ARTICLE IN PRESS

Progress in Biophysics and Molecular Biology 92 (2006) 80–85

www.elsevier.com/locate/pbiomolbio

Review

Acute effects of UVR on human eyes and skin

Antony R. Young
St John’s Institute of Dermatology, Division of Genetics and Molecular Medicine, King’s College London School of Medicine, at Guy’s,
King’s College and St Thomas’ Hospitals, King’s College London (KCL), UK
Available online 28 February 2006

Abstract

Solar UVR (295–400 nm) has acute clinical effects on the eyes and the skin. The only effect on the eye is inflammation
of the cornea (photokeratitis), which is caused by UVB (and non-solar UVC) and resolves without long-term consequences
within 48 h. The effects on the skin are more extensive and include sunburn (inflammation), tanning and
immunosuppression for which UVB is mainly responsible. Tanning is modestly photoprotective against further acute
UVR damage. Skin colour is also transiently changed by UVA-dependent immediate pigment darkening, the function of
which is unknown. Skin type determines sensitivity to the acute and chronic effects of UVR on the skin. Some of the
photochemical events that initiate acute effects are also related to skin cancer. Solar UVB is also responsible for the
synthesis of vitamin D.
r 2006 Elsevier Ltd. All rights reserved.

Keywords: Skin; Eye; Ultraviolet radiation; Sunburn

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
2. Eye. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
3. Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
4. Chromophores that initiate the skin’s response to UVR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
5. Sunburn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
6. Melanogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
7. Immunological effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
8. Concluding remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

1. Introduction

The human body is exposed to terrestrial sunlight that contains UVB (295–315 nm), UVA (315–400 nm),
visible (400–800 nm) and infrared (IR) (800 nm–1 mm) radiation. UVB wavelengths o295 nm and UVC

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E-mail address: antony.r.young@kcl.ac.uk.

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doi:10.1016/j.pbiomolbio.2006.02.005
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A.R. Young / Progress in Biophysics and Molecular Biology 92 (2006) 80–85 81

(100–280 nm) radiation are totally filtered by the stratospheric ozone layer. The ratio of UVB to UVA depends
on the solar zenith angle that depends on latitude, season and time of day. The absolute and relative quantity
of UVB is greatest when the sun is high in the sky. However, the sun is primarily a UVA source with a
maximal terrestrial UVB content of about 5%.
Visible radiation is detected by the eye and used for sight. IR is detected by the skin’s sensory system but the
body has no specialized UVR sensory system. The skin is the body’s main interface with the environment and
is frequently exposed to UVR with either intentional or unintentional exposure to the sun. The eye is also
exposed to UVR. This paper focuses on the acute effects of solar UVR on the eye and the skin, but from a
health point of view the chronic effects are more important. In this context it should be remembered that
chronic effects on the eye, such as cataracts, and the skin, such as cancer, are the consequence of decades of
multiple acute effects that are most often sub-clinical.

2. Eye

The eye is a complex multi-layered organ that receives visible radiation on its retina. The intermediate layers
attenuate UVR to different degrees and thereby protect the retina from UV photodamage. The outermost
cornea absorbs UVC and a substantial amount of UVB, which is further attenuated by the lens and the
vitreous humor in front of the retina. UVA is less well attenuated by the cornea but is attenuated by the
internal structures so it does not reach the retina (Sliney, 2001; Roberts, 2001; Johnson, 2004).
The only acute clinical effect of UVR on the eye is photokeratitis that is also known as snow blindness or
welder’s flash (Sliney, 2001; Roberts, 2001; Johnson, 2004). This is a painful transient inflammatory condition
caused by UVC and UVB-induced damage to the corneal epithelium. Typically it appears 6–12 h after
exposure and resolves, without long-term consequences, within 48 h. In some ways it can be regarded as
sunburn of the eye.

3. Skin

The skin comprises two main layers: (i) the outer cellular epidermis and (ii) the inner largely extracellular
dermis. The main epidermal cell type is the keratinocyte, a major function of which is to differentiate till death
to create the outermost cornified protective stratum corneum. Keratinocytes are regularly renewed by cell
division in the epidermal basal layer. Dendritic pigment producing melanocytes and immunocompetent
dendritic Langerhans cells (LC) are also present in the epidermis. The dermal connective tissue is mostly
collagen synthesized by fibroblasts. The dermis also contains the skin’s vascular supply.

