You are here
Home > CPD Archive > What is the Effect of a Contact Lens on the Tear Film?

What is the Effect of a Contact Lens on the Tear Film?

SASHABy Sasha Lee Price, Final year B Optom student University of Johannesburg, Department of Optometry

Reviewed by Dr Dirk J Booysen, Lecturer (Contact Lenses), University of Johannesburg, Department of Optometry


The tear film plays a vital role in ocular health (Nong and Anderson, 2010),vision and the maintenance of a uniform optical surface (Fath-Elrahman et al., 2015). A stable tear film is also necessary for defence and lubrication. In situ, contact lenses (CLs) divide the tear film into pre-lens and post-lens films (Figure 1). This compartmentalisation impacts the tear film in a number of ways, affecting both its biophysical and biochemical properties (Craig et al., 2013, Mann and Tighe, 2013).

The contact lens is approximately 10x thicker than the aqueous layer of the normal tear film and its interaction with the tear film is dependent on the lens material and the individual tear chemistry of the wearer (Mann and Tighe, 2013). The lens sits in the ocular environment and creates two active interfaces which result in interaction between the surface of the lens and the lid, leading to movement of the lens on the ocular surface. These forces are dynamic and involve both sliding and shearing forces rather than just simple compression (Mann and Tighe, 2013). Contact lens wear can deplete the tear layer of specific components and stimulate the biochemical generation of additional components, such as albumin or inflammatory mediators (Mann and Tighe, 2013). It is therefore not surprising that contact lens wearers are recognised to exhibit significantly more ocular symptoms than non-wearers (Craig et al., 2013).

Biophysical Changes

Biophysical evaluation includes non-invasive tear break up time, TBUT, meniscus height, lipid layer interferometry, maximum blink interval, tear flow rate, meniscus area, tear evaporation, Schirmer test, optical coherence tomography and ocular thermography.

Figure 1 Effect of a contact lens on the tear film

Blink Impact on Pre-Corneal and Pre-Lens Tear Film Spread and Volume

The eyelid normally covers less than 67% of the cornea (Abelson and Holly, 1977). To help maintain clear vision and ocular surface health, a blink occurs to distribute tears over the ocular surface and cornea. Two types of blink can be distinguished, complete and incomplete blinks. The proportion of incomplete blinking in healthy subjects (without contact lenses) is ± 20% (McMonnies, 2007). The movement of the eyelid over the surface of a contact lens causes frictional stimulation which may lead to a biochemical response and the release of inflammatory mediators into the tear film (Mann and Tighe, 2013). With a contact lens in situ, the following have been observed repeatedly:

  • Higher percentage of incomplete blinks in RGP wearers (Van Der Worp et al., 2008)
  • Soft lens wearers have a similar percentage of incomplete blinks to non-wearers. However, there is an association of incomplete blinks in soft contact lens wearers with corneal staining, discomfort, lens deposits and dryness (Collins et al., 2006)
  • Inter-blink interval can be increased in both RGP and soft lens wearers to compensate for tear film instability and continuous friction between contact lens, palpebral conjunctiva and the cornea (Craig et al., 2013)
  • Stagnation of the post-lens tear film with contact lens wear leads to inflammation due to prolonged retention of cells, microorganisms and debris. This leads to an increase in the cytokines interleukin, and fibronectin and a decrease in polymorphonuclear leucocyte recruitment and immunoglobulin A in the tear film (Stapleton et al., 2006).

Lipid Layer

The two major functions of the lipid layer are to; lower the tear surface tension, thereby allowing the tear film to maintain a high area-to-volume ratio, and to inhibit the aqueous tear evaporation (Craig et al., 2013). With a contact lens in situ, the aqueous layer is split in two and the thin pre-lens aqueous layer (2-6 µm) results in a deteriorating lipid layer (Craig et al., 2013, Nong and Anderson, 2010, Stapleton et al., 2006). The pre-lens tear film is influenced by lens diameter, lens type, wearing schedule, surface chemistry and lens fit (Stapleton et al., 2006). The deterioration of the lipid layer can result in patches of poor wettability and therefore, direct interaction between the lipid layer and the lens surface (Yokoi et al., 2008). Lipid deposition is especially problematic in silicone hydrogel lenses, where after continuous wear hydrophobic lipid-attractive patches readily appear over the contact lens surface (Jones et al., 2003, Mann and Tighe, 2013). Once formed, these deposits result in impaired vision and non-wetting lens surfaces with instantaneous TBUT’s (Mann and Tighe, 2013). Clinically no pre-lens lipid layer is visible with RGP lenses (Craig et al., 2013).

