HIGH ALTITUDE MEDICINE & BIOLOGY

Volume 16, Number 4, 2015

ª Mary Ann Liebert, Inc.
DOI: 10.1089/ham.2015.0109

Ultraviolet Keratitis:
From the Pathophysiological Basis
to Prevention and Clinical Management

Gabriel Willmann1,2

Abstract

Willmann, Gabriel. Ultraviolet keratitis: From the pathophysiological basis to prevention and clinical management.
High Alt Med Biol 16:277–282, 2015.—Ultraviolet keratitis is caused by the toxic effects of acute high-dose
ultraviolet radiation (UVR) reflecting the sensitivity of the ocular surface to photochemical injury. The clinical
syndrome presents with ocular pain, tearing, conjunctival chemosis, blepharospasm, and deterioration of vision
typically several hours after exposure, lasting up to 3 days. Mountaineers, skiers, and beach recreationalists are
particularly at risk to suffer from ultraviolet (UV) keratitis as the reflectivity of UVR in these environments is
extremely high. The aim of this review is to raise awareness about the potential of UV damage on the eye with an
emphasis on UV keratitis, to highlight the pathophysiological basis of corneal phototoxicity, and to provide practical
guidance for the prevention and clinical management of UV keratitis commonly known as snow blindness.

Key Words: cornea; high altitude; keratitis solaris; snow blindness; ultraviolet keratitis

Introduction is the leading cause of blindness in the developed world with sun
exposure, specifically blue light, as a major contributing risk

T he human eye is constantly exposed to ultraviolet radi-

ation (UVR). On the one hand, the eye depends on visible
light energy to ensure subsequent visual processing, but on the
other, it can be damaged by the very same light in the form of
acute high-dose or chronic UVR (Wald, 1945; Tang et al.,
2013). Associated ocular pathologies include ultraviolet (UV)
keratitis, climatic droplet keratopathy, dry eye disease, pin-
guecula, pterygium, cataract formation, solar maculopathy, age-
related macular degeneration (AMD), and eyelid malignancies
such as basal cell carcinoma or squamous cell carcinoma (Yam
and Kwok, 2014). Among these, age-related cataract formation
presents the leading cause of blindness worldwide, while AMD
factor (Sui et al., 2013). While most UV-related ophthalmic
diseases of the cornea require cumulative UVR exposure, UV
keratitis is the result of acute high-dose or suprathreshold UVR
(Pitts and Tredici, 1971; Zuclich, 1989). Here, mountaineering
at high altitude poses an extremely high risk for overexposure to
natural UVR. Many early mountaineering expeditions in the
Himalayas have reported of climbers suffering from snow
blindness, and Atkinson (1921) observed many cases during the
exploration of the Antarctic continent (Herrligkoffer, 1958). In
addition to natural UVR, artificial sources of acute UVR ex-
posure such as during welding can also cause severe UV kera-
titis unless sufficient eye protection is used (Cullen, 2002).

1
Eye Hospital, Katharinenhospital, Stuttgart, Germany.
2
Centre for Ophthalmology, University of Tübingen, Tübingen, Germany.

277
278 WILLMANN

FIG. 1. Ultraviolet radiation (UVR) can be divided into UV-A (320–400 nm), UV-B (280–320 nm), and UV-C (100–
280 nm). Visible light ranges from about 400 to 700 nm and infrared light from 700 to 1200 nm. Extremely short and high-
energy UV-C rays are almost completely absorbed by the ozone layer. The cornea absorbs a high fraction of all UV-B rays
reaching the ocular surface, making it vulnerable to develop UV keratitis upon acute exposure. Cataract formation of the
lens is mainly attributed to chronic UV-A radiation. Chronic UVR may also be responsible for other ocular surface diseases,
while age-related macular degeneration is thought to be associated with the blue light fraction of the visible light.

The energy of the radiation determines the degree of oxi-
dative photodegradation on the ocular surface of the cornea.