4. Chromophores that initiate the skin’s response to UVR

The skin contains a range of chromophores (Young, 1997) that initiate photochemical and photobiological
events. The most important is likely to be nuclear DNA that undergoes base structural change on absorption
of UVR. A wide range of photolesions are formed but the most common are di-pyrimidine lesions such as
cyclobutane pyrimidine dimers (CPD) and pyrimidine-(6–4)-pyrimidones widely known as 6–4 photoproducts
(6–4). CPDs and 6–4 are readily detected in human epidermis and dermis immediately after exposure with
solar simulation radiation (SSR), UVB and UVA (Chadwick et al., 1995; Young et al., 1998). Wavelength
dependence studies (action spectroscopy) for CPD in human skin in vivo show that UVB is 3–4 orders of
magnitude more effective that UVA (Young et al., 1998). Epidermal CPD and (6–4) are repaired by a process
called excision repair (Bykov et al., 1999; Young et al., 1996) which is dependent on a complex of repair
enzymes. Failure to repair di-pyrimidine lesions, as is the case in patients with the rare genetic disorder
xeroderma pigmentosum (XP), results in multiple skin cancers at an early age.
Trans-urocanic acid (UCA), a deamination product of histidine, is an important chromophore found in
high concentrations in the stratum corneum. Trans-UCA undergoes a photoisomerization to cis-UCA in the
presence of UVR. There is a considerable body of evidence that cis- but not trans-UCA has immunoregulatory
properties (Norval and El Ghorr, 2002). UVB is much more effective than UVA in the trans to cis
photoisomerization in human skin in vivo (McLoone et al., 2005).
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Table 1
Classification of human skin types with respect to relative response to acute and chronic solar radiation exposure

Skin type Susceptibility to sunburn Constitutive skin colour Tanning ability Susceptibility to skin cancer

I High White Very poor High

II High White Poor High
III Moderate White Good Moderate
IV Low Olive Very good Low
V Very low Brown Very good Very low
VI Very low Black Very good Very low

DNA and UCA are the most widely studied of the skin’s chromophores and are thought to be responsible
for many of the effects of UVB. Other chromophores are present but little is known about the photobiological
processes that they might initiate. Action spectroscopy had identified the presence of UVA chromophores but
these have yet to be identified with certainty.

5. Sunburn

The most obvious effect is erythema (sunburn), usually assessed at 24 h after exposure, which is highly dose
and wavelength dependent. Erythema is associated with a very wide range of molecular and cellular changes
that include the appearance of inflammatory cells in the dermis (Hawk et al., 1988; Gilchrest et al., 1983), p53
(Burren et al., 1998) and apoptotic sunburn cells (Sheehan and Young, 2002) in the epidermis. Gene and
protein expression have been observed for pro-and anti-inflammatory cytokines (Barr et al., 1999; Brink et al.,
2000), matrix matalloproteinases (MMPs), which degrade collagen, and tissue inhibitors for MMPs (Lahmann
et al., 2001; Fisher et al., 2002). MMP induction is thought to play a major role in photoageing (Fisher et al.,
2002).
The erythemal response depends on several factors that include skin type, UVR dose and emission
spectrum. Individual sensitivity to sunburn is usually determined by the visual assessment of the minimal
erythema dose (MED). In general MED increases with skin type but there is considerable overlap of MED
between skin types so that MED is not predictive of skin type (Harrison and Young, 2002), a description of
which is given in Table 1. On average the MED of a skin type IV that tans well (e.g. Mediterranean) is about
twice that of a skin type I that does not tan (e.g. Celtic) (Harrison and Young, 2002). The MED is widely used
as a dose unit in phototherapy, experimental photobiology and in the determination of a sunscreen’s sun
protection factor (SPF). Erythema is associated with increased blood flow (Young et al., 1985) and recent
studies have shown an association with increased sensitivity to thermal and mechanical stimuli (Harrison et
al., 2004). The action spectrum for erythema is very similar to that for CPD induction that suggests that DNA
photodamage in an important trigger for erythema (Young et al., 1998). Thus, UVB is much more effective
than UVA, such that the small component of UVB in sunlight is responsible for the vast majority of the
erythemal response. Laser action spectroscopy provides evidence for an additional chromophore for UVA
erythema (Anders et al., 1995) the effects of which are probably mediated via oxygen species (Auletta et al.,
1986).

