American Journal of Epidemiology Original Contribution Parkinson's Disease and Residential Exposure to Maneb and Paraquat from Agricultural Applications in the Central Valley of California
American Journal of Epidemiology Original Contribution Parkinson's Disease and Residential Exposure to Maneb and Paraquat from Agricultural Applications in the Central Valley of California
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通讯作者:
S. Costello;M. Cockburn;J. Bronstein;Xinbo Zhang;B. Ritz
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作者:
S. Costello;M. Cockburn;J. Bronstein;Xinbo Zhang;B. Ritz
Evidence from animal and cell models suggests that pesticides cause a neurodegenerative process leading to Parkinson's disease (PD). Human data are insufficient to support this claim for any specific pesticide, largely because of challenges in exposure assessment. The authors developed and validated an exposure assessment tool based on geographic information systems that integrated information from California Pesticide Use Reports and land-use maps to estimate historical exposure to agricultural pesticides in the residential environment. In 1998–2007, the authors enrolled 368 incident PD cases and 341 population controls from the Central Valley of California in a case-control study. They generated estimates for maneb and paraquat exposures incurred between 1974 and 1999. Exposure to both pesticides within 500 m of the home increased PD risk by 75% (95% confidence interval (CI): 1.13, 2.73). Persons aged 60 years at the time of diagnosis were at much higher risk when exposed to either maneb or paraquat alone (odds ratio ¼ This study provides evidence that exposure to a combination of maneb and paraquat increases PD risk, particularly in younger subjects and/or when exposure occurs at younger ages. Parkinson's disease (PD) has been reported to occur at high rates among farmers and in rural populations, contributing to the hypothesis that agricultural pesticides might be causal agents (1–4). Animal studies have linked certain pesticides to Parkinsonism and dopaminergic cell death. The pesticide rotenone can produce the behavioral and neuro-pathologic features of PD in some rodent models through chronic systemic inhibition of mitochondrial complex I (5, 6). Exposure to a combination of the fungicide maneb and the herbicide paraquat in mice leads to increased substantia nigra neuronal pathology (7), age-dependent motor degen-eration, progressive reductions in dopamine metabolites and turnover (8), and reduced tyrosine hydroxylase and dopa-mine transporter immunoreactivity (9, 10). Human evidence is insufficient to identify any particular pesticide compound, including those implicated by animal studies, as being responsible for causing PD (11). Method-ological limitations have clouded the interpretation of most epidemiologic studies exploring pesticide exposures and PD in humans. Past studies have generally relied on self-reports and recall of chemical usage, making them vulnerable to information bias and differential recall bias (12). Because pesticides applied from the air or ground may drift from their intended treatment sites, with measurable concentrations subsequently detected in the air, in plants, and in animals up to several hundred meters from application sites (13–15), accurate methods of estimating environmental exposures in rural …