Usually severe ocular pain, tearing, conjunctival chemosis,
blepharospasm, uncontrolled blinking of the eyelid, and de-
terioration of vision characterize the clinical syndrome with a
delayed onset typically several hours after exposure (Cullen,
2002). While the course of the disease is often self-limiting
and aiding treatment options are available, the only option to
prevent corneal epithelial cells from degenerating from high-
energy UVR is to minimize radiation exposure.
After an initial overview on UVR, the pathophysiological
basis of phototoxicity, followed by measures of prevention
and clinical management in respect to UV keratitis, will be
discussed.
Pathophysiological Basis of UV Keratitis
Ultraviolet radiation
UVR is invisible to human perception and presents the
shortwave electromagnetic spectrum of 100–400 nm. In
contrast, visible light ranges from about 400 to 700 nm and
infrared light from 700 to 1200 nm (Bachem, 1956). UVR can
further be divided into UV-A (320–400 nm), UV-B (280–
320 nm), and UV-C (100–280 nm) (Bachem, 1956; Pitts and
Tredici, 1971; Norren and Vos, 1974). The ozone layer, in
addition to water vapor and oxygen/carbon dioxide, is able to
absorb almost all of UV-C and >90% of UV-B radiation
(Norval et al., 2007). However, with a diminishing ozone
layer, the amount of UV-B radiation today reaching the oc-
ular surface has an increased potential for biological damage
compared with decades ago (Behar-Cohen et al., 2014).
Figure 1 provides an overview of the various effects of UVR
on the eye.
Cogan and Kinsey (1946) have first reported the action
spectrum of UVR for UV keratitis. At a wavelength of about
270 nm, only relatively little energy (0.005 J/cm2) is required
to produce UV keratitis (Kolozsvari et al., 2002). Hence, a
short wavelength of around 280 nm surmounts the damage
potential of longer wavelengths of about 300–320 nm by a
factor 600·, indicating that spectral energy increases as
wavelength decreases (Reme et al., 1996; van Norren and
Gorgels, 2011). For this reason, the International Organiza-
tion for Standardization (ISO) 8990/3 norm defines a cutoff
for potential ocular damage of 380 nm, which has been
adopted by the World Health Organization (WHO).
As direct sunlight only contributes about 50% to the am-
bient UVR, scatter and reflection play a key role in overall
ambient UVR (Sliney, 1997; Sydenham et al., 1997). Ac-
cording to Rayleigh’s law, the shorter the wavelength, the
greater the amount of scattered UVR, indicating that on a
bright sunny day, the main proportion of UV-B incident to the
eye and especially the cornea is largely contributed by diffuse
scatter. Cloud cover or haze may further increase the amount
of scatter. Another key component of the total ambient UVR
is ground reflection, which greatly varies depending on the
surface. While grass and rocks reflect at low rates (2%–5%),
water reflects at higher (10%–25%), and snow cover at much
higher rates (>90%) (Atkinson, 1921). High altitude and low
latitude further increase the ambient UVR burden, putting
high altitude mountaineers at great risk for the development
ULTRAVIOLET KERATITIS
of acute phototoxic diseases such as UV keratitis. UVR in-
creases with altitude at a rate of *4% per 1000 feet as a result
of decreased atmospheric absorption (Ellerton et al., 2009).
Other environmental factors such as season of the year have
been shown to influence the peak ocular exposure time as the
total amount of UVR reaching the eye largely depends on the
actual solar angle (Sasaki et al., 2011; Chao et al., 2013).
Compared with summer, it shifts to actual solar noon in
winter because the maximum daily solar altitude drops below
the occlusion angle (Sliney, 1999; Sasaki et al., 2011). For the
very same reason, the UVR burden to the eye may be as much
as twice as high in the morning compared with noon (Chao
et al., 2013). Finally, anatomical features as the upper orbital
rim composition, the brow, and the nose also influence the
amount of direct and reflected radiation entering the eye
(Merriam, 1996).