Tear Film Stability

Contact lenses disrupt the tear film lipid layer and reduce tear film thickness (Mann and Tighe, 2013). This disruption is most marked with RGP lenses, where typically no pre-lens lipid layer is visible clinically and tear break up (TBU) occurs within 2-3 seconds, in contrast to 5-6 seconds with soft lenses (Craig et al., 2013). Overall, tear film thinning has been shown to be significantly faster on the surface of a contact lens than on the corneal surface (Nichols et al., 2005). The location of the TBU is also different in the lens-wearing eye, occurring in the centre of the lens,  compared to the non-lens-wearing eye, where the location is more peripheral (Bruce et al., 2001). Pre-ocular TBUT is initially significantly lower after lens removal. However, over the longer term it appears to be largely unaffected by contact lens wear (Craig et al., 2013). Lower pre-ocular TBUT’s are associated with increased symptoms of discomfort with both hydrogel and silicone hydrogel lens wearers (Craig et al., 2013). Hom and Bruce, 2009 suggested a cut-off TBUT value of 3 seconds as a suitable criterion for identifying tear film dysfunction likely to cause symptoms of dryness in contact lens wearers (Hom and Bruce, 2009). Lower pre-lens TBUT can cause problems with visual acuity, which combined with changes in tear film quality and comfort may lead to increased intolerance of contact lens wear (Thai et al., 2002, Tutt et al., 2000).

Tear Film Evaporation

The normal tear film is lost from the ocular surface by evaporation, absorption, and drainage (Craig et al., 2013). However, evaporation remains the main cause of tear film thinning (King-Smith et al., 2008, Kimball et al., 2010). Due to disruption of the lipid and aqueous layers, the rate of tear film evaporation increases with contact lenses in situ (Guillon and Maissa, 2008, Refojo, 1991). Contact lens wear typically result in a 1.2 – 2.6x increase in the rate of tear evaporation independent of either lens type or water content (Craig et al., 2013). Increased evaporation rates lead to increased osmolarity, discomfort and dryness in contact lens wearers (Craig et al., 2013).

Tear Film Temperature

Due to its exposed position, the temperature of the normal ocular surface and tear film, is lower than core body temperature (32 – 36°C) (Efron et al., 1989). Pre-lens temperatures in soft lens wearers are cooler than that of the ocular surface without lenses, while the temperature of the post-lens tear film beneath the contact lens is higher (Craig et al., 2013) (Ooi et al., 2007). Higher water content lenses with corresponding rapid rate of water loss, show lower surface pre-lens temperatures (Ooi et al., 2007, Purslow et al., 2005). Silicone hydrogel lenses have higher post-lens tear temperatures than hydrogel lenses due to lower rate of water loss from these lenses (Purslow et al., 2005).

Tear Film Thickness

The pre-lens tear film initially increases when the lens is placed on the eye. This is due to reflex tearing and excess wetting solution. However, this increase is transient and fairly rapidly settles down to about 2 – 3 µm (Wang et al., 2003). Post-lens tear film is thinner (1-3 µm) and the thinning rate is higher compared to the pre-corneal tear film (Wang et al., 2003). Depletion of the post lens tear film may impact lens movement, cause lens adherence and surface staining, which can lead to contact lens complications and discomfort (Craig et al., 2013). The post-lens film has a more variable thickness than the pre-lens tear film which is possibly due to the relationship between the posterior lens surface and the corneal curvature as well as lid pressure. Factors which have an impact on the post-lens tear film are radius of the optic zone, aperture size, lens modulus, and even ethnicity. Non-Asian eyes have been found to have a thicker post-lens thickness than Asian eyes (Stapleton et al., 2006). The post-lens tear film requires optimal tear exchange to maintain a normal ocular surface and prevent complications, especially in extended wear of soft lenses. The optimal value for post-lens tear exchange has not yet been clearly determined, but the dispersive mixing model suggests that vertical and transverse lens movement are necessary (Stapleton et al., 2006). In the presence of a contact lens, the post-lens tear film has decreased tear flow which increases the potential for biochemical component absorption (Mann and Tighe, 2013, Stapleton et al., 2006). RGP lenses have less retention of debris and higher tear exchange rates in comparison to soft contact lenses. As a result, the rate of inflammatory complications is less with extended and daily RGP lens wear (Stapleton et al., 2006).

