Cole-Hunter, Thomas, Zhang, Jiawei, So, Rina, Samoli, Evangelia, Liu, Shuo, Chen, Jie, Strak, Maciej, Wolf, Kathrin, Weinmayr, Gudrun, Rodopolou, Sophia, Remfry, Elizabeth, de Hoogh, Kees, Bellander, Tom, Brandt, Jørgen, Concin, Hans, Zitt, Emanuel, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hoffmann, Barbara, Hvidtfeldt, Ulla A, Jöckel, Karl-Heinz, Mortensen, Laust H, Ketzel, Matthias, Yacamán Méndez, Diego, Leander, Karin, Ljungman, Petter, Faure, Elodie, Lee, Pei-Chen, Elbaz, Alexis, Magnusson, Patrik K E, Nagel, Gabriele, Pershagen, Göran, Peters, Annette, Rizzuto, Debora, Vermeulen, Roel C H, Schramm, Sara, Stafoggia, Massimo, Katsouyanni, Klea, Brunekreef, Bert, Hoek, Gerard, Lim, Youn-Hee, Andersen, Zorana J, IRAS OH Epidemiology Chemical Agents, University of Copenhagen = Københavns Universitet (UCPH), National and Kapodistrian University of Athens (NKUA), Utrecht University [Utrecht], Helmholtz Zentrum München = German Research Center for Environmental Health, Universität Ulm - Ulm University [Ulm, Allemagne], Queen Mary University of London (QMUL), University of Basel (Unibas), Karolinska Institutet [Stockholm], Aarhus University [Aarhus], Medizinische Universität Wien = Medical University of Vienna, Imperial College London, University of Leicester, Heinrich Heine Universität Düsseldorf = Heinrich Heine University [Düsseldorf], Danish Cancer Society Research Center [Copenhagen, Denmark] (DCSRC), University of Duisburg-Essen, University of Surrey (UNIS), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut Gustave Roussy (IGR), National Cheng Kung University (NCKU), Ludwig-Maximilians-Universität München (LMU), Lazio Regional Health Service [Rome], NNF17OC0027812, U.S. Environmental Protection Agency, EPA: R-82811201, Health Effects Institute, HEI: 4954-RFA14-3/16-5-3, Bundesministerium für Bildung und Forschung, BMBF, Karolinska Institutet, KI, Vetenskapsrådet, VR: 2017-00641, Rijksinstituut voor Volksgezondheid en Milieu, RIVM, Novo Nordisk Fonden, NNF, Deutsches Forschungszentrum für Gesundheit und Umwelt, Helmholtz Zentrum München, This study was supported by the Health Effects Institute (HEI) (#4954-RFA14-3/16-5-3) and the Novo Nordisk Foundation Challenge Programme [NNF17OC0027812]. The HEI is an organization jointly funded by the United States Environmental Protection Agency (EPA) (Assistance Award No. R-82811201) and certain motor vehicle and engine manufacturers. The contents of this article do not necessarily reflect the views of HEI, or its sponsors, nor do they necessarily reflect the views and policies of the EPA or motor vehicle and engine manufacturers. While HEI has reviewed and approved the study design, it was not involved in data collection and analysis, decision to publish, or preparation of the manuscript. We give thanks to all participants in the pooled cohort studies and the respective study teams of the ELAPSE project for their hard work and effort. Accordingly, we especially thank Marjan Tewis for conducting data management tasks when creating the pooled cohort database. In addition, we specifically thank the National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands, for their contribution to the ELAPSE project. SALT and TwinGene are sub-studies of The Swedish Twin Registry (STR), which is managed by Karolinska Institutet and receives additional funding through the Swedish Research Council (No. 2017-00641). The KORA study was initiated and financed by the Helmholtz Zentrum München – German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. The Novo Nordisk Foundation, the Swedish Research Council, the German Federal Ministry of Education and Research, and the State of Bavaria were not involved in the study design, data collection and analysis, decision to publish, or preparation of the manuscript., HAL UVSQ, Équipe, and IRAS OH Epidemiology Chemical Agents
Background: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited. Objective: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts. Methods: Within the project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders. Results: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01–1.55), NO2 (1.13; 0.95–1.34 per 10 µg/m3), and BC (1.12; 0.94–1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58–0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95–1.62) or BC (1.28; 0.96–1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5. Conclusion: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality.