Eye Health
Advis­­­­or
™
A magazine from Johnson & Johnson Vision Care
UV Radiation
EDITION THREE 2010
Eye Health
Advisor
CO NT ENT
Introduction
Eye Health AdvisorTM
A magazine from Johnson & Johnson Vision Care
EDITION THREE 2010
2
Introduction
3
Sunlight Impact onto
Human Skin
by Tatiana RubashevaVladimirovna
9
UV Damage may be
invisible, but it is there!
11
UV Radiation and the Eye
by Karen Walsh
17
UV Protection with Contact
Lenses
by Heather L. Chandler
and Jason J. Nichols
T
his ssue of the Eye Health Advisor™ newsletter is dedicated to Ultra
Violet (UV) Radiation. The consequences of exposing the skin to UV radiation are well understood in the general population with 95 per cent of people
associating UV with skin problems, but only 7 per cent of people associating
UV with eye problems.*
This issue firstly reviews some new research findings and looks specifically
at the benefits of sun-protection response of the human body along with the
skin's natural protection system. Then it analyzes the effects of UV radiation on the ocular structures and discusses the options available to reduce or
eliminate the risk or damage, particularly in relation to UV blocking contact
lenses. It looks specifically at the benefits of UV-radiation protection and
aims to help practitioners better educate patients on the importance of UV
protection in practice. It summarizes our understanding of the interaction
of UV with ocular tissues, discusses the challenges of achieving adequate
protection and finally reviews the role of UV-blocking soft contact lenses in
ocular protection.
The literature provides plenty of evidence that the eyes are at risk of damage by both acute and chronic UV exposure. These conditions have been
grouped and named "the ophthalmohelioses" derived from the Greek ophthalmos (eye) and helios (sun) to refer collectively to diseases of the eye caused
by sunlight.
The effects of ocular exposure to UV are cumulative over our lifetime with
children being at most risk. Well fitting soft contact lenses cover the entire
cornea and limbus. The addition of Class I or Class II UV blocking to lenses
has been shown to be effective in protecting the eye against all angles of
incidence, including the peripheral light focusing effect. The discussion of
UV protection with patients should become standard practice, especially with
those participating in work and leisure activities exposing them to UV radiation, to allow them to make fully informed decisions.
We hope that this edition of the Eye Health Advisor™ newsletter, dedicated
to UV Radiation, will be interesting and helpful for you and even more that it
will give you a better understanding of UV exposure and the importance of
UV protection in practice...
2
Eye Health
Advisor
*Transitions UK. Transitions European Study. 2008
A magazine from Johnson & Johnson Vision Care
Sunlight Impact onto Human Skin
Tatiana Rubasheva-Vladimirovna
S
kin photoageing is a complex of destructive
processes in the skin following the sunlight expo sure. This article reviews new research findings and
looks specifically at the benefits of sun-protection
response of the human body along with the skin's
natural protection system. It looks at the histological
signs of epidermal photodamage and UV skin damage, analyzing also the biochemistry of photoageing.
Main sun-protection facts are also presented and
sun-protection measures are suggested.
UV Radiation
Sunrays spread like electromagnetic waves with
different frequency (wavelengths) ranging from lessthan-a-nm gamma rays to the meter-wavelength radio
waves. The least frequency is pertinent to γ-rays,
then comes the roentgen part of the spectrum, then
the three types of UV radiation - UVC (200 –280
nm), UVB (280 – 320 nm) and UVA ( 320 – 400 nm).
Then comes visible light (electromagnetic radiation perceived by our eyes, with the wavelength of
400 -700 nm), infrared radiation (felt like warmth, the
wavelength is >700 nm) and, at last, radio waves.
The ozone layer of the earth makes it impossible
for γ-rays, X-rays and UVC-rays to reach the earth’s
atmosphere.
Among other t ypes of radiation, from the viewpoint of harmful impact onto human skin, UVA and
UVB seem to be the most impor tant. Depending
upon the wavelength, solar UV radiation interacts
with different skin cells in various depths. UVA
rays are the most dangerous, as they are not
absorbed by clouds, do not diffuse in the air and
hardly reflect from ground and water sur faces.
The radiation intensit y in this par t of the spec trum hardly changes during the day time. Having
the lowest energy, UVA rays have, however, the
highest penetrabilit y. In the human skin UVA rays
reach the medium dermal layers and are thought
to be related to skin photoageing triggering, mainly
due to free radicals’ release. UVA rays affect both
epidermal cells and dermal fibroblasts. Melanin
absorbs ultraviolet radiation thus protecting skin
cells from destruction, but UVA rays are able to
overcome this barrier and can produce a negative
effect onto the tissues in different ways. Usually,
UVA rays act indirectly through the free ox ygen
EDITION THREE 2010
Eye Health
Advisor
Dr Tatiana V. Rubasheva
Dr Rubasheva has a
PhD in Dermatology
& Venereology and
she is Assistant
Professor at the
Institute of Advanced
Training under the
Federal
Medical Biological Agency
( Moscow, Russia ).
She is the author
of more than 20 publications in leading
dermatological journals. Dr Rubasheva
has been invited as a keynote speaker at
numerous dermatological meetings and
conferences. She has lectured extensively and also taught at locally organized
training courses. She is a licensed dermatocosmetologist with a professional practice in Moscow.
radicals’ release. Free radicals, in their turn, acti vate lipid & transcription factors peroxidation and
may damage DNA - chains ( causing gaps ).
Medium-wavelength UV rays (UVB, 280 -320 nm)
are referred to as “burning rays”: it is UVB that cause
sunburns. UVB rays are largely absorbed by the epidermis where they mostly damage keratypocytes. To
a certain degree, UVA can also provoke the release
of free forms of oxygen, but their main role is to
produce direct destructive effect onto DNA through
activation of its special parts – transcription factors.
These factors trigger intracellular accumulation of
metalloproteinase, the ferment with high proteolytic
(disintegrating) activity towards the cell structural
proteins. UVB rays damage skin cells through the
formation of DNA thymine dimers and 6 - 4 products
of DNA exposure, which, in case of incorrect repair,
results in mutagenic effects, cell functions impairment and carcinogenesis. Together, these UV rays
produce a carcinogenic effect onto human skin. Solar
radiation is thought to be the cause of at least 90%
of all skin cancers.
3
Suntan is nothing but the natural sun-protection
response of the human body: darkened skin is a
reliable protection from solar radiation. So, at “in
advance” suntanning in a solarium UVB plays the
main role. UVA contributes to the subsequent darkening of melanin which has already been produced
by the body.
Skin natural protection system
Human skin sensibility to UV radiation is unequal.
The American dermatologist Thomas Fitzpatrick
suggested categorizing all population into 6 groups
(phototypes) according to the skin photoprotective
ability. The higher a phototype is, the better the
natural photoprotective system works. What are the
components of this system?
Urocanic acid contained in the corneous layer of
the epidermis is one of the natural sun protection
factors. The changes caused by the UV-rays of
240 – 30 0 nm trigger the production of urocanic acid
isomers conducing to the electromagnetic energy’s
transformation into thermal energy absorbed by the
body tissues.Melanin is a powerful natural photo protector. Melanin accumulation results in suntan
appearance. Melanin is produced from tyrosine
aminoacid with the aid of tyrosinase which otherwise exists in a bound state in other compounds.
At UV exposure, the released tyrosinase triggers
production of melanin the pigment. This is the
mechanism of pigment formation ( suntan) under
solar radiation. It should be specially mentioned that
the health-improving effect of UV does not need
any manifested confirmations, like intensive suntan,
and is found at the radiation volumes considerably
lower than those of suntan. The melanin absorption
spectrum covers visible light and UV radiation. Noncoupled electrons in the molecular structure enable
melanin for light quanta absorption and their energy
transformation into heat.
The colourless melanin precursors possess the pro nounced antioxidative properties allowing largely for
prevention of negative consequences of free-radical
release at UV-exposure. Their efficiency can be compared with that of a powerful antioxidant tocopherol
(vitamin E). During oxidation, they polymerize and
form the brown-and-black pigment eumelanin which
has antioxidative properties, too. Another mechanism of natural protection lies in UV-stimulation of
basal keratocytes; in this case, thickened epidermis
plays the role of a “corneous shield”.
Skin photoageing is a complex of destructive
processes in the skin following the sunlight expo -
4
sure. The term of photoageing has a number of
synonyms - “heliodermatitis”, “actinic dermatosis”
and “early skin ageing”. Skin photoageing is characterized by a number of clinical, histological and
biochemical changes that are unlike age - related
skin processes. We should differ skin photoageing
from chronological ( age - related, i.e. natural ) ageing
of the skin, but remember that photoageing usually
comes in parallel with the signs of chronological
ageing ( Figure 1). But there are some specific
symptoms which can be seen only at the former
condition but not in the latter. These symptoms
allow for categorizing this condition as a separate
nosological form related to a special pathogenic
mechanism of photodamage.
Figure 1: Hands with striking signs of photoageing
Clinical signs of photodamage can be obser ved
only in the open par ts of the body or in those
exposed to the direct sunrays – our neck, face,
arms and hands. At photodamage, accelerated line
formation, decreased skin elasticit y, enhanced
traumaticit y and slow wound healing due to dermal
disorders are obser ved. Most manifested changes
in the epidermis are related to skin colour, dyschro mias, lentigo ( senile freckle ) , telangiectasis, seb orrheic keratoses, comedo senilis ( senile acne ).
