Chemical Engineering Seminar

About 10% of the US population suffers from dry-eye syndrome and most everyone over age 65. Dry eye is exacerbated by dry, hot, and windy environments. Starting with the pioneering efforts of Gilbard in 1978, hyperosmotic tear has been implicated in the etiology of dry-eye syndrome. We present a periodic-steady tear-dynamics model explaining how tear osmolarity is set in homeostasis and what factors control tear hyperosmolarity including relative humidity, blink rate, tear supply, lipid health, and contact-lens wear. In addition to lacrimal supply, tear drainage kinetics, and tear evaporation, osmotic water supply from the cornea and conjunctiva is crucial to maintain low tear osmolarity. Calculations point to the importance of tear evaporation in setting tear osmolarity. Human tear is covered by a 100-nm oily layer of lipid (meibum) that is commonly thought to reduce evaporate rates preventing salt accumulation and subsequent corneal irritation. To date, however, there have been no direct studies confirming that thin layers of meibum actually reduce water evaporation. Using a miniature Langmuir trough, we study evaporation rates through thin lipid films of mineral oil, and bovine and human meibum at 35 degrees C under controlled humidity, and air flow for films of thickness ranging from 100 nm to 100 micrometers. Lipid films are visualized under white-light interferometry and interface temperature is gauged by infrared thermography. When uniformly spread, lipid films do reduce evaporation rate in agreement with simple dissolution/diffusion theory. However, the reduction in rate is minimal for on-eye thicknesses of 100 nm. We hypothesize that human meibum is not a simple oil, but rather also consists of debris from holocrine disintegration of gland epithelial cells. DSC, SAXS, WAXS, and rheology suggest a meibum architecture of waxy particles and cell debris dispersed in a nematic liquid crystal.