Association between ambient air pollution and Parkinson's disease: Systematic review and meta-analysis

Hu, Chengyang; Yuan, Fang; Li, Fengli; Dong, Bin; Hua, Xiao-Guo; Jiang, Wen Qi; Zhang, Heng; Lyu, Yong; Zhang, Xiujun

doi:10.1016/j.envres.2018.10.008

Cited by 71 publications

(36 citation statements)

References 63 publications

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“…Accordingly, a further meta-analysis found a slightly higher risk for the incidence of Parkinson’s disease on the basis of 15 studies, resulting in an RRs of 1.06 (95% CI 0.99–1.14) for PM2.5, 1.01 (95% CI 0.98–1.03) for NO 2 , 1.01 (95% CI 1.00–1.02) for O 3 , and 1.34 (95% CI 0.85–2.10) for CO following long-term exposure, while RR for hospital admission due to Parkinson’s disease was 1.03 (95% CI 1.01–1.05) in response to an increase in PM2.5 short-term exposure, with overall high heterogeneity between studies [ 69 ]. Stronger effect estimates for Parkinson’s Disease risk were found in a meta-analysis including 10 studies with RRs of 1.06 (95% CI 1.04–1.09) for NO x , 1.65 (95% CI 1.10–2.48) for CO, 1.01 (95% CI 1.00–1.03) for NO 2 , and 1.01 (95% CI 1.00–1.02) for O 3 , however, there was a high risk of bias [ 70 ].…”

Section: Evidence From Human and Animal Studiesmentioning

confidence: 99%

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

Hahad

Lelieveld

Birklein

et al. 2020

IJMS

252

107

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Exposure to ambient air pollution is a well-established determinant of health and disease. The Lancet Commission on pollution and health concludes that air pollution is the leading environmental cause of global disease and premature death. Indeed, there is a growing body of evidence that links air pollution not only to adverse cardiorespiratory effects but also to increased risk of cerebrovascular and neuropsychiatric disorders. Despite being a relatively new area of investigation, overall, there is mounting recent evidence showing that exposure to multiple air pollutants, in particular to fine particles, may affect the central nervous system (CNS) and brain health, thereby contributing to increased risk of stroke, dementia, Parkinson’s disease, cognitive dysfunction, neurodevelopmental disorders, depression and other related conditions. The underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests inflammation and oxidative stress to be crucial factors in the pathogenesis of air pollution-induced disorders, driven by the enhanced production of proinflammatory mediators and reactive oxygen species in response to exposure to various air pollutants. From a public health perspective, mitigation measures are urgent to reduce the burden of disease and premature mortality from ambient air pollution.

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Section: Evidence From Human and Animal Studiesmentioning

confidence: 99%

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

Hahad

Lelieveld

Birklein

et al. 2020

IJMS

252

107

View full text Add to dashboard Cite

show abstract

“…A wide range of both environmental and genetic risk factors have been implicated in the pathogenesis of PD [3]. Environmental risk factors include pesticides (specifically organochlorines) [4] and ambient air pollution [5]. Interestingly, tobacco [6], coffee [7], black tea [8], and a few pharmaceuticals including statins [9], calcium channel blockers [10] and ibuprofen [11], have shown some evidence of neuroprotective properties in a few studies.…”

Section: Introductionmentioning

confidence: 99%

Alpha-synuclein structure and Parkinson’s disease – lessons and emerging principles

Meade

Fairlie

Mason

2019

Mol Neurodegeneration

304

225

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Alpha-synuclein (αS) is the major constituent of Lewy bodies and a pathogenic hallmark of all synucleinopathathies, including Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). All diseases are determined by αS aggregate deposition but can be separated into distinct pathological phenotypes and diagnostic criteria. Here we attempt to reinterpret the literature, particularly in terms of how αS structure may relate to pathology. We do so in the context of a rapidly evolving field, taking into account newly revealed structural information on both native and pathogenic forms of the αS protein, including recent solid state NMR and cryoEM fibril structures. We discuss how these new findings impact on current understanding of αS and PD, and where this information may direct the field.

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“…The association between T. gondii infection and risk of PD was measured by OR. The HR and RR were considered to be equivalent to OR for the low incidence of PD in the population [34]. Heterogeneity across studies was tested by Cochran Q statistic, with a significant level of 0.1.…”

Section: Methodsmentioning

confidence: 99%

The Association between Toxoplasma gondii Infection and Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis

Zhou

et al. 2019

BioMed Research International

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Background. Several studies have investigated the association between Toxoplasma gondii (T. gondii) infection and risk of Parkinson’s disease (PD) with inconsistent results. Clarifying this relation might be useful for better understanding of the risk factors and the relevant mechanisms of PD, thus a meta-analysis was conducted to explore whether exposure to T. gondii is associated with an increased risk of PD. Methods. We conducted this meta-analysis according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. A rigorous literature selection was performed by using the databases of PubMed, Embase, Web of Science, Cochrane Library, and ScienceDirect. Odds ratio (OR) and corresponding 95% confidential interval (CI) were pooled by using fixed-effects models. Sensitivity analysis, publication bias test, and methodological quality assessment of studies were also performed. Results. Seven studies involving 1086 subjects were included in this meta-analysis. Pooled data by using fixed-effects models suggested both latent infection (OR, 1.17; 95% CI, 0.86 to 1.58; P=0.314) and acute infection (OR, 1.13; 95% CI, 0.30 to 4.35; P=0.855) were not associated with PD risk. Stable and robust estimates were confirmed by sensitivity analysis. No publication bias was found by visual inspection of the funnel plot, Begg’s, and Egger’s test. Conclusions. This meta-analysis does not support any possible association between T. gondii infection and risk of PD. Researches are still warranted to further explore the underlying mechanisms of T. gondii in the pathogenesis of PD and their causal relationship.

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Association between ambient air pollution and Parkinson's disease: Systematic review and meta-analysis

Cited by 71 publications

References 63 publications

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

Alpha-synuclein structure and Parkinson’s disease – lessons and emerging principles

The Association between Toxoplasma gondii Infection and Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis

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