It is interesting that chronic UV- exposure - related
complex changes of the skin had been closely
described in dermatology in the early 20th cen tur y ( “seaman’s skin”, “peasant’s skin”, “rhomb shaped atrophy of the neck”, “Favre - Racouchot
disease”, etc. )
Histological signs of epidermal photodamage.
There is a dependence between the degree of
damage and intensit y and duration of UV exposure.
At low UV- exposures, signs of hyperkeratosis can
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be obser ved in the corneous layer but epidermal
thickness of ten remains unchanged. At more
intensive UV- exposures, changes in the skin may
var y from epidermal hyper trophy to atrophy. Basal
cell membrane thickens; basal keratinocy tes loose
their abilit y for differentiation and active fission,
and along the basal membrane one can obser ve
the irregular distribution of different- sized mela tocy tes, differently pigmented and with different
quantit y of processes.
Histological signs of UV skin damage are:
a ) elastin fiber destruction1, 2 , b ) replacement of
normal collagen fibers by those with distinct dam aged par ts 3, 4 . This phenomenon is called “collagen
basophile degeneration” ( i.e., collagen destruc tion ). At severe skin photodamage, quite a number
of glucose - aminoglycan depositions ( compounds
responsible for cellular membrane stabilit y) togeth er with fragmented elastin fibers and dermal intra cellular proteins of elastin and collagen ( due to
collagen and elastin fiber destruction ) can be found
in the derma 5 . Normally, elastin fibers create a kind
of filamentar y skin carcass which suppor ts subcu taneous fat and dermal vasculature and responds
for the skin resilience, tonicit y and elasticit y. The
UV-triggered process of collagen and elastin deg radation leads to subcutaneous fat redistribution
and, consequently, to bloated faces features.
Biochemistr y of photoageing. Degradation of
filamentar y dermal carcass of the skin is a result
of UV- accelerated lipid oxidation - reduction reac tions 5 . Among the products of those chemical
processes, there are acraldehyde and 4 - hydrox y2- nonenal ( HNE ); their antibodies show high fibercidal abilit y. Additionally, it is proved by the high
efficiency of antioxidants ( their use is often justi fied at dermal involutional processes ). Increased
UV exposure considerably hampers the process of
natural decomposition of fibuline -2 ( intracellular
protein affecting the normally regular structure of
elastin fibers ).
A group of Japanese authors have studied the fac tors of skin microvascularization (vascular supply)
in 15 women aged 5 8 - 81 6 . In photodamaged skin,
they noticed the small -vessel endothelium depres sion; with low elasticit y, blood vessels became
overstretched, and this led to blood congestion
in the capillar y bed and to impaired microcircula tion. Cutaneous manifestations were abnormal
dermal vascular formations ( microhemangioma,
venous lake, ecchymoma, persistent diffuse er ythema, etc. ). Blood circulation disorders in derma
negatively affected elastin fibers that star ted to
degrade by thickening and defragmenting.
EDITION THREE 2010
Eye Health
Advisor
Solar exposure triggers production of vitamin D
( calciferol ) which is ver y impor tant for the human
organism. This vitamin is necessar y for maintain ing the constant calcium concentration in blood.
At calcium deficiency, calcium is “washed out”
from bone tissues which results in their thin ning ( osteoporosis ) , while children may get the
notorious disease of rickets leading to severe
deformations of the skeleton and other nega tive consequences. A par t from par ticipating in
calcium metabolism, vitamin D is necessar y for
proper functioning of the endocrine system ( thy roid and parathyroid glands, adrenal bodies, hypo physis ) and cholesterol exchange. A lso, vitamin
D enhances the immune system and acts as an
antioxidant. V itamin D is a physiological regulator
of proliferation ( procreation ) and dif ferentiation of
dermal cells including keratinocy tes, fibroblasts
and adipocy tes. At the aggressive photo expo sure, excessive production of vitamin D af fects a )
keratocy tes thus changing the normal thickness
of all epidermal layers, b ) fibroblasts thus chang ing the quantit y & qualit y of collagen and elastin
fibers being produced.
Moreover, in affected fibroblasts, synthesis of
pro - collagen Types 1 and 3 ( necessar y for normal
collagen fiber formation ) becomes impaired 4 ,7,
along with the accelerated disintegration of metalloproteinase which par ticipates in collagen formation and maintains its tonus7, 8 , 9 . Instead, pro collagen Type 11 is produced; new collagen fibers
become shor ter, thinner, more fragile, and cha otically ranged. Impairment of the filamentar y skin
carcass results in decreased resilience and elastic it y of the skin.
There is a wide range of dermal responses to
solar exposure: sensibilit y of hands and feet, for
example, are 4 times lower than that of midriff
and lumbar regions. Children under 5 -7 are highly
sensible to UV- radiation. Structural and functional
changes in the skin exposed to solar UV radiation
( dermatohelioses ) escalate after the age of 50, at
the onset of general evolutionar y changes10 . This is
also the age when differentiation of keratinocy tes
star ts. All those factors, along with the general
skin degradation, bear potential risks of oncologi cal consequences – mainly, of squamous cell carcinoma.
In view of this, the effect of vitamin A ( retinol )
onto cellular grow th and mitosis is demonstratively
proved. The use of retinoids ( combinations of vita min A and retinoic acid ) considerably decreases
risks of skin problems both aesthetical and onco logical. Possessing high penetrabilit y, retinoids
5
do not impact only the epidermis but also dermal
and even subdermal layers. Apar t from preventive
action, retinoids with their power ful proliferative
potential may also be efficient for the epithelial layer cancers’ treatment.
be obser ved. Grade II is characterized by a more
pronounced inflammator y response - intensive skin
redness with epidermis detachment and forma tion of blisters filled with water- like or somewhat
opaque liquid ( Figure 3 ). Full recover y of all skin
layers takes 8 -12 days.
Sunburns. The sun radiation is a beam of visible
and invisible spectral rays with different biological
activities. At the solar exposure, there is a simul taneous impact of:
•direct solar radiation;
•diffused solar radiation ( because of par tial diffu sion of the direct sunrays in the atmosphere or
their reflection from clouds );
•reflected solar radiation ( the light reflected from
surrounding sur faces ).
The volume of solar energy per a cer tain par t of
the ear th sur face depends on the position of the
sun which, in turn, depends on the latitude, the
season and time of the day.
If the sun is in its zenith point, then solar rays go
the shor test way through the atmosphere. If the
sun is at the angle of 30°, the necessar y distance
doubles, while at sunset it elongates by 35,4 times
comparing to the zenith. Diffused solar radiation is
a considerable par t of the total incoming sunrays.
It lights shadow y places; in cloudy weather, diffused radiation provides daylight. The reflection
abilit y of different par ts of the sun spectrum is not
equal and depends upon the proper ties of a surface. For example, water vir tually does not reflect
UV- radiation, and grass reflects just 2- 4% of UV,
while fresh snow reflects 8 0 - 9 0% of incoming solar
radiation. Therefore, in the mountains, on a snowcovered glacier, the volume of reflected radiation
mountaineers are exposed to is prett y equal to
that of direct sunlight, so the total solar exposure
is twice as high as on the plain. This explains the
intensive suntan and the increased risk of sunburns
in the mountains. At first sight, primar y signs of
the sun - related burns might not correspond to their
severit y; the true degree of the damage becomes
apparent somewhat later. According to the severit y, sunburns are subdivided into four grades. For
the sunburns in question, when only upper dermal
layers are affected, Grades I and II ( mild and mod erate ) are t ypical.
Figure 2: Grade I sunburn with extreme skin redness
Figure 3: Grade II sunburn with the formation of blisters
Grade I is the mildest possible degree of sun burn. Among its signs are skin redness in the place
of the burn, edema, burning sensation, pain and
to a cer tain extent skin inflammation ( Figure 2 ).
Inflammator y events are transient and soon resolve
( 3 - 5 days ). The place of the sunburn remains
pigmented; in some cases skin exfoliation can
6
After a sunburn, persistent pathological pigmen tation (freckles, chloasmas, lentigo, chronic white spot idiopathic hypomelanosis, and Civatte’s poiki loderma ) or depigmentation ( white blotches with
the new skin lacking protection and more prone to
UV- damage ) remain on the skin.
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Photose ns i bilization. A small percent of the
population has a peculiar feature – acute U V
response. Even a tiny U V exposure triggers the
allergic reaction soon leading to a severe sunburn.
P hotosensibilization is of ten c aused by some
medicaments including non - steroid antiflamma tor y drugs, painkillers, tranquilizers, peroral antid iabetic drugs, antibiotics and antidepressants.
Some food and cosmetic products, e.g. per fume
or soap, may also contain U V- sensibilizing com ponents.
The suns troke is a severe pathema with a sud den onset. It may result from the long - hour expo sure to infrared radiation from the direct sunlight
at long marching bareheaded. During hiking, the
most pronounced infra red exposure is at the
back of the head. A r terial blood ef flux and sudden
stagnation of venous blood in cerebral veins lead
to the brain edema and loss of consciousness.
The sunstroke symptoms and the first- aid actions
are the same as for the heat stroke. A hat protecting the head from direct sunlight while providing
thermal exchange with the ambient air ( ventila tion ) through the net or some eyelets, may be of
help here.