Tear Production/Turnover

An average tear turnover rate of 15.5%/minute is typical of normal young subjects without lenses (Occhipinti et al., 1988, Kok et al., 1992). Tear turnover rate decreases significantly in contact lens wear, 12.4%/minute in hydrogel lens wear, and 13.2%/minute in silicone hydrogel wear (Kok et al., 1992, Craig et al., 2013).

Tear Volume

In the normal tear system, as little as 2 – 4 µl of tear volume is required to maintain a wet surface (Craig et al., 2013). With each blink the tears are mixed and redistributed. The normal tear meniscus volume is 1.5 µl (Palakuru et al., 2007). With a contact lens on the eye the tear meniscus volume is 1 µl, this further decrease over time during lens wear (Chen et al., 2010). Lower tear meniscus volumes are related to increased ocular discomfort at the end of the day, as well as corneal staining (Craig et al., 2013).

Tear Exchange

Tear exchange or mixing during lens wear may be regulated by the interrelationships between four variables: lens diameter, movement, the blink, and tear replenishment rate (Muntz et al., 2015). The tear exchange rate beneath a soft contact lens was about 9%/minute (Paugh et al., 2001) and 0.2%/minute under a scleral lens. Based on this rate, it would take > 8 hours to replenish the fluid under a scleral lens (Vance et al., 2015).


During contact lens wear tear film osmolarity undergoes a series of changes. Initially, the insertion of a contact lens results in a reduction of osmolarity due to reflex tearing (Craig et al., 2013). A subsequent increase in osmolarity is then observed (Craig et al., 2013). Wearing soft lenses on an extended wear basis and RGP lenses on a daily wear basis significantly increased tear osmolarity. However, this did not occur while wearing soft lenses on a daily wear basis (Craig et al., 2013). No differences have been observed between hydrogel and silicone hydrogel lenses (Craig et al., 2013). The increase in tear osmolarity in contact lens wear have been attributed to two factors; reduced tear production due to reduced corneal sensitivity, and excessive evaporation due to disrupted tear film and reduced tear film stability (Gilbard et al., 1986).

Tear pH

The tear film pH varies throughout the day shifting from acid to alkaline (0.6 units) (Craig et al., 2013). The tear film is more acidic in contact lens wear, decreasing between 0.27-0.53 units due to increased tearing and blinking. Whereas, eyelid opening leads to alkalisation due to equalisation of the partial pressure of CO2 to that of the surrounding air (Craig et al., 2013). This acidification (decrease in pH) has been observed in the post-lens tear film in both RGP and soft lenses and have been attributed to the lens preventing CO2 loss from the ocular surface and tear fluid (Chen and Maurice, 1990).


Normal human tears have viscosity rates of 1 -10 mPa depending on the shear rate (Craig et al., 2013). Although, it was initially thought that the main contributor to tear viscosity was mucin, recent studies have shown that proteins and lipids also play a role (Gouveia and Tiffany, 2005). The effect of contact lens wear on viscosity is currently not known (Craig et al., 2013).

Surface Tension

Tear film surface tension is around 2/3rds of that of water or saline (Miller, 1969, Zhao and Wollmer, 1998). Higher the surface tension leads to faster the TBUT. Tear film lipids are probably the most important contributors to surface tension due to the amphipathic nature of their polar components. Not much information is available on the effect of a contact lens on the tear surface tension. However, the lipid layer is disturbed by the presence of a lens and one can therefore assume that the surface tension will also be influenced (Craig et al., 2013).

