Fine particulate matter is a potential determinant of Alzheimer's disease: A systemic review and meta-analysis.

ABSTRACT

Air pollution is a modifiable and preventable factor, and it is a possible risk factor for dementia. However, evidence from epidemiological studies is still limited. We conducted a systematic review and meta-analysis to summarize the epidemiological evidence for long-term effects of particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) on dementia/Alzheimer's disease (AD). Our inclusion criteria for eligible studies were longitudinal cohort study design, no overlap in study population, age of study subject ≥50 years, detailed description of exposure assessment for PM2.5, outdoor assessment of exposure to PM2.5, usage of a clear definition of dementia/AD, and accessibility of sufficient information for meta-analysis. Six databases were searched for eligible studies. The random-effect model was used to synthesize the associations between PM2.5 and dementia. After exclusion of all irrelevant studies, we analyzed the results of four cohort studies conducted in Canada, Taiwan, the UK, and the US during 2015-2018 among more than 12 million elderly subjects aged ≥50 years (N = 12,119,853). Our meta-analysis reveals that exposure to a 10 µg/m3 increase in PM2.5 was significantly and positively associated with dementia (pooled HR = 3.26, 95% CI 1.20, 5.31). In subgroup analyses, exposure to a 10 µg/m3 increase in PM2.5 was found to be positively associated with AD (pooled HR = 4.82, 95% CI 2.28, 7.36). Analysis of current epidemiological research on PM2.5 and dementia confirmed that exposure to PM2.5 was positively associated with a higher risk for dementia. However, it is to be noted that the included studies mainly relied on claim-based diagnosis and showed large differences in methods of exposure assessment, hence further epidemiological studies with well validated outcomes and with standardized exposure assessment models are required to ascertain the relationship between PM2.5 and dementia/AD.