6. Melanogenesis

Skin darkening in response to UVR occurs via two distinct mechanisms: melanogenesis, also known as
delayed tanning (DT), and immediate pigment darkening (IPD). Both processes are influenced by genetic
factors and are more pronounced with darker constitutive pigmentation.
During melanogenesis melanin is produced by the dendritic melanocytes of neural crest origin. Confined
mainly to the basal layer, melanocytes form a complex inter-relationship with proximal keratinocytes on
which they depend for both differentiation and function. Melanin is synthesized in specific ovoid organelles
called melanosomes and transported via dendrites to adjacent keratinocytes. Within individual melanocytes or
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keratinocytes melanin often accumulates as a nuclear ‘‘cap’’ that is thought to shield DNA from UVR.
Melanocyte density varies with body site and declines with age (Whiteman et al., 1999).
Melanogenesis is evident 3–4 days post-irradiation and can increase over 8 weeks depending on complexion
and UVR dose protocol (Caswell, 2000; Sheehan et al., 1998, 2002). It may take several weeks for the skin to
return to its base constitutive colour. There is evidence that melanogenesis is mediated via DNA photodamage
(Gilchrest and Eller, 1999) with an action spectrum that is similar to erythema (Parrish et al., 1982), which is
similar to that for CPD (Young et al., 1998). Thus, UVA-induced melanogenesis is 2–3 orders of magnitude
less efficient per unit dose than UVB and has an earlier onset, often directly after IPD. Furthermore, there is
evidence that, unlike UVB, UVA-induced melanogenesis is oxygen dependent (Auletta et al., 1986).
Melanin is synthesised either as dark-coloured brown–black insoluble eumelanin or light-coloured
red–yellow, alkali soluble, sulphur-containing phaeomelanin. The structure of melanin in the skin has not been
determined but is thought to be a complex polymer with eumelanin and phaeomelanin (Zanetti et al., 2001).
Skin types I–III demonstrate an increase in epidermal eumelanin content correlating with higher skin types,
however no correlation has been observed for phaeomelanin (Thody et al., 1991). Eumelanin is thought to be
the major factor in the photoprotective properties of melanin, which when induced in white skin types, results
in a protection factor of about 2–3 against DNA photodamage and erythema (Agar and Young, 2005). There
is in vitro evidence that products relating to eumelanogenesis may have photosensitising properties (Hill and
Hill, 2000) and it has been suggested that this may be a factor in the skin cancer susceptibility of people with
red hair (Vincensi et al., 1998).
IPD starts during UV irradiation as a greyish colouration that gradually fades to a brown colour over a
period of minutes to days depending on UVR dose and individual complexion. These changes are not due to
new melanin synthesis but rather oxidation of pre-existing melanin, and redistribution of melanosomes from a
perinuclear to peripheral dendritric location. The colour change may be so subtle as to be almost undetectable
in fair-skinned individuals but is easily observed in skin types IV (or darker). The transient nature of IPD has
made understanding of this phenomenon difficult. Significantly, no photoprotective effect for IPD has been
established hence its biological function remains unknown (Routaboul et al., 1999). The action spectrum for
IPD shows a broad peak in the UVA region (Irwin et al., 1993), and is completely different from the action
spectrum for DT, which indicates that they are mechanistically different processes.

7. Immunological effects

The skin is the body’s first barrier to infectious agents and is a major immunological organ. Epidermal LC
recognize the antigens encountered by the skin and migrate and present them to lymphocytes in the regional
draining lymph nodes. LC are sensitive to acute UVR exposure which results in their loss of numbers and
dendricity. These changes, that generally require at least 2MED (Novakovic et al., 2001) are probably the
result of migration initiated by the release of tumour necrosis factor alpha (TNFa) (Griffiths et al., 2005),
possibly from keratinocytes. In addition to TNFa, exposure of the skin to UVR results in enhanced gene and
protein expression of a range of immunoregulatory cytokines (Barr et al., 1999; Brink et al., 2000) that are
probably initiated via DNA photodamage (Yarosh et al., 2002).
Acute exposure to UVR has an effect on cellular immune function that can be clinically assessed using the
normal contact hypersensitivity (CHS) or delayed-type hypersensitivity (DTH) responses. This can be done in
two basic ways described in more detail by Fourtanier et al. (2005). Novel antigens encountered by the skin are
processed by the LC, termed sensitisation, to create a population of lymphocytes that will recognize that
specific antigen when encountered again and provoke an inflammatory reaction, termed elicitation. Exposure
of the skin to UVR prior to sensitisation results in a failure to sensitise such that there is a diminished response
at the elicitation stage. In skin types I/II a single sub-erythemal of solar simulated radiation (SSR) suppresses
sensitisation of the CHS response whereas erythemal exposures are required with skin types III/IV (Kelly
et al., 2000). The CHS and DHS elicitation responses are also sensitive to UVR but this generally requires
higher doses or repeated exposures (Moyal and Fourtanier, 2003; Damian and Halliday, 2002).
There is ample evidence from mouse studies that UVR-induced immunosuppression plays a major role in
skin cancer (Ullrich, 2002). A similar role is suspected in humans but there no direct evidence for this though it
is well known that patients with organ transplants that are maintained with immunotherapy are very prone to
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skin cancer (Bordea et al., 2004). One study suggested that humans could be divided into UVR-susceptible and
UVR-resistant populations in terms of the suppression of the sensitisation phase of the CHS response and that
this could be related to skin cancer risk (Yoshikawa et al., 1990). However, several other authors have found
that its is possible to suppress this acute response in all healthy people (Wolf et al., 2003; Baron et al., 2003;
Kelly et al., 1998) with a single UVR exposure. This suggests some evolutionary advantage in the acute
suppression of the CHS response and this may be to down-regulate immunological reactions to antigens,
especially photoantigens (van de Pas et al., 2004).

8. Concluding remarks

Solar UVR has adverse acute effects on the eyes and the skin. Vitamin D synthesis is the only recognized
benefit of UVR, specifically UVB, exposure of the skin. The acute effects on the skin are mediated by at least
two chromophores, viz. DNA and UCA. There is considerable evidence that DNA is also a chromophore for
skin cancer, especially non-melanoma skin cancer. UCA may play a role in the immunomodulatory effects
that are though to be important in skin cancer. Skin cancer is the consequence of chronic UVR exposure,
though patterns of exposure are different for different types of skin cancer. Chronic exposure is, in practice,
multiple acute exposures. Minimizing damage from acute exposures by strategies such as sun avoidance and
photoprotection is likely to minimize the risk of skin cancer, especially in sun-sensitive vulnerable skin types.

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