Air pollution was found to create DED-related inflammation in individuals. Photo: Getty Images. Click image to enlarge.

Dry eye disease (DED) is a multifactorial disease where homeostasis of ocular surface tear film is dysregulated and accompanied by ocular symptoms including tear film instability and hyperosmolarity, ocular surface inflammation and damage and neurosensory abnormality. In recent years, with the aggravation of air pollution, the prevalence of DED has increased year by year. A previous study by researchers in Shanghai found that particulate matter 2.5 (PM_2.5), or tiny particles or droplets in the air that are 2.5µm or less in width, was a potential risk of DED. Their most recent study explored the reaction’s pathogenesis and showed that PM_2.5 can cause DED-related inflammatory reactions on corneal epithelial cells.

The researchers conducted animal exposure and cell-based studies to evaluate the pathogenic effect of PM_2.5 exposure on the ocular surface and DED etiological mechanisms. Lab mice were exposed to filtered air and PM_2.5 aerosol, and the research team assessed health conditions and inflammation of the ocular surface by corneal fluorescein staining and immunohistochemistry. In parallel, cultured human corneal epithelial cells were treated with PM_2.5, followed by characterization of cell viability, intracellular ATP level, mitochondrial activity and expression level of DED-relevant mRNA and proteins.

In mice, PM_2.5 exposure induced severe superficial punctate keratopathy and inflammation in the cornea. In cultured human corneal epithelial cells, cell proliferation and reactive oxygen species (ROS) generation followed a dose-response and time-dependent manner; meanwhile, mitochondrial ROS level increased and mitochondrial membrane potential level decreased.

The study further explored the reaction’s mechanism: ROS from mitochondrial dysfunctions of corneal epithelial cells after PM_2.5 exposure inhibited the expression of anti-inflammatory protein Nrf2 and led to the activation of inflammatory protein NF-κB P65 and its downstream molecules, which finally caused inflammation reaction.

“The toxic reaction of PM_2.5 was mainly manifested in the inflammatory reaction on the ocular surface,” the study authors wrote in their paper. “The eyes are directly exposed to the air for a long time, so the impact of particulate matter on the ocular surface is prominent.”