To summarise, the presence of a contact lens divides the tear film into a pre-lens and post-lens tear film and creates new interfaces with and within the ocular environment. The biophysical changes to the tear film properties introduced include; decreased tear film stability, decreased tear turnover rate, decreased pre-lens lipid layer thickness, decreased tear volume, and an increase in evaporation rate. Additionally, tear osmolarity increases, tear temperature decreases, and pH becomes more acidic.

Biochemical Changes

The lens is the guest and the ocular environment is the host. Interaction between the two will be affected by both the characteristics of the guest, such as material, modulus, permeabilities and coefficient of friction,  as well as those of the host, such as individual tear chemistry, level of adaptation and duration of lens wear (Mann and Tighe, 2013). As soon as the lens is inserted it will be coated by components of the tear film including lipids, proteins and mucins. The movement of the lens over the surface of the lens causes friction and mechanical stimulation which can upregulate the inflammatory response. The reduced tear flow between the posterior surface of the lens and cornea, due to a less dynamic interaction between the tears and the corneal epithelium, can lead to alterations in protein deposits on the posterior surface compared to the anterior surface of the lens and its sequelae (Mann and Tighe, 2013).


As mentioned earlier, the pre-lens tear film lipid layer’s thickness and stability is disrupted by the presence of a contact lens on the eye and silicone hydrogel lenses are particularly prone to lipid interaction and deposition (Mann and Tighe, 2013, Craig et al., 2013). Exposure to oxygen and UV light leads to lipid oxidation, a process known as auto-oxidation, which in combination with enzymes break down the lipids from their native states to the end products of lipid oxidation – peroxide and hydroperoxide (Mann and Tighe, 2013). The presence of these end products and their effect on contact lens wear has not been fully investigated. However, they may contribute to “end of day” discomfort in symptomatic contact lens patients (Mann and Tighe, 2013).


Protein denaturation, or a change in conformation of the protein, results in the protein losing its native biological function or properties. Protein denaturation on the lens surface (and in lens matrix) may be due to interaction with lens surface, material, tear chemistry changes, lens drying, and solution interactions (Mann and Tighe, 2013). Denatured protein is not recognised as “self” and has been linked to CLPC or GPC (Mann and Tighe, 2013). Additionally, plasma-derived proteins (albumin and plasmin) can be found in the tears of contact lens wearers. This indicates that the tear-blood barrier is compromised. This is probably due to some level of material-induced plasma leakage, increased vascular permeability, and/or changes in indigenous protein secretion such as IgA from the lacrimal gland (Mann and Tighe, 2013). Plasmin can cause epithelial abnormalities due to its proteolytic activity (Mann and Tighe, 2013). Albumin is useful as a marker for vascular leakage into the ocular environment. Although contact lens wear leads to leakage of albumin into the tears, levels decrease rapidly upon lens removal, indicating that once the stimulus is removed the plasma leakage subsides (Mann and Tighe, 2013). The presence of albumin in tears suggest that other plasma derived components such as cytokines should also be present and indeed lens wear has been shown to have an influence on cytokine levels in the tear film (Mann and Tighe, 2013, Craig et al., 2013).


Contact lens wear and cleaning solutions are associated with a decrease in the amount of secreted mucins at the ocular surface as well as damage to the glycocalyx formed by transmembrane mucins (Craig et al., 2013). This is in part due to a decrease in the number of conjunctival goblet cells (Mann and Tighe, 2013). Mechanical interaction of the contact lens, the epithelial surface and the blinking forces of the lid are involved in the formation of mucin balls. Mucin balls are usually seen with silicone hydrogel soft contact lenses and form between the corneal epithelium and posterior lens surface. They cause marked indentation to both these surfaces, which recovers when the lens is removed. Contributing factors are predisposition of the individual such as higher amounts of post-lens debris and steep corneal curvature, or properties of the lens material such as surface wettability. Dehydration of the post-lens tear film causing mucin matrix collapse may also be a causative factor for mucin ball formation. The clinical consequences of mucin balls appear to be insignificant (Stapleton et al., 2006). Mucin fragmentation and degradation was observed in asymptomatic contact lens wearers as a result of a new material leading to increased discomfort (Mann and Tighe, 2013, Craig et al., 2013).


