TY - JOUR
T1 - Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort
T2 - An ELAPSE study
AU - Cole-Hunter, Thomas
AU - Zhang, Jiawei
AU - So, Rina
AU - Samoli, Evangelia
AU - Liu, Shuo
AU - Chen, Jie
AU - Strak, Maciej
AU - Wolf, Kathrin
AU - Weinmayr, Gudrun
AU - Rodopolou, Sophia
AU - Remfry, Elizabeth
AU - de Hoogh, Kees
AU - Bellander, Tom
AU - Brandt, Jørgen
AU - Concin, Hans
AU - Zitt, Emanuel
AU - Fecht, Daniela
AU - Forastiere, Francesco
AU - Gulliver, John
AU - Hoffmann, Barbara
AU - Hvidtfeldt, Ulla A.
AU - Jöckel, Karl Heinz
AU - Mortensen, Laust H.
AU - Ketzel, Matthias
AU - Yacamán Méndez, Diego
AU - Leander, Karin
AU - Ljungman, Petter
AU - Faure, Elodie
AU - Lee, Pei Chen
AU - Elbaz, Alexis
AU - Magnusson, Patrik K.E.
AU - Nagel, Gabriele
AU - Pershagen, Göran
AU - Peters, Annette
AU - Rizzuto, Debora
AU - Vermeulen, Roel C.H.
AU - Schramm, Sara
AU - Stafoggia, Massimo
AU - Katsouyanni, Klea
AU - Brunekreef, Bert
AU - Hoek, Gerard
AU - Lim, Youn Hee
AU - Andersen, Zorana J.
N1 - Publisher Copyright:
© 2022 The Authors
PY - 2023/1
Y1 - 2023/1
N2 - 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.
AB - 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.
KW - Adults
KW - Air pollution
KW - Long-term exposure
KW - Low-level exposure
KW - Parkinson's Disease
KW - Pooled-cohort study
UR - http://www.scopus.com/inward/record.url?scp=85143661053&partnerID=8YFLogxK
U2 - 10.1016/j.envint.2022.107667
DO - 10.1016/j.envint.2022.107667
M3 - Article
C2 - 36516478
AN - SCOPUS:85143661053
SN - 0160-4120
VL - 171
JO - Environment International
JF - Environment International
M1 - 107667
ER -