Pathophysiological basis of phototoxicity to the cornea
Oxidative photodegradation is largely dependent on three
factors: radiation exposure at a specific wavelength, tissue
type containing a specific chromophore for that wavelength,
and oxygen. The degree of damage depends on time of ex-
posure and energy of radiation. Due to its high content in
protein and nucleic acid, the cornea, particularly the corneal
epithelium, absorbs predominantly UV-B in the range of
280–300 nm, acting as a major protection shield against UVR
for the eye. However, when the threshold radiation dose for
biological damage is reached, absorption of UVR leads to the
generation of reactive oxygen species (ROS) as a result of an
imbalance between ROS generation and antioxidant defense
(Cullen, 2002; Chao et al., 2013).
The production of ROS leads to the disruption of important
cellular components such as cellular membranes, DNA, and
proteins with the consequence of biological dysfunction and
damage (Bergendi et al., 1999). Mainly hydroxyl radicals
induce the oxidative degradation of cellular membranes in
the form of lipid peroxidation (Esterbauer et al., 1991). In
addition, upon UVR, the hydroxyl radical can react with a
number of DNA components targeting purine and pyrimidine
FIG. 2. The mechanisms involved in phototoxicity to the
cornea include oxidative stress by reactive oxygen species
(ROS) formation, induction of inflammation with the pro-
duction of proinflammatory cytokines, and apoptotic cell
death through necrotic receptor activation. Evidence sug-
gests that multiple enzymatic and nonenzymatic antioxi-
dants of the cornea and tear film play a crucial role in
protecting the ocular surface from the damaging oxidative
effects of UVR.
279
bases and the deoxyribose backbone to alter DNA structure
(Liu et al., 1996; Cai et al., 1998; Halliwell, 1998). Finally,
proteins are targeted by ROS. Specifically, amino acids,
cysteine, and methionine are affected by oxidative stress,
resulting in structural and functional inactivation (Dean et al.,
1997). Furthermore, high-dose UVR causes upregulation of
proinflammatory cytokines by activation of nuclear factor
kappa-light-chain-enhancer of activated B cells (NF-jB) and
leads to apoptosis in corneal cells by direct cell membrane
damage through necrotic receptor activation (Black et al.,
2011). Figure 2 presents an overview of the pathophysio-
logical mechanism of UV keratitis.
The antioxidant defense system
The cornea together with the tear film and aqueous humor
present the first barrier against UVR. Thus, the ocular surface
has developed a cellular defense system to protect the eye.
Various enzymatic and nonenzymatic antioxidants play a key
role in protecting ocular tissues against oxidative damage by
scavenging and neutralizing ROS. An antioxidant is a molecule
that inhibits the oxidation of other molecules. To terminate the
process of oxidative photodegradation, antioxidants remove
free radical intermediates by being oxidized themselves.
Therefore, antioxidants are often reducing agents.
An important factor in protecting the cornea from UVR
insult is the corneal crystalline aldehyde dehydrogenase,
ALDH3A1 (Chen et al., 2013). It comprises a large portion of
soluble proteins of the cornea and acts through metabolism of
toxic aldehydes, generation of reduced nicotinamide adenine
dinucleotide phosphate (NADPH), scavenging of ROS, and
chaperone-like activity (Estey et al., 2007). It may even ab-
sorb UV light directly. Another important small-molecule
antioxidant is glutathione, which is differentially distributed
within the cornea with highest levels reaching in the epithe-
lium (Dalton et al., 2004). In conditions of oxidative stress, it
can counteract against free radicals as well as regenerate
other antioxidants, such as vitamin C and E, and protect the
integrity of cellular membranes (Watson et al., 2003). As-
corbic acid itself (vitamin C) is known to promote healing of
damaged corneal tissue by serving as a cofactor for collagen
synthesis (Piatigorsky, 2001; Pappa et al., 2003). Other im-
portant antioxidants of the cornea include L cysteine, L-
tyrosine, a-tocopherol, retinol, albumin, ferritin, superoxide
dismutase, and catalase (Marchitti et al., 2011).
