# Long-term exposure to ambient particulate matter and its association with Alzheimer’s disease: influencing factors and a systematic review with meta-analysis

## TL;DR

This study finds that long-term exposure to certain air pollutants is linked to a higher risk of Alzheimer's disease, suggesting the need for stricter emission controls.

## Contribution

A systematic review and meta-analysis quantifying the association between ambient particulate matter and Alzheimer's disease risk.

## Key findings

- PM2.5, PM10, NO2, and NOx exposure increases Alzheimer's disease risk with statistically significant hazard ratios.
- Ozone exposure shows no significant association with Alzheimer's disease due to high heterogeneity.
- Subgroup analyses confirm that study design, region, and follow-up duration modify the observed associations.

## Abstract

Alzheimer’s disease (AD) poses a pressing public health burden globally. Evidence linking long-term ambient particulate matter exposure to AD risk remains inconsistent, necessitating systematic quantification to inform prevention policies.

We searched PubMed, Embase, Web of Science, and Cochrane Library up to September 2025 for cohort studies with ≥1 year of particulate exposure (PM2.5, PM10, NO2, NOx, O3) and incident/diagnosed AD. Quality was assessed via the Newcastle–Ottawa Scale (NOS), with random-effects models pooling hazard ratios (HRs) and 95% CIs; subgroup analyses explored heterogeneity by study design, region, and follow-up duration.

Twenty-five high-quality (NOS ≥ 7/9) cohort studies involving over 170 million participants were included. Meta-analyses showed higher AD risk with each 5 μg/m3 increase in PM2.5 (HR = 1.24, 95%CI: 1.10–1.39), 10 μg/m3 in PM10 (HR = 1.16, 95%CI: 1.01–1.33), 10 μg/m3 in NO2 (HR = 1.06, 95%CI: 1.00–1.12), and 10 μg/m3 in NOx (HR = 1.05, 95%CI: 1.03–1.07). For O3, four included studies showed no significant association (HR = 1.23, 95%CI: 0.65–2.31) with extremely high heterogeneity (I2 = 99.8%), indicating inadequate and unstable evidence. Subgroup analyses confirmed effect modification by study design, region, and follow-up duration; publication bias was low for most pollutants.

We recommend high-risk population screening, stricter emission standards, and prioritizing emission reduction in AD primary prevention—aligning with global efforts to address environmental determinants of neurological health.

PROSPERO with the registration number CRD420251174986, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420251174986.