The impact of long-term exposure to ambient air pollution and second-hand smoke on the onset of Parkinson disease: a review and meta-analysis

被引:38
|
作者
Han, C. [1 ]
Lu, Y. [2 ,3 ]
Cheng, H. [4 ]
Wang, C. [1 ,5 ,6 ]
Chan, P. [1 ,5 ,6 ]
机构
[1] Capital Med Univ, Natl Clin Res Ctr Geriatr Disorders, Xuanwu Hosp, 45 Changchun Rd, Beijing, Peoples R China
[2] Chinese Acad Med Sci, Inst Lab Anim Sci, NHC Key Lab Human Dis Comparat Med, Beijing Engn Res Ctr Expt Anim Models Human Crit, 5 Pan Jia Yuan Nan Li, Beijing, Peoples R China
[3] Peking Union Med Coll, Comparat Med Ctr, 5 Pan Jia Yuan Nan Li, Beijing, Peoples R China
[4] Huangpi Dist Hosp Tradit Chinese Med, Obstet & Gynecol Dept, 48 Banqiao Rd, Wuhan, Hubei, Peoples R China
[5] Capital Med Univ, Xuanwu Hosp, Clin Ctr Parkinsons Dis, Dept Neurobiol Neurol & Geriatr,Beijing Inst Geri, Beijing, Peoples R China
[6] Beijing Inst Brain Disorders, Parkinson Dis Ctr, Beijing Key Lab Parkinsons Dis, Key Labs Neurodegenerat Dis,Minist Educ, 45 Changchun Rd, Beijing, Peoples R China
基金
国家重点研发计划;
关键词
Air pollution; Second-hand smoke; Parkinson disease; PASSIVE SMOKING; PARTICULATE MATTER; PROSPECTIVE COHORT; GLOBAL BURDEN; RISK; NEUROINFLAMMATION; INFLAMMATION; MARKERS;
D O I
10.1016/j.puhe.2019.09.020
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Objectives: Long-term exposure to particulate and gaseous air pollution (AP) may trigger the development of Parkinson disease (PD), but this association remains controversial. The relationship between second-hand smoke (SS) and PD risk is also inconclusive. We aimed to systematically review epidemiological studies investigating the association between these AP exposures and PD risk. Study design: This was a systematic review and meta-analysis of studies investigating the relationship of ambient AP and SS with PD risk. Methods: PubMed, Embase, Web of Science, Cochrane Library, and Google Scholar databases were searched. We used a random-effects model to derive pooled estimates of relative risk (RR) and corresponding 95% confidence intervals (CIs) per increment in pollutant concentration. The studied AP included particulate matter with aerodynamic diameter <2.5 mu m (PM2.5), <10 mu m (PM10), nitrogen dioxides (NO2, NOx), ozone (O-3), and carbon monoxide (CO). Results: In total, 21 studies with 222,051 patients with PD were eligible for inclusion. We found marginally significant increased risk of PD with per 10-mu g/m(3) increase in concentration of PM2.5 (RR = 1.08, 95% CI = 0.98-1.19), NO2 (RR = 1.03, 95% CI = 0.99-1.07), and O-3 (RR = 1.01, 95% CI = 1.00-1.02). A positive but non-significant association was also detected for CO (RR = 1.32, 95% CI = 0.82-2.11). Furthermore, an inverse PD-SS relationship was noted irrespective of exposure occasions and timing (at home: RR = 0.73, 95% CI = 0.56-0.95; at work: RR = 0.82, 95% CI = 0.57-1.17; in children: RR = 0.91, 95% CI = 0.76-1.08). Both sensitivity and subgroup analyses generated results comparable with those of the overall analyses. Conclusions: Our study suggested that exposure to PM2.5, NO2, and O-3 might contribute to higher risk of PD, whereas SS conferring reduced PD risk. Public and environmental health strategies that aim at reducing outdoor AP levels might reduce the burden of PD. More prospective cohort studies with personal exposure measurements are warranted in the future. (C) 2019 The Royal Society for Public Health. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:100 / 110
页数:11
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