Prevention and Clinical Management
Prevention
UVR generally poses a risk for the eye throughout life.
However, when acute high ocular UV exposure is encoun-
tered during high altitude mountaineering or skiing, one is at
great risk of developing UV keratitis unless preventative
measures are in place. Less than two hours of UV radiation
reflected from snow has been reported to be enough to cause
UV keratitis (Dolin and Johnson, 1994).
Individual predisposition factors such as orbital anatomy,
corneal thickness, or pupil size also determine the overall UV
burden to the eye. Photosensitizing drugs such as tetracy-
clines or chloroquine may also increase the susceptibility to
UVR damage and should be avoided. General prevention
strategies to avoid the risk of UV keratitis include wearing a
hat to block exposure from above and more importantly the
280
use of sunglasses or contact lenses, also to block low-angle
and reflected UV radiation (Sasaki et al., 2011).
While all sunglasses have at least some UV-blocking
characteristics, the amount of UV absorption varies widely
(Borgwardt et al., 1981). In one study, 75% of all lenses
tested failed to provide the 95% UV-A protection re-
commended by the US Food and Drug Administration
(Velpandian et al., 2005). In addition, neither brand nor price
seems to predict the quality of UV protection available in
sunglasses (Bazzazi et al., 2015). The type of sunglass should
be chosen according to the environmental terrain and planned
activity (Butler, 1999). Respective dark lens sunglasses,
which transmit much less visible light in combination with
side shields, should be used in snowy conditions or at high
altitude. However, dark lens sunglasses may also cause pupil
dilation and have been shown to actually increase UV
transmission into the eye (Pitts and Tredici, 1971; Sliney,
2011). Nevertheless, sunglasses without side shields signifi-
cantly increase UV exposure as UVR coming in from the
sides is not blocked and therefore back reflection from
the antireflective coatings of the sunglasses is increased
(Rosenthal et al., 1988; Sliney, 2001). This increase in back
reflection adds to the overall UVR burden. Finally, under
extreme environmental conditions (wind, cold), snow gog-
gles with respective UV filters may also be useful and can be
recommended.
UV-blocking soft contact lenses that completely cover the
pupil and limbus seem to be a particularly good option to
prevent UV rays from damaging the cornea and reaching
internal structures of the eye (Walsh and Bergmanson, 2011).
UVR coming in from the sides is totally blocked and back
reflection is not an issue (Kwok et al., 2003). The initial
development of contact lenses years ago showed variable UV
absorption in respect to UV-A (Anstey et al., 1999). How-
ever, the characteristics of newer soft contact lenses available
today are much improved and some even exhibit enhanced
UV-filtering capabilities up to a wavelength of about 390 nm.
One example of a soft contact lens capable of filtering all of
UV-B and a major portion of UV-A is the Acuvue Ad-
vanve (Lira et al., 2009). Nevertheless, the use of contact
lenses has to be carefully assessed in remote wilderness areas
or at high altitude as these conditions provide a challenge for
appropriate contact lens wear and care with a potential risk of
infections (Bauer, 2015).
Clinical manifestation and management
In the event of UV keratitis, the primary strategy is to avoid
further exposure to UVR. One should reassess if all measures
of appropriate prevention have been applied and avoid any
further exposure to damaging UVR. It is important to note
that all symptoms usually resolve within 24–72 hours de-
pending on the degree of UV damage (Dolin and Johnson,
1994; McIntosh et al., 2011).
The clinical manifestation of the typically bilateral oc-
curring UV keratitis ranges from a mild superficial punctate
keratitis to severe cases with total epithelial desquamation.