Sk i n c a n c e r may develop in any person, but
some people are more prone to this condition
( Figure 4 ) . T he special skin - photot y pe system was
developed for definition of those predisp osed to
skin c ancer. T here are six grades according to the
skin colour and abilit y to sunt an. T he p opulations
belonging to Groups I or II according to their skin
photot y pes, are predisp osed to skin c ancer; they
Figure 4: Skin cancer
EDITION THREE 2010
Eye Health
Advisor
are especially prone to b as al - cell and squamous cell c arcinomas and melanomas. People belong ing to Groups III and I V are less susceptible to
basal - cell and squamous - cell c arcinomas, though
the high risk of melanoma still remains. Bas al - cell
and squamous - cell c arcinomas and melanomas
are rarely seen in people with skin t y pes V and
V I. If they get melanoma, it is usually lo c alized on
p alm and soles ( acrolentigo melanoma ) or muco s ae ( e.g., bucc al or genit al mucos a ) . T he fre quenc y of sunburns with blisters and tot al solar
radiation a person has got during his / her lifetime,
are the indices of the melanoma risk . Ac tually,
sunburns direc tly af fec t the risk of melanoma. In
a research rep or t it was said that melanoma risk
increases by 2. 5 - 6 . 3 in those who ex perienced
sunburns with blisters ≥ 3 times. T herefore, the
risk of melanoma is higher for medic al specialists
and of fice workers working indo ors and ex p osed
to occ asional but intensive solar radiation. Tot al
volume of solar radiation is a direct precondition
for b as al - cell and squamous - cell skin c ancers.
People who regularly spend much time outdo ors
( farmers, fishermen, builders etc. ) belong to the
high - risk p opulation for non - melanomic skin c an cer development.
12 main sun-protection facts
1. Harmful solar radiation has a cumulative nature.
Each and ever y UV- exposure, either shor t or
long, is added to the total UV dosage the body
has already got, and may lead to the early lines’
formation, dermal depigmentation and skin
cancer.
2. There is no such thing as “healthy suntan”.
Suntan is a human body protective response on
UV- damage of the skin.
3. Avoid being in the sun bet ween 10 a.m.
and 2 p.m. when UV- radiation is the most
intensive. Schedule all outdoor events on the
early morning or evening.
4. Apply sunscreen onto the open par ts of the
body.
5. Remember the peculiarities of solar radiation at
high altitudes. The sun - absorbing atmospheric
layer is thinner there, so the risk of getting a
sunburn is higher.
6. UV- radiation is more intensive near the equator
where the sun rays come down at the right
angle.
7. Use protective clothes and sunscreens even
in cloudy weather. In such days UV radiation
may be less intensive but still it penetrates the
cloudy barrier and adds new skin damage to
those already existing.
7
8. UV- radiation reflected from sand, concrete and
snow, increases U V- exposure. U V- rays can
reflect and diffuse, so being in the shade does
not protect from sunburns.
9. Do not suntan in the solarium. Though in the
ar tificial solar units mainly UVA -t ype of radiation
is used, excessive solar exposure may lead to
the sunburns. Besides, UVA accelerate skin
ageing and increase the risk of skin cancer.
10.The population prone to skin cancers ( people
with skin t ypes I and II, or regularly working
outdoors, or those with skin cancer in histor y,
or those with the high photosensibilit y- related
disorders ) , should use sunscreen ever y day.
11.S o m e
medical
drugs
( sulfanilamides,
tetracyclines, contraceptive and other overthe - counter drugs ) and cosmetic products
( e.g., lime oil ) may sensibilize the skin to the
sunlight.
12.Protect children from solar radiation. Star t
to use a sunscreen when the child begins
to toddle. Only moderate solar exposure is
acceptable for children.
Sunscreens
1. A sunscreen should absorb both UVA and UVB
and have the UV-factor to be equal or more
15.
2. Avoid aromatized sunscreens : they may
provoke contact dermatitis or photodermatits.
P- aminobensoic acid is another risk factor for
contact dermatitis, so now many sunscreens do
not contain this ingredient.
3. Though some sunscreens are proclaimed to be
water- & friction - resistant and providing “all day protection”, be careful to use them again
after you have sweated or had a swim.
4. Tablets for suntan are not safe as they contain
c anthaxanthin which has side ef fects like
nausea, diarrhea, itching, dermal stigmas, night
blindness and drug - induced hepatitis. Selftan lotions are nothing more than paints for
skin, so they are safe in use, but keep in mind
that colourants do not protect your skin from
UV- damage.
This ar ticle reviewed new research findings and
looked at the benefits of sun - protection response
of the human body along with the skin's natural
protection system. Although the current level of
awareness of skin UV exposure is high, patients
should all be continuously aler ted and educated. It
isn’t possible or practical to completely avoid sun light, and it would be unwise to reduce the level
of activit y to avoid being outdoors. But too much
8
sunlight can be harmful. There are some steps that
can be taken to limit the amount of exposure to UV
rays. Following some practical steps can help to
protect from the effects of the sun. These steps
complement each other and they provide the best
protection when used together.
References
1. Suwabe, H., A. Serizawa, H. Kajiwara, M. Ohkido, and Y.
Tsutsumi. 1999. Degenerative processes of elastic fibers
in sun-protected and sun-exposed skin: immunoelectron
microscopic observation of elastin, fibrillin-1, amyloid P
component, lysozyme and alpha1-antitrypsin. Pathol. Int
49:391–402.
2. Bernstein, E., Y. Chen, K. Tamai, K. Shepley, K. Resnik,
H. Zhang, R. Tuan, A. Mauviel, and J. Uitto. 1994.
Enhanced elastin and fibrillin gene expression in chronically
photodamaged skin. J. Investig. Dermatol
3. Schwartz, E., F. A. Cruickshank, C. C. Christensen, J. S.
Perlish, and M. Lebwohl. 1993. Collagen alterations in
chronically sun-damaged human skin. Photochem. Photobiol
58:841–844.
4. Talwar, H. S., C. E M. Griffiths, G. J. Fisher, T. A. Hamilton,
and J. J. Voorhees. 1995. Reduced type I and type III
procollagens in photodamaged adult human skin. J. Investig.
Dermatol 105:285–290.
5. Chung, J. H., J. Y. Seo, H. R. Choi, M. K. Lee, C. S. Youn,
G. Rhie, K. H. Cho, K. H. Kim, K. C. Park, and H. C. Eun.
2001. Modulation of skin collagen metabolism in aged
and photoaged human skin in vivo. J. Invest. Dermatol
117:1218–1224.
6. Toyoda M, Nakamura M, Luo Y, Morohashi M (2001)
Ultrastructural characterization of microvasculature in
photoaging. J Dermatol Sci 27(Suppl 1):S32–S41
7. Pascual-Le Tallec, L., C. Korwin-Zmijowska, and M. Adolphe.
1998. Effects of simulated solar radiation on type I and type
III collagens, collagenase (MMP-1) and stromelysin (MMP-3)
gene expression in human dermal fibroblasts cultured in
collagen gels. J. Photochem. Photobiol. B: Biol 42:226–232.
8. Brenneisen, P., J. Oh, M. Wlaschek, J. Wenk, K. Briviba, C.
Hommel, G. Herrmann, H. Sies, and K. Scharffetter-Kochanek.
1996. Ultraviolet B wavelength dependence for the regulation
of two major matrix-metalloproteinases and their inhibitor
TIMP-1 in human dermal fibroblasts. Photochem. Photobiol
64:877–885.
9. Herrmann, G., M. Wlaschek, T. Lange, K. Prenzel, G. Goerz,
and K. Scharffer-Kochanek. 1993. UVA irradiation stimulates
the synthesis of various matrix-metalloproteinases (MMPs) in
cultured human fibroblasts. Exp. Dermatol 2:92–97.
10.Lavker, G., G. Gerberick, D. Veres, C. Irwin, and K. Kaidbey.
1995. Cumulative effects from repeated exposures to
subthreshold dose of UVB and UVA in human skin. J. Am.
Acad. Dermatol 32:53–62.
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UV Damage may be invisible, but it is there!
J
ust like UV radiation, UV damage is invisible but it is there. Dermatologists in the USA led by Professor David
McDaniel have used ultraviolet (UV) photography to reveal the damage on the skin caused by the sun which is invisible under normal conditions. In the following patient photographs, the photograph on the left in each series was taken
in ordinary light and show what is visible to the naked eye. The picture on the right was taken with a UV-light camera
and illustrates the amount of damage that lies beneath the surface of the skin.
18 months - Researchers had to go as young as 18
months to find a child without sun damaged skin.
37 years - This 37-year-old woman has subsurface sun
damage, which is clearly visible in the photo on the right.
4 years - At the age of 4 years, early sun damage is evident. Notice the freckling across the nose and cheeks.
52 years - Wrinkling and other signs of premature aging are
beginning to show on the surface of the skin. The significantly sun-damaged skin is visible in the ultra-violet light.
17 years - The photograph above shows that this
17-year-old girl already has significant sun damage. The
reasons for this are deliberate tanning on the beach and
in tanning salons.
64 years - This 64-year-old beach community resident
has a skin that chronicles a lifetime of chronic sun exposure. UV photography is not necessary to see that her
skin is dry, inelastic, wrinkled, and heavily mottled.
Photos provided courtesy of: David H. McDaniel, MD FAAD. Director, Institute of Anti-Aging Research. Co-Director, Hampton University Skin of
Color Research Institute. Adjunct Professor in the School of Science, Hampton University. Assistant Professor of Clinical Dermatology and Plastic
Surgery. Eastern Virginia Medical School. 125 Market Street, Virginia Beach, VA 23462.
Source: http://www.skincarephysicians.com/agingskinnet/uv_photography.html
EDITION THREE 2010
Eye Health
Advisor
9
UV Eye Damage may be invisible, but it is there!
An Australian group of researchers, led by Professor
Minas Coroneo have developed a method to detect precursors of ocular sun damage, using ultraviolet fluorescence
photography (UVFP). Presence of areas of increased fluorescence was detected by UVFP, or presence of pinguecula
was detected by standard photography.
