World Journal of Pharmaceutical
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ISSN: 2583-6579


Impact Factor: 6.916

ABSTRACT

A PRISMA-BASED SYSTEMATIC REVIEW: IMPACT OF AMBIENT AIR POLLUTION ON OCULAR SURFACE DISEASE

Namrata Srivastava*, Aleem Iqbal

Background: Ambient air pollution is increasingly recognized as an important environmental determinant of ocular surface disease (OSD), including dry eye disease (DED), conjunctivitis, blepharitis, keratitis, and allergic ocular disorders. The ocular surface is continuously exposed to environmental pollutants, making it highly vulnerable to toxic airborne particles and gases. Objective: This systematic review aims to synthesize epidemiological and mechanistic evidence examining the impact of ambient air pollutants—particularly particulate matter (PM₂.₅, PM₁₀), nitrogen dioxide (NO₂), ozone (O₃), and sulfur dioxide (SO₂)—on ocular surface health. Methods: A systematic review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was conducted. Literature searches were performed across PubMed, Embase, Scopus, Web of Science, and MEDLINE for studies published between 2018 and 2025. Studies investigating ambient air pollution exposure and ocular surface outcomes in human populations or experimental models were included. Results: A total of approximately 125 studies were included in the qualitative synthesis. Epidemiological studies consistently demonstrated associations between exposure to particulate matter and nitrogen dioxide and increased risk of dry eye disease, ocular inflammation, and meibomian gland dysfunction.[1,2,6,7] Clinical studies reported increased symptom severity, tear film instability, and elevated inflammatory cytokines in individuals exposed to higher pollution levels.[6,7] Mechanistic studies showed that particulate matter induces oxidative stress, epithelial damage, inflammatory signaling, and disruption of tear film integrity.[8,9,10] Conclusions: Ambient air pollution represents a significant modifiable environmental risk factor for ocular surface disease. Further longitudinal and interventional studies are required to establish causal relationships and develop targeted prevention strategies.

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