Severity may also vary between individuals as light- versus
dark-skinned humans or individuals with pre-existing ocular
conditions, such as dry eye syndrome, keratokonus, or post-
operative refractive surgery (e.g., LASIK), may even be more
likely to develop severe forms of UV keratitis. While mild
forms may only present with a red eye and increased foreign
body sensation, severe cases usually have significant ocular
WILLMANN
pain, lacrimation, chemosis, blepharospasm, and decreased
visual acuity. Interestingly, the clinical syndrome is charac-
terized by a lag time between exposure and beginning of
clinical symptoms. While increased redness of the conjunc-
tiva, chemosis, foreign body sensation, and lacrimation may
occur quite rapidly after exposure, the absence of ocular pain
for about 6–12 hours is characteristic for UV keratitis. This
phenomenon has been attributed to the loss and return of
corneal sensitivity in an experimental study (Millodot and
Earlam, 1984). Due to the fast reepithelialization of the
cornea, the resolution of clinical symptoms is often rapid and
permanent damage is extremely rare.
Apart from the primary strategy of avoiding further UV
exposure, there are several therapeutic approaches to aid
clinical symptoms and gain faster recovery. Vision is usually
blurred due to epithelial trauma, resulting in constant tearing.
Moreover, uncontrollable blinking over the exposed corneal
surface causes pain and blepharospasm. The frequent use of
topical lubrication, ideally with preservative artificial tears
containing antioxidative properties such as Artelac EDO
(Bausch+Lomb, Bridgewater, NJ), is recommended (Rieger,
2001). Indeed, artificial tears should also be used as a mea-
sure of prevention, especially when at high attitude, as tear
film stability due to increased evaporation is significantly
reduced (Willmann et al., 2014). Topical anesthetics should
not be used as they delay and prevent corneal re-
epithelialization (Burstein, 1980; Patel and Fraunfelder,
2013). However, in emergency situations, for example, when
a stricken climber at high altitude needs to descend to safety,
short-term application of topical anesthetics may be consid-
ered to stop the crucial pain and constant blinking (Sliney,
2001). Otherwise, for comfort and relief of pain, a bandage
contact lens in addition to lubrication is usually sufficient. In
addition, topical antibiotic ointment (e.g., erythromycin
drops) should be used in moderate and severe cases to prevent
infection. In severe cases, additional nonsteroidal anti-
inflammatory eye drops and oral acetaminophen or other
narcotic analgesics can be used to alleviate symptoms of
discomfort and redness of conjunctival tissue. Cycloplegic
eye drops (cyclopentolate 1%) may also be considered for
pain relief, but result in a wide pupil, altering visual acuity
and increasing glare. Although very efficient for pain relief,
they may not be appropriate for use in a wilderness setting.
People at risk, particularly mountaineers travelling to re-
mote snow-covered areas or to high altitude, should be fa-
miliar with the prevention and clinical management of UV
keratitis as this usually benign condition may result in inca-
pacitation, requiring assistance in severe cases. Therefore, a
first aid kit should always contain at least spare sunglasses
and/or contact lenses, artificial tears for lubrication, and a
topical antibiotic ointment. In Addition, a topical anesthetic
for emergency use only may be considered.
Conclusion
Acute suprathreshold UVR ultimately leads to UV keratitis
unless appropriate protective measures are applied. With a
diminishing ozone layer, preventing the eye from UVR be-
comes even more important. When wearing sunglasses, side
shields should be used to avoid back reflection caused by
antireflective coatings and dark versus light lenses should be
chosen depending on environmental conditions. UV-filtering
contact lenses might be a particularly good option as they
ULTRAVIOLET KERATITIS
automatically filter light from all angles. When being out-
doors, it is important to keep in mind that the UV burden on
the eye might peak at hours different to the skin due to the
increase in direct and reflected sunlight to the eye at lower
solar angles. Due to the antioxidant defense mechanism of the
cornea and the ability for fast reepithelialization, clinical
symptoms are often self-limiting within a few days. For ef-
fective relief of the clinical symptoms encountered, relatively
easy-to-follow treatment regimes are available.
Author Disclosure Statement
No competing financial interests exist.