Percentage of subjects with ocular changes
consistent with pinguecula
3x
Established pingueculae, on standard photography, were
seen in 10% of the children; on UVFP, all of these pingueculae demonstrated fluorescence (Figure 1). In total, 32%
have increased fluorescence detected on UVFP, including
the 30% with pingueculae. Of the remaining 70%, the
changes were only detectable using UVFP (Figures 2, 3).
Fluorescence on UVFP was seen in children aged 9 years
and above, with prevalence increasing with age. The presence of fluorescence was 0% for children aged 3 to 8 years,
26% for those aged 9 to 11 years, and 81% of those aged
12 to 15 years.
32 %
10 %
Standard (Control)
Photography
Ultraviolet Fluorescence
Photography (UVFP)
UV Fluorescence photography reveals early sun damage
not seen in standard photography*
Control photograph
demonstrates an
established pinguecula
Corresponding
UV-fluorescence
photograph illustrates
fluorescence at the side
of the pinguecula
Figure 1: Left nasal interpalpebral region of a 13-year-old boy with an established pinguecula.
Control photograph
is apparently normal
Corresponding
UV-fluorescence photograph
demonstrates an area of
fluorescence in the
right temporal
interpalpebral region
Figure 2: Right temporal interpalpebral region of an 11-year-old girl without pinguecula.
Control photograph
is apparently normal
Corresponding
UV-fluorescence photograph
demonstrates an area of
fluorescence in the left
nasal interpalpebral region
Figure 3: Left nasal interpalpebral region of an 11-year-old girl without pinguecula.
Photos provided courtesy of: Professor Minas T. Coroneo Department of Ophthalmology, 2nd Floor, South Wing, Edmund Blacket Building, Prince
of Wales Hospital, Randwick NSW 2031 AUSTRALIA.
* Ooi J, Sharma N, Papalkar D, Sharma S, Oakey M, Dawes P, and Coroneo M. Ultraviolet Fluorescence Photography to Detect Early Sun
Damage in the Eyes of School-Aged Children. American Journal of Ophthalmology, 2006 Feb; 141(2): 294 -298.
10
A magazine from Johnson & Johnson Vision Care
UV Radiation and the Eye*
Karen Walsh+
T
he consequences of exposing the skin to ultraviolet
(UV) radiation are well understood in the general population with 95 per cent of people associating UV with skin
problems and 85 per cent knowing about the risk of skin
melanoma.1 This level of understanding is substantially
different when it comes to the eye however, with only 7
per cent of people associating UV with eye problems.1
It has been said that aside from skin, the organ most
susceptible to sunlight-induced damage is the eye. 2 This
article summarises our understanding of the interaction
of UV with ocular tissues, discusses the challenges of
achieving adequate protection and finally reviews the role
of UV-blocking soft contact lenses in ocular protection.
What is UV radiation?
It is important to begin with a clear understanding of
what UV radiation is. This may be more clearly pictured
by defining what it is not: UV is not light; it does not
form part of the visible light spectrum. It sits adjacent to
the blue end of the visible portion of the electromagnetic spectrum. Wavelengths from 400-100nm sit within
the UV spectrum (Figure 1) which is further categorised
as: UVA 400-315nm, UVB 315-280nm, UVC 280-200nm
and UV vacuum 200-100nm. 3 The sun is a natural source
of ultraviolet energy. The shorter and arguably more
toxic wavelengths of UVC and UV-vacuum are blocked
from reaching the earth by ozone in the stratosphere. 3 It
is therefore more relevant to concentrate on the action
of UVA and UVB in this article.
°¸²Ÿíì
°¯¯¬±·¯Ÿíì ±·¯¬²°´Ÿíì ²°´¬³¯¯Ÿíì
ÓçäŸ
Ä÷âèìäñ
Ëàòäñ
UVC
UVB
³¯¯¬·¯¯Ÿíì
accelerate skin aging. UVA does not damage DNA directly
like UVB, but can generate highly reactive chemical intermediates, such as hydroxyl and oxygen radicals, which in
turn can damage DNA. Because UVA does not cause reddening of the skin (erythema), it cannot be measured in
sunlight protection factor (SPF) testing for sunscreens.
UV radiation at shorter wavelengths, designated as
UVB, causes damage at the molecular level to the fundamental building block of life: deoxyribonucleic acid
(DNA).4 DNA readily absorbs UVB radiation. This commonly changes the shape of the molecule via disruption
to hydrogen bonds, formation of protein-DNA aggregates
and strand breaks (Figure 2). Changes in the DNA molecule often mean that protein-building enzymes cannot
“read” the DNA code at that point on the molecule. As a
result, distorted proteins can be made, or cells can die.
Incoming UV
Healthy DNA
Figure 2: UV radiation can disrupt chemical bonding with DNA, resulting in
absent or misplaced nucleotide UVR
½Ÿ·¯¯Ÿíì
UVA
Ôëóñàõèîëäó
ÕèòèáëäŸËèæçó
Figure 1: The visible spectrum, broken down by wave length
Mode of action
Some effects of UV are helpful, such as its role in the formation of Vitamin D by the skin. However the same wavelengths of UVA also cause sunburn on human skin.4 UVA
and UVB can both damage collagen fibres and thereby
DNA with point
mutation after UVR
exposure
Consequences of exposure to
the skin
UV radiation is a major causative
factor in the development of skin
cancer.5 It is well known that an
increased incidence of malignant
skin melanomas has been attributed to severe sunburn
and/or exposure to excessive sunlight at an early age.6
Chronic UV exposure has also been shown to be the leading predisposing factor to the development of squamous
cell carcinoma of the lid.7 Also, the incidence of basal cell
carcinoma is significantly higher on the side of the nose
Èíåñàñäã
* First published in Optician, 2009; 237 (6204): 26-33
+ Summary by Ioannis G. Tranoudis, PhD, Senior Manager, Professional Affairs, Central and Southeastern Europe, Johnson & Johnson Vision Care.
EDITION THREE 2010
Eye Health
Advisor
11
than other parts of the face exposed to direct sun, with
the curved shape of the eye creating a focusing effect
and producing UV hot spots on the side of the nose.8
What can UV radiation do to ocular tissues?
Absorption characteristics of ocular tissue
It has already been illustrated that UVA and UVB
exert different effects on biological tissue, determined
by their respective wavelengths. Equally, there are also
differences in the absorption characteristics of ocular
tissue to UV radiation. The cornea and the intraocular
lens are the most important tissues in the eye for
absorbing UV radiation. Below 300nm (UVB), it is the
cornea that absorbs most radiation; the lens primarily
absorbs UVA of less than 370nm (Figure 3). 9
Lens
Cornea
Vitreous
λ nm
< 280
300
320
340
360
% Absorption
100
92
6
2
45
16
36
1
37
14
48
1
34
12
52
2
%
%
%
%
Both the corneal epithelium and endothelium (which cannot regenerate) are vulnerable to UV radiation. Increased
UVB exposure causes damage to the antioxidant protective mechanism, resulting in injury to the cornea and other
parts of the eye.14 A significant amount of UVB is absorbed
by corneal stroma, so thinning with keratoconus or refractive surgery allows more UVB to reach the lens.
Whilst many of the pathologies associated with UV exposure are chronic, taking years to develop, photokeratitis is
an obvious example of an acute response to UV radiation.
Also known as snow-blindness, this reversible condition is
characterised by severe pain, lacrimation, blepharospasm
and photophobia.15 The corneal epithelium and Bowman’s
layer absorbs about twice as much UVB radiation than the
posterior layers of the cornea. It is the superficial epithelium that becomes irritated in photokeratitis. A one hour
exposure to UV reflected off snow or a six to eight hour
exposure reflected off light sand around midday is enough
to cause a threshold photokeratitis. At levels below this
there may still be mild symptoms of ocular discomfort.
Climactic droplet keratopathy, or spheroidal degeneration, is a permanent pathological change characterised by
an acculmulation of droplet-shaped lesions in the superficial corneal stroma.9
Anterior Chamber
Aqueous
Iris
Cornea
Retina
Figure 3: Intraocular filtering of UV radiation by ocular tissues
Conjunctiva
The conjunctiva is easily damaged by UV, which activates a complex series of oxidative reactions and distinct
pathways of cell death.10 Squamous cell carcinomas of
the conjunctiva are possible and frequently begin at the
limbus.7 A study showed ocular melanomas, such as
choroidal melanoma, to be eight to 10 times more common in caucasians than blacks.11
The antioxidant ascorbic acid (vitamin C) is present in high
concentration in the aqueous humour. It is able to scavenge
free radicals in the aqueous and protect against UV-induced
DNA damage of the lens.16 Its presence acts as a filter for
both UVA and UVB radiation, and it has been suggested that
it has a protective role in the pathogenesis of cataract.17
Crystalline Lens
Over time, the lens yellows and loses its transparency,
primarily due to irreversible lens protein changes caused
by aging, heredity and UV exposure.18 Exposure to UV
There is strong epidemiological evidence to support
an association between chronic UV exposure and the
formation of a pterygium.12 This wing-shaped thickening of the conjunctiva and cornea is particularly seen
in people who live in sunny climates and those who
work outdoors (Figure 4). The prevalence of pterygia
occurring on the nasal conjunctiva has been explained
by peripheral light focussing onto the medial anterior
chamber beneath the limbal corneal stem cells.
