Association Between PM2.5 Exposure and Type 2 Diabetes Across the Cardiovascular–Kidney–Metabolic (CKM) Continuum (APEX-T2D): An Umbrella Review of Systematic Reviews and Meta-Analyses

Aims: Long-term exposure to fine particulate matter (PM2.5) is a near-universal and modifiable exposure. We synthesised the systematic review-level evidence linking PM2.5 to type 2 diabetes (T2D) and examined how far agreement between reviews reflects independent replication rather than repeated analysis of shared primary studies. Methods and Results: We searched PubMed, Embase, Scopus, Web of Science and Google Scholar to 10 May 2026 (PROSPERO CRD42025642487), appraised reviews with the JBI checklist, and graded certainty using GRADE separately for each outcome domain. Thirteen systematic reviews and meta-analyses were included, spanning more than 200 million cumulative participant observations. All seven reviews reporting incident T2D found a positive association; six clustered at hazard or relative risks of 1.10–1.16 per 10 µg/m3, with a dose–response gradient and comparable estimates in Asian and Western populations. Associations were also reported for prevalent T2D (OR 1.12–1.25), diabetes-related mortality (RR 1.08, 1.03–1.13) and fasting plasma glucose (+1.18%, 0.86–1.50); HOMA-IR was null. Positive associations persisted in populations with annual means near the WHO guideline value of 5 µg/m3. Certainty was low for incident T2D—the ceiling attainable for an non-randomisable observational exposure—and very low for secondary outcomes; heterogeneity exceeded 90%, and because the reviews draw on shared primary studies their agreement is not independent replication. Conclusions: Across the whole review-level literature, long-term PM2.5 exposure is consistently associated with a 10–16% higher risk of T2D per 10 µg/m3. Because exposure is near-universal, an association of this size at the individual level implies a substantial attributable burden, greatest in South Asia. PM2.5 belongs within cardiometabolic prevention and within the cardiovascular–kidney–metabolic continuum, although causality and reversibility remain untested.