References
Anstey A, Taylor D, Chalmers I, and Ansari E. (1999). Ultra-
violet radiation-blocking characteristics of contact lenses:
Relevance to eye protection for psoralen-sensitised patients.
Photodermatol Photoimmunol Photomed 15:193–197.
Atkinson SC. (1921). SNOW-BLINDNESS: Its causes, effects,
changes, prevention, and treatment. Br J Ophthalmol 5:49–54.
Bachem A. (1956). Ophthalmic ultraviolet action spectra. Am J
Ophthalmol 41:969–975.
Bauer IL. (2015). Contact lens wearers’ experiences while trekking
in the Khumbu region/Nepal: A cross-sectional survey. Travel
Med Infect Dis 13:178–184.
Bazzazi N, Heydarian S, Vahabi R, Akbarzadeh S, and Fouladi
DF. (2015). Quality of sunglasses available in the Iranian
market; a study with emphasis on sellers’ license. Indian J
Ophthalmol 63:152–156.
Behar-Cohen F, Baillet G, de Ayguavives T, Garcia PO, Krutmann
J, Pena-Garcia P, Reme C, and Wolffsohn JS. (2014). Ultraviolet
damage to the eye revisited: Eye-sun protection factor (E-
SPF(R)), a new ultraviolet protection label for eyewear. Clin
Ophthalmol 8:87–104.
Bergendi L, Benes L, Durackova Z, and Ferencik M. (1999).
Chemistry, physiology and pathology of free radicals. Life
Sci 65:1865–1874.
Black AT, Gordon MK, Heck DE, Gallo MA, Laskin DL, and
Laskin JD. (2011). UVB light regulates expression of anti-
oxidants and inflammatory mediators in human corneal epi-
thelial cells. Biochem Pharmacol 81:873–880.
Borgwardt B, Fishman GA, and Vander-Meulen D. (1981).
Spectral transmission characteristics of tinted lenses. Arch
Ophthalmol 99:293–297.
Burstein NL. (1980). Corneal cytotoxicity of topically applied
drugs, vehicles and preservatives. Surv Ophthalmol 25:15–30.
Butler FK, Jr. (1999). The eye at altitude. Int Ophthalmol Clin
39:59–78.
Cai CX, Birk DE, and Linsenmayer TF. (1998). Nuclear ferritin
protects DNA from UV damage in corneal epithelial cells.
Mol Biol Cell 9:1037–1051.
Chao SC, Hu DN, Yang PY, Lin CY, Nien CW, Yang SF, and
Roberts JE. (2013). Ultraviolet-A irradiation upregulated
urokinase-type plasminogen activator in pterygium fibro-
blasts through ERK and JNK pathways. Invest Ophthalmol
Vis Sci 54:999–1007.
Chen Y, Thompson DC, Koppaka V, Jester JV, and Vasiliou V.
(2013). Ocular aldehyde dehydrogenases: Protection against
ultraviolet damage and maintenance of transparency for vi-
sion. Prog Retin Eye Res 33:28–39.
Cogan DG, and Kinsey VE. (1946). Action spectrum of keratitis
produced by ultraviolet radiation. Arch Ophthal 35:670–677.
Cullen AP. (2002). Photokeratitis and other phototoxic effects
on the cornea and conjunctiva. Int J Toxicol 21:455–464.
281
Dalton TP, Chen Y, Schneider SN, Nebert DW, and Shertzer HG.
(2004). Genetically altered mice to evaluate glutathione homeo-
stasis in health and disease. Free Radic Biol Med 37:1511–1526.
Dean RT, Fu S, Stocker R, and Davies MJ. (1997). Biochem-
istry and pathology of radical-mediated protein oxidation.
Biochem J 324(Pt 1):1–18.
Dolin PJ, and Johnson GJ. (1994). Solar ultraviolet radiation
and ocular disease: A review of the epidemiological and
experimental evidence. Ophthalmic Epidemiol 1:155–164.