It is clear that substantial changes occur in the tear film with contact lens wear. However, although it is difficult to understand the implications of the individual changes, the literature is shows that they have a large impact on the dryness, inflammation and end of day comfort experienced by contact lens patients.  Future lens materials and cleaning products (solutions) will no doubt address the biophysical and biochemical tear layer changes associated with lens wear and thereby hopefully improve the comfort and health of our contact lens patients significantly.


ABELSON, M. B. & HOLLY, F. J. 1977. A tentative mechanism for inferior punctate keratopathy. Am J Ophthalmol, 83, 866-9.

BRUCE, A., C. MAINSTONE, J. & R. GOLDING, T. 2001. Analysis of tear film breakup on Etafilcon A hydrogel lenses.

CHEN, F. S. & MAURICE, D. M. 1990. The pH in the precorneal tear film and under a contact lens measured with a fluorescent probe. Exp Eye Res, 50, 251-9.

CHEN, Q., WANG, J., TAO, A., SHEN, M., JIAO, S. & LU, F. 2010. Ultrahigh-resolution measurement by optical coherence tomography of dynamic tear film changes on contact lenses. Invest Ophthalmol Vis Sci, 51, 1988-93.

COLLINS, M. J., ISKANDER, D. R., SAUNDERS, A., HOOK, S., ANTHONY, E. & GILLON, R. 2006. Blinking patterns and corneal staining. Eye Contact Lens, 32, 287-93.

CRAIG, J. P., WILLCOX, M. D. P., ARGÜESO, P., MAISSA, C., STAHL, U., TOMLINSON, A., WANG, J., YOKOI, N. & STAPLETON, F. 2013. The TFOS International Workshop on Contact Lens Discomfort: Report of the Contact Lens Interactions With the Tear Film Subcommittee. Investigative Ophthalmology & Visual Science, 54, TFOS123-TFOS156.

EFRON, N., YOUNG, G. & BRENNAN, N. A. 1989. Ocular surface temperature. Curr Eye Res, 8, 901-6.

FATH-ELRAHMAN, N., MERGHANI, I., ABDU, M. & BINNAWI, K. 2015. The effects of rigid gas-permeable contact lens wear on tear film of eyes with keratoconus. Sudanese Journal of Ophthalmology, 7, 6-9.

GILBARD, J. P., GRAY, K. L. & ROSSI, S. R. 1986. A proposed mechanism for increased tear-film osmolarity in contact lens wearers. Am J Ophthalmol, 102, 505-7.

GOUVEIA, S. M. & TIFFANY, J. M. 2005. Human tear viscosity: an interactive role for proteins and lipids. Biochim Biophys Acta, 1753, 155-63.

GUILLON, M. & MAISSA, C. 2008. Contact lens wear affects tear film evaporation. Eye Contact Lens, 34, 326-30.

HOM, M. M. & BRUCE, A. S. 2009. Prelens tear stability: relationship to symptoms of dryness. Optometry, 80, 181-4.

JONES, L., SENCHYNA, M., GLASIER, M. A., SCHICKLER, J., FORBES, I., LOUIE, D. & MAY, C. 2003. Lysozyme and lipid deposition on silicone hydrogel contact lens materials. Eye Contact Lens, 29, S75-9; discussion S83-4, S192-4.

KIMBALL, S. H., KING-SMITH, P. E. & NICHOLS, J. J. 2010. Evidence for the Major Contribution of Evaporation to Tear Film Thinning between Blinks. Investigative Ophthalmology & Visual Science, 51, 6294-6297.

KING-SMITH, P. E., NICHOLS, J. J., NICHOLS, K. K., FINK, B. A. & BRAUN, R. J. 2008. Contributions of evaporation and other mechanisms to tear film thinning and break-up. Optom Vis Sci, 85, 623-30.

KOK, J. H., BOETS, E. P., VAN BEST, J. A. & KIJLSTRA, A. 1992. Fluorophotometric assessment of tear turnover under rigid contact lenses. Cornea, 11, 515-7.

