Dry eye disease (DED) is a highly prevalent multifactorial chronic condition, with reported prevalence rates ranging widely from 5% to 50% across populations. DED significantly impacts ocular health, leading to blurred vision, instability of the tear film, increased risk of damage to the ocular surface such as scarring of the cornea, and changes in the eye including the neurosensory system. Given its substantial burden, there is an urgent need for targeted public health strategies to mitigate DED risk factors, enhance early detection, and implement effective management protocols. Epidemiological evidence confirms associations between DED incidence and modifiable lifestyle factors (e.g., visual display terminal (VDT) usage duration, sleep patterns) and environmental exposures (e.g., smoking, air pollution). However, the precise mechanisms by how these factors contribute to disease pathogenesis remain poorly defined. Emerging research also suggests a critical role for genetic susceptibility and gene-environment interactions in DED development.
This study therefore proposes to (1) How do modifiable lifestyle factors (e.g., visual display terminal (VDT) usage duration, sleep patterns, smoking) independently and cumulatively influence DED risk? (2) To what extent do environmental exposures (e.g., air pollution, occupational metals) contribute to DED pathogenesis? (3) What is the role of genetic susceptibility and gene-environment interactions in mediating DED development?
Utilizing large-scale cohort with longitudinal data enables the robust adjustment for confounders (e.g., age, sex, comorbidities) when examining exposure-disease relatio. By leveraging integrated genetic, lifestyle, and environmental data, this study will help to elucidate mechanistic pathways driving DED, enabling future targeted interventions.