A weaker link has been found between UV radiation and
the formation of pingueculae with a high prevalence found
in populations that live in both sunny and snow covered
environments.13
12
Figure 4: Pterygium (With permission of Rachael Peterson, University of
Waterloo, Canada)
A magazine from Johnson & Johnson Vision Care
radiation has been shown to lead to the development of
cataract in animal models and the link between UV and
cataract formation in humans is well established.19
viewing.26 It is clear from this evidence that provision of UV
protection from a young age, sustained throughout life is
extremely important.
The lens absorbs both UVA and UVB. It is exposed to
three times more UVA, but both types of radiation are
known to damage the lens via different mechanisms. 20
A significant positive correlation has been reported
between UVB and cortical cataract; there is also a possible association with posterior sub-capsular cataract. 21
Sources of exposure
EDITION THREE 2010
Eye Health
Advisor
0.03
0.02
21st September
0.01
17:00
16:00
15:00
0.00
14:00
The effect of UV is cumulative over our lifetime. Also,
many people have more leisure time and choose to spend
it outdoors. This, coupled with the fact that life expectancy
is rising, increases the opportunity for exposure and gives
time for the induced tissue changes to develop.3 The larger
pupils and clearer ocular media of children make them
especially vulnerable to UV. Fluorescence photography
makes it possible to view examples of early sun damage
to young eyes that are not visible under normal white light
0.04
13:00
Cumulative effect
21st November
12:00
UV radiation levels are affected by altitude; as the atmosphere is thinner at higher elevations, it absorbs less UV
radiation, increasing exposure. UV doses increase with
decreasing latitude; equatorial regions receive highest UV
radiation levels.25
0.05
11:00
Altitude and latitude
0.06
10:00
Atmospheric ozone provides a crucial protective barrier
from shorter wavelength radiation. Not only does it filter
out the harmful UVC and UV-vacuum portions of the UV
spectrum; it also attenuates the proportion of UVB reaching
the earth. The amount of ozone present in the upper atmosphere, which varies by location, time of year and time of
day, determines the amount of UVB and lower end UVA, up
to 330nm, that we are exposed to at the earth’s surface.23
The thinning of the ozone layer is particularly relevant when
discussing UV exposure and will result in an increase of UVB
reaching the earth. Following the ban on the widespread use
of chlorofluorocarbons (CFCs), it has been estimated that
ozone levels may not significantly recover until 2050.24
9:00
Ozone depletion
It has previously been quoted that around 80 per cent of
UV radiation reaches the surface of the earth between the
hours of 10am and 2pm, with levels being particularly high
in the summer months.27 More recent research measured
the ocular exposure to UVB throughout the day and at different times in the year.28 This Japanese study found that
ocular UV exposure is greatest during early morning and
late afternoon for all seasons except winter. During spring,
summer and autumn, the exposure in these peak periods
of early morning and late afternoon was nearly double that
seen in the middle of the day (Figure 5). The conclusion
that can be drawn from this is to acknowledge the difficulty the general public have in knowing when they are
most exposed to ocular UV radiation.
8:00
Risk of exposure
Exposure at unlikely times
7:00
Although the amount of UV radiation reaching the retina
in the adult eye is very low, with protection by the filtering
power of the crystalline lens (1 per cent UV below 340nm
and 2 per cent between 340-360nm), studies have linked the
early development of age-related macula degeneration with
greater time spent outdoors, while some studies have found
no association. More recently a significant link between the
10-year incidence of early age-related macula degeneration
and extended exposure to summer sun was reported.22
Hourly Average UVB Intensity (V)
Retina
Exposure from both scattered sources as UV passes
through the atmosphere, and reflected sources such
as snow, buildings and water are arguably more important. The amount of scattered or reflected UV radiation
is dependant on the surface type; for example, snow
reflects 80 to 94 per cent of UVB rays compared to water
reflecting 5 to 8 per cent. Not only is this type of indirect
exposure responsible for 50 per cent of the UV radiation
we receive,27 but it also represents a form of exposure that
may not be obvious to the general public. Similarly, most
clouds do not protect from UV; making overcast days,
where people may not take steps to protect themselves,
particularly dangerous.
Time of Day ( 7:00 am to 5:00 pm)
Figure 5: Average UVB Intensity from sunrise to sunset (after Sasaki)
Challenges of protection
The shape of the orbit and eyebrow provide some anatomical protection from direct UV radiation, and in bright
13
Sunglasses only
Sunglasses plus UV-blocking
contact lenses
UV blocking
Spectacle Lens
UV blocking
Spectacle Lens
UV blocking
Contact Lens
Exposure to UV from peripheral sources is still possible even when wearing UV blocking spectacle lenses.
The use of a UV blocking contact lens provides
additional protection.
Figure 6: Peripheral light focussing effect
light the exposure is further reduced by squinting. It has
been demonstrated however, that reflected light can still
strike the orbits,29 and the anatomy of the ocular adnexa is
such that it makes it particularly vulnerable to scattered or
reflected sources of UV, for example, reflected by the tear
film interface. It has been shown experimentally that the
use of a brimmed hat can reduce UV exposure to the eyes
by up to a factor of four.30 The frequent use of sunglasses
has been associated with a 40 per cent decrease in the
risk of posterior sub-capsular cataract.21
Peripheral light focussing effect
It is argued that peripheral UV rays are in fact the most
dangerous. Coroneo presented a hypothesis in the early
1990s as to why pterygia are more common on the nasal
side of the conjunctiva.31 Initial studies showed the cornea acts as a side on lens, focussing light incident on the
temporal cornea onto the opposite side of the eye. The
anatomy of the nose prevents this effect from occurring
in the opposite direction, that is, light incident at the nasal
limbus is not of such a peripheral angle as to allow a focussing effect onto the temporal limbus. The amount of limbal
focussing is determined in part by the corneal shape and
anterior chamber depth, perhaps explaining why certain
individuals in particular environments are affected.32
It has been calculated that, via the peripheral light focussing (PLF) effect, the peak light intensity at the nasal
limbus is approximately 20 times higher than the intensity
of incident light. Furthermore, light is also concentrated by
the same mechanism on the nasal crystalline lens, with a
peak intensity of between 3.7 and 4.8 times greater than
normal incident light. It is thought that PLF is a factor in the
development of cortical cataracts, and this is supported
by the fact that they most commonly occur in the inferior
nasal quadrant.32
The PLF has been shown to occur over a range of
incidence angles, including very oblique trajectories that
14
originate from behind the eye’s frontal plane. While wellmade sunglasses block nearly all UV radiation that enters
through the lens, most designs provide inadequate side
protection. In fact it has been shown that non wrap-around
sunglasses provide little or no protection from peripherally
focussed UV radiation (Figure 6).33
UV-blocking contact lenses
Well fitting soft contact lenses cover the entire cornea
and limbus. Adding a UV-blocker into a soft lens provides
protection to both this area and the interior of the eye from
direct and reflected UV rays. Unlike some sunglasses, they
are also effective at protecting from the PLF effect. This
has been demonstrated experimentally where the presence of a UV-blocking contact lens, etafilcon A, was found
to significantly reduce the intensity of UV peripheral light
focussing at the nasal limbus (Figure 7).33
The impact of UV-absorbing silicone hydrogel contact
lenses on the prevention of UV-induced pathological
changes in the cornea, aqueous humour and crystalline lens has been measured by a team at Ohio State
University. Matrix-metalloproteinases (MMPs) can be
induced within the cornea by UV exposure and are associated with many pathologic inflammatory cascades.
Levels of MMPs and anterior chamber ascorbic acid following exposure to UV were measured with and without
the presence of a UV-blocking contact lens. The authors
concluded that this is one of the first studies to show that
UV-blocking lenses are capable of protecting the cornea,
aqueous humour and crystalline lens from UV-induced
pathological processes.34
Some soft contact lenses provide UV protection,
with the amount of UV absorbed and transmitted by a
lens depends on the material and design. UV-blocking
contact lenses need to meet certain standards specified by the Food and Drug Administration (FDA), along
with the International Standards organisation (ISO),
A magazine from Johnson & Johnson Vision Care
100
100%
ÔÕÁ
100%
85%
80
79%
60
40
20
5%
UV-blocking
contact lens
(Class II)
Non-UV-blocking
contact lenses
Aviator-style
sunglasses
Figure 7: Peripheral light focussing effect – UV detection at the nasal
limbus (after Kwok et al)
based on their absorptive capacity at minimum thickness (often taken to be –3.00D); 35 for example, Class I
must block at least 90% of UVA and at least 99% UVB
and Class II must block at least 70% UVA and at least
95% UVB.
ACUVUE ® brand contact lenses (Johnson & Johnson
Vision Care) are unique in that all lenses available
contain UV-blocking agents meeting either Class I or
Class II standards (Figure 8). The UV-blocking capabilities of ACUVUE ® contact lenses are achieved by
co-polymerising a benzotriazole UV-absorbing monomer with the lens monomer, for example etafilcon A,
during manufacture. Benzatriazole absorbs UVA and
UVB radiation and is known to be particularly stable
once polymerised. 27 It has been shown that the addition of a UV-blocker to ACUVUE ® contact lenses has
A study that examined the UV attenuating properties of various lenses 37 showed that senofilcon A had
the lowest UV transmittance of all the lenses tested
( 8.36 per cent), meeting the ANSI standard for UV
blocking. 38 There was a statistically significant difference in the UV transmittance of senofilcon A and
galyfilcon A compared with the other SiHs tested
without UV-blockers. The authors also calculated a
protection factor for each of the test lenses which
is designed to quantify the UV protection of a CL in
a similar manner to the protection factor with sunscreen. Senofilcon A was found to have a superior
UV protection factor to the other silicone hydrogels
tested.
