The Protective Effect of a Topical Mucin Secretagogue on Ocular Surface Damage Induced by Airborne Carbon Black Exposure

Abstract

PURPOSE. Exposure to airborne particulate matter can induce ocular surface damage and inflammation. We evaluated the effects of a topical mucin secretagogue on the mitigation of ocular surface damage induced by exposure to airborne carbon black (CB). METHODS. Sprague-Dawley rats were exposed to ambient CB for 2 hours twice daily for 5 days. Corneal staining score and tear lactic dehydrogenase (LDH) activity were measured to evaluate ocular surface damage. Serum immunoglobulin (Ig) G and IgE levels and the sizes of cervical lymph nodes were also measured. The expressions of interleukin (IL)-4, IL-17, and interferon (IFN)-c were measured by Western blot analysis. Diquafosol tetrasodium was instilled six times a day for 5 days, and the extent of ocular surface damage was evaluated. RESULTS. After exposure to airborne CB, the median corneal staining score and LDH activity were significantly increased. Serum IgG and IgE levels and the sizes of cervical lymph nodes were also significantly increased. Additionally, the expression of IL-4 and IFN-c was elevated in the anterior segment of the eyeball. Furthermore, the expression of IL-4, IL-17, and IFN-c was elevated in the cervical lymph nodes. When exposed to airborne black carbon, topical diquafosol tetrasodium significantly increased tear MUC5AC concentration and decreased tear LDH activity. CONCLUSIONS. Exposure to airborne CB induced ocular surface damage and increased proinflammatory cytokines in the eyes and cervical lymph nodes. Topical mucin secretagogues seem to have a protective effect on the ocular surface against exposure to airborne particulate matters.

Evidence of air pollution-related ocular signs and altered inflammatory cytokine profile of the ocular surface in Beijing

“…Tau 16 found that human corneal and conjunctival epithelial cells incubated with diesel exhaust particles showed cytotoxicity and an inflammatory response mediated by the cytokine IL-6. Li 17 considered rat animal model exposure to airborne carbon black that induced corneal fluorescein staining (CFS) increased and upregulation of IL-4 and interferon (IFN)-γ in the anterior segment. Activation of inflammatory pathways and oxidative stress are considered potential mechanisms involved in the pathogenesis of ocular surface diseases after air pollution exposure 18 , 19 .…”

Detection of Ambient Black Carbon in Conjunctival Sac Washed Fluid Reveals the Ocular Exposure Risks of Particulate Pollution

“…However, due to the complexity of the influencing factors, no significant association was found in the regression analyses after multivariable adjustment. In addition, the deposition of particles at the ocular surface may be related to ocular damage, − so multicollinearity may exist between ocular damage and environmental factors, affecting the fitting process. Despite that, the rates of detection of black carbon showed some differences relative to smoking, transport mode, living location, etc.…”

The environment and dry eye—manifestations, mechanisms, and more

“…Furthermore, an increased level of apoptosis was noted in the corneal superficial and basal epithelia in the PM 10 -treated group (specific data not provided; p < 0.05 for each) ( Li et al, 2017 ). Other in vitro human ( Tau et al, 2013 ) and animal model studies ( Li et al, 2019 ) have similarly reported increased tear cytokines after exposure to air pollutants. Another noted mechanism is corneal epithelial oxidative stress— an in vitro Chinese study that studied the effects of air pollution (up to 320 μg/100 μL of PM) on human corneal epithelial cells found a dose–response relationship between PM concentration and oxidative stress (via 8-hydroxy-2' -deoxyguanosine (8OHdG): 214 ± 6.50 pg/mL with 5 μg/100 μL of PM vs. 400 ± 38.8 pg/mL with 80 μg/100 μL of PM; p < 0.005) ( Xiang et al, 2016 ).…”