The report by
Nichols et al.
1 on the use of fluorescence quenching to demonstrate characteristics of tear thinning is perhaps the capstone of a concerted effort to understand the mechanisms of tear thinning, and likely tear film breakup. King-Smith et al. have undertaken a series of studies using multiple custom interferometers that follow the classic hypothesis-driven path to understand a fundamental question: what causes tear film thinning and instability?
2 This group postulated three potential mechanisms for tear film thinning and have investigated them systematically. The proposed mechanisms for tear thinning are epithelial absorption, tangential (or transverse) flow across the corneal surface, and evaporation.
2
Tear absorption has been discounted by analysis of epithelial and contact lens thickness data that demonstrated no thickening of either layer during eye opening.
3 Tangential flow, driven by surface tension gradients, while important in the thinning and dark area formation occurring with several local ocular surface phenomena, such as meniscus-induced thinning, corneal elevations, and during the immediate (within 2 seconds) upward flow of lipid and tear film following a complete blink, also has been disproven as the major mechanism of tear thinning. The evidence for this includes the absence of tear film thinning with the eye open under goggle (i.e., 100% relative humidity) conditions,
4 and new data in the study of Nichols et al.
1
Nichols et al. used the elegant experimental approach of simultaneous tear thickness and fluorescence quenching measurement to demonstrate a more rapid rate of fluorescent intensity loss under quenching conditions.
1 The differential was about 4- to 6-fold, and highly statistically significant, yet tear thickness decrease was similar for high and low fluorescein concentrations in normal subjects. Taken together, this body of work, including the present study, provides convincing evidence for evaporation as the major cause of tear thinning and likely tear breakup.