Education in practice
Once the benefits of UV protection have been
explained to the patient, the interest in UV-blocking
contact lenses is high. Patient literature can be used
in the reception area about ocular protection from UV
radiation. During history and symptoms, include questions on lifestyle and medications to identify high-risk
patients. When discussing actions following the examination, include ways in which the patient can minimise their UV exposure, such as use of wrap-around
sunglasses whenever outdoors and the benefits of
UV-blocking contact lenses.
UVA-blocking
97.1%
86.0%
4.4%
6.3%
AIR OPTIX™ NIGHT & DAY®
Biofinity™
PureVision®
10.0%
s$!9 ACUVUE® MOIST®
s$!9 ACUVUE® TrueEye™
Biofinity™ 9.6%
AIR OPTIX™ NIGHT & DAY® 12.2%
0
23.8%
40
AIR OPTIX™
% of UVA-blocking
52.4%
PureVision®
Class I UV blocking
Class II UV blocking
60
20
20.4%
s$!9 ACUVUE® MOIST®
s$!9 ACUVUE® TrueEye™
ACUVUE® ADVANCE®
ACUVUE® OASYS®
0
AIR OPTIX™
% of UVB-blocking
60
40
80
93.3%
Class I UV blocking
Class II UV blocking
80
20
96.1%
100
99%
99.8%
99.8%
100
100%
UVB-blocking
ACUVUE® ADVANCE®
8%
0
not affected their clinical performance in daily wear. 36
Galyfilcon A and senofilcon A lenses, both with Class
I UV-blocking, were the first to receive the World
Council of Optometry’s global seal of acceptance for
their UV protection.
ACUVUE® OASYS®
% of albedo UV detected at nasal limbus
ÔÕÀ
Figure 8: UV-blocking for a range of contact lenses
EDITION THREE 2010
Eye Health
Advisor
15
Conclusion
The effects of UV radiation are cumulative over our
lifetime, and young eyes are particularly vulnerable.
Importance should be placed on starting ocular UV protection from a young age. Maximum exposure to ocular
UV occurs at unlikely times and is relatively unaffected by
cloud, making protection important year round. The peripheral light focussing (PLF) effect is implicated in the formation of nasal pterygia and cortical cataract. Sunglasses
without adequate side protection do not prevent the
PFL effect. Use of Class I or II UV-blocking soft contact
lenses significantly reduces exposure of the nasal limbus
to peripheral light. UV-blocking lenses provide protection
to the cornea, limbus and internal structures of the eye in
situations where sunglasses are not appropriate. Perhaps
the most comprehensive message to patients should
be to advise them on the use of combined protection: a
wide brimmed hat; good quality wrap-around well fitting
sunglasses and, for those who require vision correction,
UV-blocking contact lenses.
About the author
Optometrist Karen Walsh is Professional Affairs Manager
at Johnson & Johnson Vision Care. She has worked in
both independent and multiple high street practice and
is currently finishing her Master in Optometry at City
University.
References
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34.Chandler H, Nichols J, Reuter K. The impact of UV-blocking
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38.ANSI/Z80.3. Non-prescription sunglasses and fashion eyewear
requirements.
A magazine from Johnson & Johnson Vision Care
UV Protection with Contact Lenses
Heather L. Chandler and Jason J. Nichols
I
ntroduction
Sunlight is the primar y source of radiation reach ing the human eye. The solar ultraviolet ( U V ) radi ation spectrum is t ypically classified according to
wavelength into the following based on biological
ef fect : U VA ( 4 0 0 - 320 nm ) , U V B ( 320 -29 0 nm ) ,
and U VC ( 29 0 -10 0 nm ) .1 Solar U V that reaches
the Ear th’s sur face is comprised of approximately
9 5% U VA and 5% U V B.1 U VA exposures produce
tanning of the skin and photosensitivit y reactions.
U V B radiation has impor tant influences on biologi cal processes, and is strongly absorbed by atmo spheric ozone ( in both the stratosphere and the
lower atmosphere ) . Reductions in stratospheric
ozone are therefore impor tant because of the
corresponding increase in U V B radiation reaching
the Ear th’s sur face. U VC wavelengths are com pletely filtered by the ozone layer such that they
are ef fectively not found in nature. W hile some
U V radiation is needed to synthesize vitamin D,
which is necessar y for human health, increases
in U V radiation are also harmful for human health.
Increases in U V radiation can increase damage to
a wide range of organic molecules, including DN A ,
and generally leads to increased harm to a diverse
range of biological and physical processes.
It is well established that both acute and chronic
U V ex p osure c an lead to various ophthalmic
p atholo gies. T he t y pe and ex tent of d amage
from U V radiant energy is associated with the
wavelength, duration, intensit y, and size of the
exposure. This ar ticle will discuss the impact of
U V exposure on ocular tissue and the need for
adequate U V protect, with par ticular emphasis on
U V- blocking contact lenses.
The biology of UV-induced tissue damage
U V radiation is invariably damaging to ocular tis sue by many mechanisms such as protein cross linking, dysfunction of enz ymes, ion pump inhibi tion, genetic mutations, and membrane damage. 2 , 3
These ef fects of U V on biologic targets may be due
to direct or indirect damage. In indirect reactions,
U V- activated intermediates such as free radicals
actually mediate the ef fects of U V. This results in
EDITION THREE 2010
Eye Health
Advisor
the formation of activated ox ygen species, includ ing peroxides, superoxides anion, and hydrox yl
radicals. Production of these free radicals, will
neutralize antioxidant defenses and cause cellular
damage. 2 , 3 Direct U V damage to pyrimidines in
DN A and RN A can lead to potentially mutagenic
pyrimidine dimers and ( 6,4 ) - photoproducts. 2 , 3 A ll
cells possess some abilit y to repair themselves
following U V exposure, but of ten times, U V irradia tion can lead to programmed cell death. 2 , 3 The eye
is par ticularly susceptible to photochemical reac tions due to the high concentration of pigmented
molecules including the visual pigments. 4 Damage
can occur from either acute or chronic exposure,
and the degree of damage is dependent on the
wavelength and exposure time of radiation.
UV-induced ocular changes
The eye is shielded from ambient UV by the brow
and eyelids, so that over land about 5% ambient UV
reaches the unprotected eye. 5,6 Repeated exposure of
the eyes to UV radiation causes both short-term eye
conditions and permanent eye damage. Short-term
complaints include mild irritations such as excessive
blinking, swelling, or difficulty looking at strong light.
UV exposure can also cause acute photo keratopathy,
essentially a sunburn of the cornea, such as snow
blindness or welders flash burns.1
Exposure to UV radiation over long periods can
result in more serious damage to the eyes. This
includes cataracts, pterygium, solar keratopathy,
cancer of the conjunctiva, and skin cancer of the
eyelids and around the eyes ( Figure 1).1,7-11 It is
estimated that almost half of the 8,60 0 cases of
pterygium treated annually in Australia are caused
by sun exposure.12,13 In the more temperate climate
of the northeastern United States, a significant
relationship has been found between the cumula tive dose of solar UVA and UVB and the prevalence
of pterygium.1,7,8 It has been estimated that 10%
of cataracts are potentially due to UV radiation
exposure to the eye.12 An analysis of data that con trolled for age, sex, race, income, and medical prac tices, found that the probability of cataract surger y
17
a
b
between UV radiation and age - related macular
degeneration (AMD ) is tenuous, it is possible that
damage to the retina may be indirectly associated
with UV exposure. Aside from induction of DNA
fragmentation, one potential role for UV-induced
cell death involves production of reactive oxygen
species ( ROS ). 21 The retina is an ideal environment
for generation of ROS: oxygen consumption is high,
photoreceptors are composed of polyunsaturated
fatty acids readily oxidized, RPE cells contain an
abundance of photosensitizers, and finally photore ceptor phagocytosis processes generate high levels
of ROS by itself. A substantial body of laborator y evidence underlies the association of oxidative stress
has been linked to many age -related diseases, such
as AMD. While currently unsupported by scientific
studies, it is possible that UV-induced generation of
ROS may indirectly contribute to AMD formation or
progression.
UV exposure and children
Figure 1: Examples of the UV-associated ocular pathologies (a) pterygium
and (b) cortical cataract.
increases by 3% for each degree south in latitude
in the USA .15 By the year 2050, assuming a 5 -20%
ozone depletion, there will be 167,0 0 0 - 830,0 0 0
more cases of cataract.16,17 This will result in an
increase in cataract operations resulting in added
costs of $ 563 million to $ 2.8 billion.16,17 In Australia,
approximately 160,0 0 0 cataracts are treated annu ally in excessive of $ 320 million.18 Such data demonstrating UV-induced anterior segment pathologies
are especially convincing because they have been
derived from a number of different study designs
in a number of different populations with varying
levels of other known risk factors.
Most UV radiation is absorbed by the cornea,
aqueous humor, and crystalline lens, with less than
1% of radiation below 340 nm reaching the retina
compared to over 10% of incident light at the 40 0
nm wavelength reaching the retina.19 Despite this,
all UV-radiations are genotoxic and UVB exposure
can alter the function of the retina. 20 This makes
aphakic or pseudophakic eyes more vulnerable to
UV induced retinal damage. While an association
18
As eye damage from UV radiation is cumulative,
it is important to maximally protect the eyes begin ning in childhood. A recent study in Australia found
that 80% of children has signs of UV-induced dam age by the age of 15. 22 Exposure of very young children to UV radiation should be limited, especially
when UV levels are moderate or high. Children are
particularly vulnerable to UV damage because they
have larger pupils and have clearer lenses. 23,24 In
the crystalline lens, 75% of UV radiation is transmitted in children under the age of 10, compared to
10% transmittance for individuals older than 25. 24,25
In addition, children tend to spend more time outdoors than adults, exposing them to higher levels
of UV. Recent studies estimated that only 3% of
children regularly wear sunglasses and that 23% of
lifetime UV exposure occurs by the age of 18. 26,27
During times of peak UV exposure, it is important
that all children wear sun protection. Once children
are old enough to manage wearing sunglasses and
UV- absorbing contact lenses they should be encouraged to do so if they are outside at times of high
UV levels.
