Indoor Environmental Exposures and Dry Eye Disease: Mechanisms, Clinical Impact, and Prevention Strategies

Dry eye disease (DED) is a complex ocular surface disorder characterized by tear film instability, discomfort, hyperosmolarity, inflammation, and neurosensory dysfunction. Since individuals spend a significant amount of time inside buildings, exposure to indoor environments has emerged as a noteworthy and adjustable factor influencing ocular surface disorders. This analysis consolidates recent findings connecting indoor air contaminants, such as particulate pollutants, volatile organic substances, formaldehyde, and other gaseous irritants, as well as tobacco and cooking fumes, heavy metals, organophosphate flame retardants, and liquid crystal compounds, with the mechanisms and symptoms associated with DED. Research suggests that indoor environmental factors can exacerbate DED by triggering interconnected mechanisms such as oxidative damage, inflammation, lipid degradation, meibomian gland issues, decreased tear production, impairment of goblet cells and the mucin layer, disruption of tight junctions, and damage to the corneal or conjunctival epithelium. The most robust clinical evidence currently pertains to tobacco smoke, particulate matter, indoor air pollution, low humidity, and poor ventilation. In contrast, although biological plausibility exists for heavy metals, flame retardants, and liquid crystal monomers, the supporting data remain relatively sparse, indirect, and less comprehensive. Harmonized exposure assessments, prospective cohort studies, analyses of pollutant mixtures, and experimental intervention trials are needed to better characterize dose-response relationships and to establish effective preventive measures. Assessment of environmental history and improvement of indoor air quality should be regarded as integral and interrelated components in the prevention and management of DED.