Ellerton JA, Zuljan I, Agazzi G, and Boyd JJ. (2009). Eye
problems in mountain and remote areas: Prevention and on-
site treatment—Official recommendations of the International
Commission for Mountain Emergency Medicine ICAR
MEDCOM. Wilderness Environ Med 20:169–175.
Esterbauer H, Schaur RJ, and Zollner H. (1991). Chemistry and
biochemistry of 4-hydroxynonenal, malonaldehyde and re-
lated aldehydes. Free Radic Biol Med 11:81–128.
Estey T, Piatigorsky J, Lassen N, and Vasiliou V. (2007). ALD-
H3A1: A corneal crystallin with diverse functions. Exp Eye Res
84:3–12.
Halliwell B. (1998). Can oxidative DNA damage be used as a
biomarker of cancer risk in humans? Problems, resolutions
and preliminary results from nutritional supplementation
studies. Free Radic Res 29:469–486.
Herrligkoffer KM. (1958). [Protection against snow burn; ex-
periences from two Himalaya expeditions with corodenin,
Diwag-light protection ointment and labiosan]. Munch Med
Wochenschr 100:1856–1858.
Kolozsvari L, Nogradi A, Hopp B, and Bor Z. (2002). UV
absorbance of the human cornea in the 240- to 400-nm range.
Invest Ophthalmol Vis Sci 43:2165–2168.
Kwok LS, Kuznetsov VA, Ho A, and Coroneo MT. (2003).
Prevention of the adverse photic effects of peripheral light-
focusing using UV-blocking contact lenses. Invest Ophthal-
mol Vis Sci 44:1501–1507.
Lira M, Dos Santos Castanheira EM, Santos L, Azeredo J,
Yebra-Pimentel E, and Real Oliveira ME. (2009). Changes in
UV-visible transmittance of silicone-hydrogel contact lenses
induced by wear. Optom Vis Sci 86:332–339.
Liu ZG, Baskaran R, Lea-Chou ET, Wood LD, Chen Y, Karin M,
and Wang JY. (1996). Three distinct signalling responses by
murine fibroblasts to genotoxic stress. Nature 384:273–276.
Marchitti SA, Chen Y, Thompson DC, and Vasiliou V. (2011).
Ultraviolet radiation: Cellular antioxidant response and the
role of ocular aldehyde dehydrogenase enzymes. Eye Contact
Lens 37:206–213.
McIntosh SE, Guercio B, Tabin GC, Leemon D, and Schi-
melpfenig T. (2011). Ultraviolet keratitis among mountain-
eers and outdoor recreationalists. Wilderness Environ Med
22:144–147.
Merriam JC. (1996). The concentration of light in the human
lens. Trans Am Ophthalmol Soc 94:803–918.
Millodot M, and Earlam RA. (1984). Sensitivity of the cornea after
exposure to ultraviolet light. Ophthalmic Res 16:325–328.
Norren DV, and Vos JJ. (1974). Spectral transmission of the
human ocular media. Vision Res 14:1237–1244.
Norval M, Cullen AP, de Gruijl FR, Longstreth J, Takizawa Y,
Lucas RM, Noonan FP, and van der Leun JC. (2007). The
effects on human health from stratospheric ozone depletion
and its interactions with climate change. Photochem Photo-
biol Sci 6:232–251.
Pappa A, Chen C, Koutalos Y, Townsend AJ, and Vasiliou V.
(2003). Aldh3a1 protects human corneal epithelial cells from
ultraviolet- and 4-hydroxy-2-nonenal-induced oxidative
damage. Free Radic Biol Med 34:1178–1189.
282
Patel M, and Fraunfelder FW. (2013). Toxicity of topical oph-
thalmic anesthetics. Expert Opin Drug Metab Toxicol 9:983–
988.
Piatigorsky J. (2001). Enigma of the abundant water-soluble
cytoplasmic proteins of the cornea: The ‘‘refracton’’ hy-
pothesis. Cornea 20:853–858.