UV protection from sunglasses
Ocular exposure to U V can be substantially
reduced through personal protection, such as wear
a hat with a brim and sunglasses. 5 ,6 Unfor tunately,
most individuals do not realize that the vast majorit y of sunglasses do not prevent all UV rays from
reaching the eyes. While it is true that well - made
sunglasses will block nearly all UV light that enters
A magazine from Johnson & Johnson Vision Care
through the lenses, only goggles and extreme
wrap - around st yles have lenses that provide com plete coverage. Some research has suggested that
dark sunglasses may undermine UV protection by
disabling the eye’s natural reactions to sunlight
such as squinting and may initiate counterproduc tive responses such as pupil dilation. 2 8 , 2 9 Most
other sunglass st yles allow direct and reflected
light to enter the eye from the sides, top, and
bottom of the glasses, with the result that some
sunglasses block as little as 50% of UV rays. 6 , 2 8 , 3 0
This can result in the peripheral light focusing
effect where tangential light rays will be directed
onto the nasal aspect of the eye. 9, 31 Unfor tunately,
these peripheral UV rays can be ver y damaging
to the eye. The intensit y of light passing through
most sunglasses is 20 times stronger at the nasal
limbus and up to 5 times stronger at the nasal lens
cor tex. 31- 3 3 Studies have shown that these UV rays
entering the eye from the side or top of sunglasses
are focused at the nasal limbus, where pter ygia
most frequently occur, and the nasal lens cor tex,
the most likely site for cor tical cataracts. When
UV- blocking contact lenses are used, they can
help absorb the peripheral light that sunglasses
cannot block ( Figure 2 ). 3 2, 3 4 , 3 5 Kwok and colleagues
demonstrated a significant decrease in the inten sit y of peripheral light focused on the nasal limbus
when UV- absorbing contact lenses were worn. 3 2
In addition, UV- absorbing contact lenses cover the
limbal region including the Palisades of Vogt. As a
result, these contact lenses can help protect the
vital stem cells of the cornea and conjunctiva that
reside in this region against UV rays that enter tan gentially and temporally.
UV protection from contact lenses
Currently, silicone hydrogel contact lenses make
up over 6 0 % of fits in the United States. 3 6 Silicone
hydrogels that of fer U V- protection are labeled
as Class I and Class II, with each of the dif ferent classes indicating the level of U V protection.
Class II U V- absorbing polymers have been avail able in contact lenses for several years ; most
recently Class I U V- absorbing silicone hydrogel
polymers have been introduced, providing the
highest level of U V protection. Previously, lit tle
data concerning the U V- absorbing characteristics
of silicone hydrogel polymers was available ; 3 5 , 3 7
however, measurements from a recent stud y
found that the lens polymers Senofilcon A and
Galy filcon A could ef fectively reduce U V radiation
to safe levels. 3 8 Senofilcon A or Galy filcon A are
the polymers present in Class I silicone hydrogel
contact lenses.
According to the American National Standards
Institute’s ( ANSI ) standard for aphakic and cos metic contact lens wear, Class I contact lenses
block 9 0% of UVA ( 316 – 4 0 0 nm wavelengths ) and
9 9% of UVB ( 28 0 – 315 nm wavelengths ). Class II
contact lenses must block at least 70% of UVA and
9 5% of UVB radiation. Non - UV blocking contact
lenses have been documented to absorb only 10%
UVA and 30% of UVB, on average. It is thought
that the unique materials found within Class I and
II could provide protection relative to UV- induced
ophthalmic exposures. 3 9 - 4 6 In this regard, a hydro gel contact lens is in intimate contact with the
ocular sur face, therefore potentially protecting the
ÈíóäíòèóøŸîåŸëèìáàëŸëèæçóŸåîâôòŸèíŸãèååäñäíó
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Òôíæëàòòäò
ÂëäàñŸÂË
ÔÕ¬áëîâêèíæÂË
ÄøäöäàñŸóøïä
Figure 2a: presents the relative intensity of peripherally focused UVB
measured using the mannequin head model in three insolation
conditions. In all environments, the UV-blocking contact lens
produced significantly lower intensities than no eyewear
(*P<0.056)32
EDITION THREE 2010
Eye Health
Advisor
±´
¯
Íîíä
Òôíæëàòòäò
ÂëäàñŸÂË
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Figure 2b: presents the relative intensity of peripherally focused UVA
measured using the mannequin head model in three insolation
conditions. In all environments, the UV-blocking contact lens
produced significantly lower intensities than no eyewear
(*P<0.02)32
19
sur face it covers in addition to the internal struc tures of the eye that are vulnerable to UV induced
damage.
Research on UV-absorbing contact lenses
U V ex p osure is b ased on a number of fac tors
such as environment al conditions ( altitude, geo g raphy, cloud cover) and personal fac tors ( ex tent
and nature of outdo or ac tivities ) . U V - blo cking
cont ac t lenses help provide protec tion ag ainst
such ex p osure to harmful U V radiation. Recent
studies supp or t the hy p othesis that U V - blo cking
c ont ac t lenses c an at tenu ate the amount of
peripherally fo cused U V light , sug gesting that
the risk of eye diseases such as pter ygium and
cor tic al c at arac ts may be reduced through use
of U V - blo cking cont ac t lenses. 3 2 , 3 4 Due to their
smaller diameter, g as permeable cont ac t lenses
c ap able of blo cking U V radiation, c an only pro tec t the central cornea from U V ex p osure. T he
peripheral cornea is lef t ex p osed and research
has demonstrated evidence of U V - induced d am age in such situations. 4 2 Silicone hydro gel con t ac t lenses are c ap able of covering the entire
cornea and limbus, increasing the p otential for
protec tion from U V ex p osure. T his is of consid erable signific ance since this is the lo c ation of
epithelial stem cells that continuously rep opulate
the corneal epithelium. C oncern over increased
c o r n e a l d a m a g e d u e to t h e c o m b i n a t i o n of
cont ac t lens wear and U V ex p osure has been
minimized by previous studies. 4 3 , 4 4 A hmed bhai
and Cullen demonstrated that removal or a rigid
cont ac t lens from a cont ac t lens ad apted eye
did not increase the risk of d amage to that eye
comp ared to the non - ad apted eye subjec ted to
20
Fold Change in
Total MMP-2 Expression
30
25
20
15
10
5
ns
n-U
V
co blo
nt ck
ac in
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UV
co -blo
nt ck
ac in
t le g
ns
tac
t le
Exposed to UV
no
co
n
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tac
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0
no
Currently there are five Class I cont ac t lenses
that have rec ei ve d the A meric an O ptometric
A sso ciation ( AOA ) seal of accept ance b ased on
FDA st and ards ( Acuvue ® Oasys ® , Acuvue ®
Oasys ® for Astigmatism, Acuvue ® A dvance ® ,
Acuvue ® A dvance ® for Astigmatism, and 1• Day
Acuvue ® Tr u Eye ™ ) . According to a V ist akon ®
B r a n d H e a l t h M o n i to r i n g S u r vey, p e r fo r m e d
in 20 0 5 , 5 7% of resp ondents did not know if
their current cont ac t lenses provided U V protec tion and 3 9 % believed that all cont ac t lenses
provided appropriate U V protec tion. In a 20 0 6
G allup sur vey, 5 7% of cont ac t lens considerers
rated U V protec tion as the most desired feature
in a cont ac t lens. 47 T his d at a provides strong
incentive to educ ate cont ac t lens consumers
on appropriate U V protec tion and U V - absor bing
cont ac t lenses.
35
Not Exposed to UV
Treatment Group
Figure 3: MMP expression following UV exposure. A significant increase
(*P = 0.03) in MMP expression was found in corneas exposed
to UV wearing non-UV-absorbing contact lenses compared to
corneas exposed to UV but wearing UV-absorbing contact lenses.
the s ame ex p osure of U V. 4 4 It was noted that
biomicroscopic dif ferences in the appearance of
the o cular reac tion, d amage, and recover y were
similar. 4 4 T he second stud y determined that eyes
ex p osed to U V while wearing sof t cont ac t lenses
were at no greater risk than eyes not wearing
cont ac t lenses. 4 3 Such d at a supp or ts the use of
U V - absor bing cont ac t lenses to protec t the o cu lar sur face.
