Abstract / Summary
BackgroundAir pollution is increasingly recognized as a potentially modifiable environmental determinant of age-related ocular disease, but its association with cataract remains incompletely characterized. Epidemiological evidence remains heterogeneous across pollutants and study methods, although emerging experimental findings support biological plausibility for pollution-related lens injury.ObjectivesTo systematically evaluate the epidemiologic evidence linking air-pollution exposure with cataract-related outcomes and to quantitatively synthesize pollutant-specific associations where sufficiently comparable data were available.MethodsPubMed, Embase, Scopus, Web of Science, and Google Scholar were searched through August 10, 2026 for observational studies reporting cataract-specific associations with specific air pollutants. Risk of bias was assessed using ROBINS-E for longitudinal follow-up studies and the WHO air-quality epidemiology instrument for cross-sectional and aggregate studies. Comparable hazard ratios (HRs) were synthesized using restricted maximum-likelihood random-effects models in Stata 18, with Knapp–Hartung sensitivity analyses.ResultsFifteen studies were included in the systematic review, of which seven contributed to at least one meta-analysis. The pooled HR was 1.036 (95% CI, 0.988–1.086) per 1 µg/m3 increase in PM₂.₅, 1.041 (95% CI, 1.013–1.070) per 10 µg/m3 increase in NO₂, and 1.010 (95% CI, 0.983–1.038) per study-specific interquartile-range increase in black carbon. Heterogeneity was substantial for PM₂.₅ (I2 = 99.68%) and NO₂ (I2 = 86.04%) but lower for black carbon (I2 = 33.41%). The highest-versus-lowest quartile analysis also showed a positive association for NO₂ (HR, 1.094; 95% CI, 1.057–1.133; I2 = 0.11%), whereas corresponding PM₂.₅ and PM₁₀ estimates were not statistically significant. Knapp–Hartung adjustment widened the NO₂ confidence intervals, indicating sensitivity to the small number of contributing studies.ConclusionNO₂ showed the most consistent association with cataract outcomes, whereas evidence for PM₂.₅ remained heterogeneous and that for black carbon was limited. Although these findings support further investigation of traffic-related and other ambient pollution mixtures in cataract epidemiology, the sensitivity of NO₂ estimates to small-study inference precludes firm causal conclusions. Independent prospective studies with improved exposure assessment and standardized cataract phenotyping are needed.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/recorddashboard#, identifier CRD420261509514.