MANN, A. & TIGHE, B. 2013. Contact lens interactions with the tear film. Exp Eye Res, 117, 88-98.

MCMONNIES, C. W. 2007. Incomplete blinking: exposure keratopathy, lid wiper epitheliopathy, dry eye, refractive surgery, and dry contact lenses. Cont Lens Anterior Eye, 30, 37-51.

MILLER, D. 1969. Measurement of the surface tension of tears. Arch Ophthalmol, 82, 368-71.

MUNTZ, A., SUBBARAMAN, L. N., SORBARA, L. & JONES, L. 2015. Tear exchange and contact lenses: A review. Journal of Optometry, 8, 2-11.

NICHOLS, J. J., MITCHELL, G. L. & KING-SMITH, P. E. 2005. Thinning rate of the precorneal and prelens tear films. Invest Ophthalmol Vis Sci, 46, 2353-61.


OCCHIPINTI, J. R., MOSIER, M. A., LAMOTTE, J. & MONJI, G. T. 1988. Fluorophotometric measurement of human tear turnover rate. Curr Eye Res, 7, 995-1000.

OOI, E. H., NG, E. Y., PURSLOW, C. & ACHARYA, R. 2007. Variations in the corneal surface temperature with contact lens wear. Proc Inst Mech Eng H, 221, 337-49.

PALAKURU, J. R., WANG, J. & AQUAVELLA, J. V. 2007. Effect of blinking on tear dynamics. Invest Ophthalmol Vis Sci, 48, 3032-7.

PAUGH, J. R., STAPLETON, F., KEAY, L. & HO, A. 2001. Tear exchange under hydrogel contact lenses: methodological considerations. Invest Ophthalmol Vis Sci, 42, 2813-20.

PURSLOW, C., WOLFFSOHN, J. S. & SANTODOMINGO-RUBIDO, J. 2005. The effect of contact lens wear on dynamic ocular surface temperature. Cont Lens Anterior Eye, 28, 29-36.

REFOJO, M. F. 1991. Tear Evaporation Considerations and Contact Lens Wear. In: FLATTAU, P. E. (ed.) Considerations in Contact Lens Use Under Adverse Conditions: Proceedings of a Symposium. . National Academies Press (US).

STAPLETON, F., STRETTON, S., PAPAS, E., SKOTNITSKY, C. & SWEENEY, D. F. 2006. Silicone hydrogel contact lenses and the ocular surface. Ocul Surf, 4, 24-43.

THAI, L. C., TOMLINSON, A. & RIDDER, W. H. 2002. Contact lens drying and visual performance: the vision cycle with contact lenses. Optom Vis Sci, 79, 381-8.

TUTT, R., BRADLEY, A., BEGLEY, C. & THIBOS, L. N. 2000. Optical and visual

impact of tear break-up in human eyes. Invest Ophthalmol Vis Sci, 41, 4117-23.

VAN DER WORP, E., DE BRABANDER, J., SWARBRICK, H. & HENDRIKSE, F. 2008. Eyeblink frequency and type in relation to 3- and 9-o’clock staining and gas permeable contact lens variables. Optom Vis Sci, 85, E857-66.

VANCE, K. D., MILLER, W. & BERMANGSON, J. 2015. Measurement of tear flow in scleral contact lens wearers. American Academy of Optometry meeting. New Orleans.

WANG, J., FONN, D., SIMPSON, T. L. & JONES, L. 2003. Precorneal and pre- and postlens tear film thickness measured indirectly with optical coherence tomography. Invest Ophthalmol Vis Sci, 44, 2524-8.

YOKOI, N., YAMADA, H., MIZUKUSA, Y., BRON, A. J., TIFFANY, J. M., KATO, T. & KINOSHITA, S. 2008. Rheology of tear film lipid layer spread in normal and aqueous tear-deficient dry eyes. Invest Ophthalmol Vis Sci, 49, 5319-24.

ZHAO, J. & WOLLMER, P. 1998. Surface activity of tear fluid in normal subjects. Acta Ophthalmol Scand, 76, 438-41.