Pitts DG, and Tredici TJ. (1971). The effects of ultraviolet on
the eye. Am Ind Hyg Assoc J 32:235–246.
Reme C, Reinboth J, Clausen M, and Hafezi F. (1996). Light
damage revisited: Converging evidence, diverging views?
Graefes Arch Clin Exp Ophthalmol 234:2–11.
Rieger G. (2001). Anti-oxidative capacity of various artificial
tear preparations. Graefes Arch Clin Exp Ophthalmol 239:
222–226.
Rosenthal FS, Bakalian AE, Lou CQ, and Taylor HR. (1988).
The effect of sunglasses on ocular exposure to ultraviolet
radiation. Am J Public Health 78:72–74.
Sasaki H, Sakamoto Y, Schnider C, Fujita N, Hatsusaka N,
Sliney DH, and Sasaki K. (2011). UV-B exposure to the
eye depending on solar altitude. Eye Contact Lens 37:191–
195.
Sliney DH. (1997). Ocular exposure to environmental light and
ultraviolet—The impact of lid opening and sky conditions.
Dev Ophthalmol 27:63–75.
Sliney DH. (1999). Geometrical assessment of ocular exposure
to environmental UV radiation—Implications for ophthalmic
epidemiology. J Epidemiol 9:S22–S32.
Sliney DH. (2001). Photoprotection of the eye—UV radiation
and sunglasses. J Photochem Photobiol B 64:166–175.
Sliney DH. (2011). Intraocular and crystalline lens protection
from ultraviolet damage. Eye Contact Lens 37:250–258.
Sui GY, Liu GC, Liu GY, Gao YY, Deng Y, Wang WY, Tong
SH, and Wang L. (2013). Is sunlight exposure a risk factor for
age-related macular degeneration? A systematic review and
meta-analysis. Br J Ophthalmol 97:389–394.
Sydenham MM, Collins MJ, and Hirst LW. (1997). Measure-
ment of ultraviolet radiation at the surface of the eye. Invest
Ophthalmol Vis Sci 38:1485–1492.
WILLMANN
Tang PH, Kono M, Koutalos Y, Ablonczy Z, and Crouch RK.
(2013). New insights into retinoid metabolism and cycling
within the retina. Prog Retin Eye Res 32:48–63.
van Norren D, and Gorgels TG. (2011). The action spectrum of
photochemical damage to the retina: A review of mono-
chromatic threshold data. Photochem Photobiol 87:747–753.
Velpandian T, Ravi AK, Kumari SS, Biswas NR, Tewari HK,
and Ghose S. (2005). Protection from ultraviolet radiation by
spectacle lenses available in India: A comparative study. Natl
Med J India 18:242–244.
Wald G. (1945). Human vision and the spectrum. Science 101:
653–658.
Walsh JE, and Bergmanson JP. (2011). Does the eye benefit
from wearing ultraviolet-blocking contact lenses? Eye Con-
tact Lens 37:267–272.
Watson WH, Chen Y, and Jones DP. (2003). Redox state of
glutathione and thioredoxin in differentiation and apoptosis.
Biofactors 17:307–314.
Willmann G, Schatz A, Fischer MD, Schommer K, Zrenner E,
Bartz-Schmidt KU, Gekeler F, and Gekeler K. (2014). Ex-
posure to high altitude alters tear film osmolarity and breakup
time. High Alt Med Biol 15:203–207.
Yam JC, and Kwok AK. (2014). Ultraviolet light and ocular
diseases. Int Ophthalmol 34:383–400.
Zuclich JA. (1989). Ultraviolet-induced photochemical damage
in ocular tissues. Health Phys 56:671–682.
Address correspondence to:
Gabriel Willmann, MD
Eye Hospital
Katharinenhospital
70174 Stuttgart
Germany
E-mail: gabriel.willmann@googlemail.com
Received November 8, 2015;
accepted in final form November 15, 2015.