Smog and Dry Eye Disease: A Comprehensive Review (2019–2024)

Abstract

Background: Smog, a complex mixture of particulate and gaseous pollutants, has become an increasingly prevalent environmental hazard due to industrialization, vehicular emissions, and urban expansion. While its respiratory and cardiovascular effects are well recognized, recent research highlights its emerging impact on ocular surface integrity and tear film stability. The eye, continuously exposed to environmental factors, is highly susceptible to the oxidative and inflammatory stress induced by airborne pollutants, positioning smog as a significant but modifiable risk factor for ocular disease. Objective: This review consolidates recent clinical, epidemiological, and experimental evidence (2019–2024) regarding the association between smog-related air pollution and dry eye disease (DED), with emphasis on pathophysiological mechanisms, environmental modifiers, and potential preventive approaches. Methods: A comprehensive literature review was performed using studies published between 2019 and 2024 that evaluated particulate matter (PM₂.₅, PM₁₀) and gaseous pollutants (O₃, NO₂, SO₂, CO) in relation to ocular surface inflammation, tear film disruption, and meibomian gland function. Both human and experimental models were analyzed. Results: Recent multicenter and mechanistic studies consistently demonstrate that pollutant exposure leads to oxidative stress, mitochondrial dysfunction, cytokine activation (IL-6, IL-8, TNF-α), and tear film instability. Epidemiological data confirm higher DED incidence and symptom severity during high-smog episodes, often exacerbated by low humidity and temperature extremes. Conclusion: Smog-related air pollution contributes to DED through oxidative, inflammatory, and evaporative mechanisms. Standardized exposure metrics, longitudinal monitoring, and interventional trials are essential to mitigate this preventable cause of ocular morbidity.