Whole-Body Lifetime Occupational Lead Exposure and Risk of Parkinson's Disease Steven Coon,1 Azadeh Stark,2 Edward Peterson,1 Aime Gloi,3 Gene Kortsha,4 Joel Pounds,5 David Chettle,6 and Jay Gorell4 1Department of Biostatistics and Research Epidemiology, and 2Department of Pathology, Henry Ford Health System, Detroit, Michigan, USA; 3Department of Radiology, St. Vincent Hospital, Green Bay, Wisconsin, USA; 4Department of Neurology, Henry Ford Health System, Detroit, Michigan, USA; 5Department of Molecular Biosciences, Pacific Northwest National Laboratory, Richland, Washington, USA; 6Medical Physics and Applied Radiation Sciences Department, McMaster University, Hamilton, Ontario, Canada 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 = 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. Key words: case control, chronic toxicity, K-X-ray fluorescence, lead exposure, neurodegeneration, occupational exposure, Parkinson's disease. Environ Health Perspect 114:1872–1876 (2006) . doi:10.1289/ehp.9102 available via http://dx.doi.org/ [Online 18 August 2006] Address correspondence to S. Coon, Department of Biostatistics and Research Epidemiology, Henry Ford Health System, 1 Ford Pl., Suite 3E, Detroit, MI 48202 USA. Telephone: (313) 874-6229. Fax: (313) 874-6730. E-mail: scoon1@hfhs.org This article is dedicated in memory of J.M. Gorell. Financial support was provided by the National Institute of Environmental Health Sciences (grant ES 06418) , and by the William T. Gossett Parkinson's Disease Center and Louis Hayman Parkinson's Disease Research Fund, both of the Department of Neurology, Henry Ford Health System. The authors declare they have no competing financial interests. Received 15 February 2006 ; accepted 17 August 2006. The full version of this article is available for free in HTML or PDF formats. |