data on participants from 18 years of age until the age at enrollment, and an industrial hygienist determined the duration and intensity of environmental Pb exposure. We employed physiologically based pharmacokinetic modeling to combine these data, and we estimated whole-body lifetime Pb exposures for each individual. Logistic regression analysis produced estimates of PD risk by quartile of lifetime Pb exposure. Results: Risk of PD was elevated by > 2-fold [odds ratio = 2.27 (95% confidence interval, 1.13–4.55); p = 0.021] for individuals in the highest quartile for lifetime lead exposure relative to the lowest quartile, adjusting for age, sex, race, smoking history, and coffee and alcohol consumption. The associated risk of PD for the second and third quartiles were elevated but not statistically significant at the α = 0.05 level. Conclusions: These results provide an objective measure of chronic Pb exposure and confirm our earlier findings that occupational exposure to Pb is a risk factor for PD.
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“Lead is predominantly stored in bone, replacing calcium. When the bone is remodeled, lead is released into the bloodstream, thus serving as a long‐term endogenous exposure source many years or decades after the original inhalation or ingestion events.”
From Risk factors for amyotrophic lateral sclerosis: A regional United States case‐control study (2021) · cites this paper as [39]
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Wirdefeldt, K., Adami, H.-O., Cole, P., Trichopoulos, D., & Mandel, J. (2011) · European Journal of Epidemiology · doi:10.1007/s10654-011-9581-6 · Cited by 1,199
Neuromelanin of the Human Substantia Nigra: An Update
Zucca, F. A., Basso, E., Cupaioli, F. A., Ferrari, E., Sulzer, D., Casella, L., & Zecca, L. (2014) · Neurotoxicity Research · doi:10.1007/s12640-013-9435-y · Cited by 243
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Metadata
- Authors
- Coon, S., Stark, A., Peterson, E., Gloi, A., Kortsha, G., Pounds, J., Chettle, D., & Gorell, J.
- Affiliations
- Department of Biostatistics and Research Epidemiology and
- Department of Pathology, Henry Ford Health System, Detroit, Michigan, USA
- Department of Radiology, St. Vincent Hospital, Green Bay, Wisconsin, USA
- Department of Neurology, Henry Ford Health System, Detroit, Michigan, USA
- Department of Molecular Biosciences, Pacific Northwest National Laboratory, Richland, Washington, USA
- Medical Physics and Applied Radiation Sciences Department, McMaster University, Hamilton, Ontario, Canada
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2006-08-18
- Volume
- 114
- Issue
- 12
- Pages
- 1872-1876
- ISSN
- 0091-6765
- 1552-9924
- PMC
- PMC1764163
- Cited by
- 161
- References
- 2
- Language
- en
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