Exploring causality of the association between smoking and Parkinson's disease

被引:100
作者
Gallo, Valentina [1 ,2 ,3 ]
Vineis, Paolo [2 ]
Cancellieri, Mariagrazia [1 ,4 ,5 ]
Chiodini, Paolo [6 ]
Barker, Roger A. [7 ]
Brayne, Carol [7 ]
Pearce, Neil [3 ]
Vermeulen, Roel [8 ,9 ]
Panico, Salvatore [10 ]
Bueno-de-Mesquita, Bas [2 ,11 ,12 ,13 ]
Vanacore, Nicola [14 ]
Forsgren, Lars [15 ]
Ramat, Silvia [16 ]
Ardanaz, Eva [17 ]
Arriola, Larraitz [18 ,19 ,20 ]
Peterson, Jesper [21 ]
Hansson, Oskar [22 ]
Gavrila, Diana [23 ]
Sacerdote, Carlotta [24 ,25 ]
Sieri, Sabina [26 ]
Kuehn, Tilman [27 ]
Katzke, Verena A. [27 ]
van der Schouw, Yvonne T. [8 ,28 ]
Kyrozis, Andreas [28 ,29 ]
Masala, Giovanna [30 ]
Mattiello, Amalia [10 ]
Perneczky, Robert [2 ,31 ,32 ,33 ]
Middleton, Lefkos [2 ]
Saracci, Rodolfo [34 ]
Riboli, Elio [2 ]
机构
[1] Queen Mary Univ London, Blizard Inst, Ctr Primary Care & Publ Hlth, Yvonne Carter Bldg,58,Turner St, London E1 2AB, England
[2] Imperial Coll London, Sch Publ Hlth, London, England
[3] London Sch Hyg & Trop Med, Epidemiol & Med Stat Unit, London, England
[4] Univ Campania Luigi Vanvitelli, Sch Hyg & Prevent Med, Naples, Italy
[5] AUSL Imola, Dept Publ Hlth, Hyg & Publ Hlth Unit, Bologna, Italy
[6] Univ Campania Luigi Vanvitelli, Med Stat Unit, Naples, Italy
[7] Univ Cambridge, Inst Publ Hlth, Cambridge, England
[8] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands
[9] Univ Utrecht, Inst Risk Assessment Sci, Div Epidemiol, Utrecht, Netherlands
[10] Univ Naples Federico II, Dipartimento Med Clin & Chirurgia, Naples, Italy
[11] Natl Inst Publ Hlth & Environm, Bilthoven, Netherlands
[12] Univ Med Ctr, Dept Gastroenterol & Hepatol, Utrecht, Netherlands
[13] Univ Malaya, Fac Med, Dept Social & Prevent Med, Kuala Lumpur, Malaysia
[14] Italian Natl Inst Hlth, Natl Ctr Dis Prevent & Hlth Promot, Rome, Italy
[15] Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden
[16] Univ Florence, Careggi Hosp Univ, Dept Neurosci Psychol Drug Res & Child Hlth, Florence, Italy
[17] IdiSNA, Navarra Publ Hlth Inst, Pamplona, Spain
[18] CIBERESP, CIBER Epidemiol & Publ Hlth, Madrid, Spain
[19] Basque Govt, Publ Hlth Dept Gipuzkoa, Vitoria, Spain
[20] Hosp Univ Donostia, Neurosci Area, Biodonostia Res Inst, Donostia San Sebastian, Spain
[21] Lund Univ, Dept Neurol, Lund, Sweden
[22] Lund Univ, Dept Clin Sci Malmo, Clin Memory Res Unit, Lund, Sweden
[23] IMIB Arrixaca, Murcia Reg Hlth Council, Dept Epidemiol, Murcia, Spain
[24] Ctr Canc Prevent CPO Piemonte, Canc Epidemiol Unit, Turin, Italy
[25] Human Genet Fdn HuGeF, Turin, Italy
[26] Fdn IRCCS Ist Nazl Tumori, Epidemiol & Prevent Unit, Milan, Italy
[27] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany
[28] Hellen Hlth Fdn, Athens, Greece
[29] Univ Athens, Dept Neurol 1, Athens, Greece
[30] Inst Canc Res Prevent & Clin Network ISPRO, Canc Risk Factors & Lifestyle Epidemiol Unit, Florence, Italy
[31] Ludwig Maximilians Univ Munchen, Dept Psychiat & Psychotherapy, Munich, Germany
[32] German Ctr Neurodegenerat Disorders DZNE, Munich, Germany
[33] Munich Cluster Syst Neurol SyNergy, Munich, Germany
[34] IARC, Lyon, France
基金
英国惠康基金; 欧洲研究理事会; 瑞典研究理事会;
关键词
Parkinson's disease; smoking; smoking patterns; passive smoking; causal inference; cohort study; EPIC; NeuroEPIC4PD; CIGARETTE-SMOKING; ACETYLCHOLINE-RECEPTORS; TOBACCO USE; RISK; ALCOHOL; TRAITS;
D O I
10.1093/ije/dyy230
中图分类号
R1 [预防医学、卫生学];
学科分类号
100235 [预防医学];
摘要
Background: The aim of this paper is to investigate the causality of the inverse association between cigarette smoking and Parkinson's disease (PD). The main suggested alternatives include a delaying effect of smoking, reverse causality or an unmeasured confounding related to a low-risk-taking personality trait. Methods: A total of 715 incident PD cases were ascertained in a cohort of 220 494 individuals from NeuroEPIC4PD, a prospective European population-based cohort study including 13 centres in eight countries. Smoking habits were recorded at recruitment. We analysed smoking status, duration, and intensity and exposure to passive smoking in relation to PD onset. Results: Former smokers had a 20% decreased risk and current smokers a halved risk of developing PD compared with never smokers. Strong dose-response relationships with smoking intensity and duration were found. Hazard ratios (HRs) for smoking <20 years were 0.84 [95% confidence interval (CI) 0.67-1.07], 20-29 years 0.73 (95% CI 0.56-0.96) and >30 years 0.54 (95% CI 0.43-0.36) compared with never smokers. The proportional hazard assumption was verified, showing no change of risk over time, arguing against a delaying effect. Reverse causality was disproved by the consistency of dose-response relationships among former and current smokers. The inverse association between passive smoking and PD, HR 0.70 (95% CI 0.49-0.99) ruled out the effect of unmeasured confounding. Conclusions: These results are highly suggestive of a true causal link between smoking and PD, although it is not clear which is the chemical compound in cigarette smoking responsible for the biological effect.
引用
收藏
页码:912 / 925
页数:14
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