S eve r a l s c ie nt i f i c s tu d ie s h ave d e m o ns t r ate d
t h at fo ll ow in g a c u te U V ex p o su re, t h e c o r n e a
is p a r t i c u l a r l y v u ln e r a b l e to U V - in d u c e d d a m a g e. 4 0 - 4 6 F o ll ow in g ir r a d i at i o n , c o r n e a s n ot p ro te c te d by U V - a b s o r b i n g c o nt a c t l e n s e s , h a d
p ro n o u n c e d c o r n e a l h a ze a n d e d e m a w i t hin t h e
e n d ot h e liu m a n d s t ro m a . 4 0 U s e of U V - a b s o r b in g
c o nt a c t l e ns e s n ot o nl y p reve nte d t h e s e c h a n g e s to c o r n e a l hyd r at i o n , b u t d e g e n e r at i o n a n d
fr a g m e nt at i o n of c o r n e a l e p i t h e li a l c e lls a n d
ke r ato c y te s w a s n e g ate d . 4 0 E x p re s si o n of p ro te i n s a s s o c i a te d w i t h i nf l a m m a t i o n a n d c e l l
d e at h h ave b e e n o b s e r ve d in c o r n e a s ex p o s e d
to a c u te U V ir r a d i at i o n . 4 6 I n e a r lie r re s e a rc h
s tu d ie s , U V B h a s b e e n sh ow n to in d u c e m at r i x
m et a ll o p rotein a s e s ( M M P s ) in hu m a n c o r n e a l
c e ll s . 4 8 T his U V in d u c t i o n of M M P p ro d u c t i o n
a n d a c t i v at i o n like l y p l ay s a ro l e in ini t i at in g
o r m a int a inin g e nh a n c e d p rote o l y t i c a c t i v i t y in
c o r n e a s w i t h ke r at i t is . Fu r t h e r, infl a m m ato r y
c e lls re c r u i te d to c o r n e a s af fe c te d w i t h ke r at i t is
u n d o u bte d l y su s t a in a n d a m p li f y M M P a c t i v i t y.
N ew d at a d e m o ns t r ate s t h at u s e of U V - b l o c k in g
A magazine from Johnson & Johnson Vision Care
EDITION THREE 2010
Eye Health
Advisor
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UV
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ac in
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0.0
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In addition to corneal changes, damage asso ciated with U V exposure has been noted in the
aqueous humor and cr ystalline lens. U V- induced
reduction of aqueous humor ascorbate levels, an
antioxidant know to protect the cr ystalline lens,
was minimized in rabbits wearing U V- absorbing
cont act lenses ( Figure 4 ) . 4 6 T his shielding of
aqueous humor antioxidant levels will likely aid
in protec tion ag ainst c at arac to genesis. W hile
U V- associated cataract formation requires chronic
exposure, a recent study utilizing acute U V, dem onstrated that U V- blocking contact lenses were
capable of decreasing lens epithelial cell death. 4 6
This is one factor known to contribute to cata ract formation. Bergbauer and colleagues found
that longer U V exposures to guinea pig eyes,
resulted in changes that occur during human lens
ageing and cataractogenesis, such as increased
pigmentation, fluorescence, and disulfide cross linking. 4 5 Eyes that wore U V - blocking contact
lenses showed reduced U V- associated damage in
the guinea pig lens. 4 5 To date, neither chronic nor
clinical studies in humans have been per formed
to demonstrate that wearing U V- blocking contact
lenses reduce the risk of developing cataracts or
other ocular disorders.
A large body of evidence suppor ts the ben efit of wearing U V- absorbing contact lenses to
prevent detrimental ocular damage associated
with acute U V exposure. W hile it is ver y likely
that U V- absorbing contact lenses can mitigate
the ef fects of U V irradiation over longer periods
of time, additional research must be per formed
to c onfir m this hy p othesis. D espite the lack
of conclusive biologic or clinical evidence, U V
protecting contact lenses should be considered
for a large number of patients. Children who
are either emmetropic or myopic may benefit
from U V- absorbing contact lenses by reducing
lifetime o cular U V ex p osure. O ther inst ances
where an U V- blocking contact lens would be
indic ated include aphakia or those who have
received refractive surger y, as the removal of
stromal thickness might alter the corneas abilit y
to naturally filter U V light. Increasing public and
practitioner awareness is of critical impor tance.
In the future, emphasis of the impor tance of
U V ocular safet y and education on U V protec tion in all forms should be strongly encouraged.
It’s impor tant to note that U V- blocking contact
lenses should not be viewed as a stand - alone solu tion. Contact lenses do not protect the eyelids,
face, or areas of the eye not covered by the lens.
The most complete measure of U V protection can
be achieved with a combination of U V- absorbing
sunglasses, a wide - brimmed hat, and U V- blocking
Ascorbate Expression
Programmed cell death through apoptotic mech anisms is frequently obser ved in corneas that
receive exposure to U V B. Chandler et al. docu mented that use of U V- blocking contact lenses
could significantly reduce levels of U V- induced
cell death, likely due to prevention of apoptosis,
in the cornea compared to eyes wearing non U V - b lo ck ing c ont ac t lenses. 4 6 Fur ther ex p eri mentation has found that irradiated eyes wearing
U V- absorbing contact lenses maintained normal
corneas, while eyes wearing standard hydrogel
lenses showed pronounced cell loss and changes
in the epithelial, stromal, and endothelial cells. 41
W hile full recover y from U V induced damage
is possible in the corneal epithelium, damage
to the stromal keratocy tes and endothelium is
considered permanent. This has implications on
how the cornea can deal with future trauma or
surger y. Cumulative examination of data relating
to U V- induced corneal changes, suggests that
long -term exposure to solar U V could be a major
factor in the etiology of cer tain keratopathies and
might be responsible for premature age - related
corneal changes. 8 This provides fur ther justifica tion for protecting the cornea with U V- absorbing
contact lenses.
Conclusions and future directions
no
sili c o n e hyd ro g e l c o nt a c t l e ns e s si g ni f i c a nt l y
re d u c e d ex p re s si o n of t h e s e p ote nt i a ll y d et r i m e nt a l p rote s a s e s ( F i g u re 3 ) . 4 6
Exposed to UV
Not Exposed to UV
Treatment Group
Figure 4: Aqueous humor ascorbate levels following UV exposure. A
significant decrease (*P = 0.03) in aqueous humor ascorbate
was observed in eyes exposed to UV while wearing non-UVabsorbing contact lenses compared to UV exposed eyes wearing
UV-absorbing contact lenses.
21
contact lenses. These contact lenses can provide
practitioners, patients, and parents with the reas surance that contact lens wearers have at least
some protection without the supplemental pro tection of hats and sunglasses. Additionally, the
protection provided by U V- blocking contact lenses
is provided all day long, allowing the wearer with
one layer of U V- protection with minimal ef for t and
obstruction to daily life. Patients with refractive
error can utilize U V- blocking contact lenses to
provide an impor tant, additional means for reduc ing ocular exposure to the damaging ef fects of
U V.
Heather L. Chandler,
PhD FAAO is a faculty member at the
Ohio State University
College of Optometry.
She
is
primarily
responsible for conducting research and
examines the molecular mechanisms by
which cataracts and
posterior
capsule
opacification form. She is also actively involved
in corneal wound healing research and frequently collaborates with the College of Veterinary
Medicine. She has received research funding
from several foundations and industrial partners
including the American Kennel Club, American
College of Veterinary Ophthalmologists, Acri.Vet,
and Vistakon. Dr. Chandler has authored over
20 peer-reviewed manuscripts and 75 abstracts
in the field of vision science. She serves as a
reviewer for many influential journals such as
Investigative Ophthalmology and Visual Science,
Molecular Vision, and Experimental Eye Research.
In addition to her research efforts, Dr. Chandler is
responsible for teaching ocular anatomy to professional optometry students at the Ohio State
University.
Jason J. Nichols,
OD MPH PhD FAAO
is a faculty member
at the Ohio State
University College
of
Optometr y,
where he is responsible for teaching
coursework on the
tear film, dry eye,
corneal physiology
and contact lenses.
He has received research funding from the
National Eye Institute of the National Institutes
of Health to study contact lens-related dry
eye in addition to the American Optometric
Foundation, and a variety of industrial partners
including CIBA Vision, Vistakon, Advanced
Medical Optics, Alcon, Menicon, Allergan,
Ocusense, and Inspire Pharmaceuticals, Inc.
He has authored over 50 peer-reviewed
manuscripts and 100 abstracts on these topics. He is currently Editor of Contact Lens
Spectrum, serves on the editorial board for
Eye and Contact Lens and is also a diplomate
in the American Academy of Optometry’s
sections of Public Health and Environmental
Optometry and Cornea, Contact Lenses, and
Refractive Technology.
Note: UV absorbing contact lenses are not substitutes for UV-blocking sunglasses as they do not
completely cover the eye and the surrounding area.
References
1. Taylor H. The biological effects of UVB on the eye.
Photochem Photobiol. 1989; 50:489 - 492.
2. Sinha RP, Hader DP. UV-induced DNA damage and repair: a
review. Photochem Photobiol Sci. 2002;1:225 -236.
3. Klums D, Schwartz T. Molecular mechanisms of UV-induced
apoptosis. Photodermatol Photoimmunol Photomed.
22
2000;16:195 -201.
4. Reme C, Reinboth J, Clausen M. Light damage revisited:
converging evidence, diverging views? Graefes Arch Clin
Exp Ophthalmol. 1996;224:2-11.
5. Rosenthal FS, Phoon C, Bakalian AE, Taylor HR. The ocular
dose of ultraviolet radiation to outdoor workers. Invest
A magazine from Johnson & Johnson Vision Care
Ophthalmol Vis Sci. 1988;29:649 - 656.
6. Rosenthal FS, Bakalian AE, Lou CQ, Taylor HR. The effect of
sunglasses on ocular exposure to ultraviolet radiation. Am J
Pub Health. 1988;78:72-74.
7. Taylor HR. Ultraviolet radiation and the eye: an
epidemiologic study. Trans Am Ophthalmol Soc.
1989;87:802-853.
8. Taylor HR, West SK, Rosenthal FS, Munoz B, Newland HS,
Emmett EA. Corneal changes associated with chronic UV
irradiation. Arch Ophthalmol. 1989;107:1481–1484.
9. Coroneo MT. Pterygium as an early indicator of ultraviolet
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