Responses to sunlight of Human Skin

INTRODUCTION
Exposure to sunlight can bave both beneficial and harmful effects of the human body,
depending on the length and frequency of exposure, the intensity of the sunlight, and the
sensitivity of the individual concerned. For light to interact with any material, it needs to be
absorbed. Once the light is absorbed, it raises the absorbing molecule to an excited state. The
excited molecule may then produce photoproducts that may initiate biochemical reactions.
The skin reaction to sunlight that we are most familiar with is sunburn. A sunburn reaction,
observed 8-24 hours after exposure, may include erythema (redness), edema (swelling),
blistering, pain, and delayed pigmentation, with the intensity of the reaction being
proportional to the length of exposure. A whole body sunburn experience will result in
buming, stinging, pain, and possibly sunstroke (including headache, stomach upset, and in
severe cases vomiting). Lighter pigmented individuals are more likely to experience a
sunbum reaction the first time they are exposed to sun afer the winter months. While sunburn
is associated with light-skinned individuals, it is also experienced by dark-skinned individuals
upon exposure to adequate doses of sunlight. The only difference is that the erythema
(redness) that follows may be difficult to perceive under native pigment. The sensations of
sunburn are similar for dark skinned and light skinned individuals.
The most recognized sign of overexposure to the sun is an erythema, which develops in six
to eight hours after exposure. The intensity of the sunbum reaction is related to the length of
exposure. The erythema is followed by a tanning reaction that appears three to five days after
exposure. In the last 50 years a tan has been considered a symbol of well-being. In the
nineteenth century and the early part of the twentieth century people remained out of the sun,
and a tan was a sign of working out of doors (farmer, sailor, etc). A tan is also considered as
the bodys natural mechanism of protection to subsequent exposures, along with epidermal
thickening. While erythema is the most familiar result of a sunburn, the cellular component of
the skin responds to sunlight by releasing proteins (cytokines), inducing an
immunosuppression a whole cascade of cellular and molecular events.
SKIN OPTICS
Light
Light is the visible part of the electromagnetic spectrum, with a wavelength range of 400700nm. Ultraviolet radiation is electromagnetic radiation of wavelengths shorter than visible
light, 100-400 nm. Infrared radiation occupies the wavelengths longer than visible light, 70040.000 nm. The UV is wave divided into three ranges, UVA, UVB, and UVC (UVA: 320-400
nm: UVB: 280-320 nm: UVC 200-280 nm). Of these ranges only UVA and UVB exist in
terrestrial sunlight all three exist in interplanetary sunlight.
The molecules that absorb UV (UVA and UVB) radiation (chromophores) in the skin include
DNA, proteins, 7-dehydrocholesterol (provitamin D3), NADH (ulcotinarnide adeaine
dinucleotide),
melanin, hemoglobin, and urocanic acid. Visible absorbed by the
chromopbores melanin, hemoglobin, bilirubin, -carotene, porphyrins, and water. The energy
content of each photon is given by plancks law, E = h .v, where E is the energy of each
photon, h is plancks constant (6.6 x 10-27 erg/sec), and v the frequency (for UV photons the
frequency is in the range of 1015 Hz). The energy of each photon in the UV and visible

ranges of the electromagnetic spectrum is enough to either raise a chromophore to an excited

state or break bonds. The act of breaking chemical bonds results in the fomation of free
radicals, that is, short-lived reactive species.

PENETRATION OF LIGHT INTO SKIN

Light that falls on the skin interacts with each of the skin components and is attenuated by
absorption and scattering. Absorption occurs when a photon interacts with a chromophore,
and the chromophore is thus excited to a higher energy state; scattering occurs when a photon
suffers a change in its direction of travel by some organelle, due to a change in index of
refraction. Light interacts first with the stratum corneum, then with the viable epidermis, and
finally with the dermis after it traverses the epidermis. The penetration of light into the skin is
limited in the short wavelengths of the UV. It has been shown that wavelengths shorter than
290 nm are very effective in producing DNA damage, with effects limited to the upper two
thirds of the epidermis. At wavelength longer than 300 nm DNA damage is found throughout
the epidermis as well as in the dermal fibroblasts and the keratinocytes of the out or root
sheath of the hair follicles. DNA damage includes cross-links that interfere with DNA
replication, such as the production of cyclobutane pyrimidine dimers and 6-4 photoproducts.
Absorption by proteins is the principal source of attenuation of UV radiation in the skin.
Incident radiation at about 300 nm is attenuated to 1% at a depth of 28 nm in the skin, but
radiation at 400 nm is reduced to the same level at a depth of 240nm.
ACTION SPECTRUM
An action spectrum is a map of how the threshold of a biological reaction changes in relation
to the wavelength of electromagnetic radiation that causes. If the desired "action" is the dose
to produce a threshold erythema response, the "action spectrum" represents the dependence of
the skin's sensitivity to UV radiation on wavelenght (Fig. 1.4). The -action spectrum usually
requires a monochromatic source (a souirce capable of producing.single wavelengths at a
time) such as a-tunable laser.

Figure 1.4. Two erythema action spectra are plotted versus wavelength. The solid curve was obtained
with a tunable pulsed laser and the dashed curve was obtained with a filtered mercury-xenon arc
lamp, the output of which went through a monochromator. The subjects were fair-complexioned
Caucasians; the skin sites were on the backfor the dashed curve and on the ventral forearm for the
solid curve. (MEDminimal erythema dose)

The ordinate of the graph is the reciprocal of the threshold dose to produce the action
(erythema) and therefore corresponds to sensitivity. The more sensitive the skin is to a
particular wavelength, the lower the threshold dose and the higher the value of its reciprocal.
Biological responses (end points) need not have the sarne mechanisrn of action at all
wavelengths. This becomes particularly clear in the case of pigmentation. The end point for
UV radiation-induced neomelanogenesis (new pigrnent formation) is the minimum dose of
UV radiation to produce a threshold response seven days after exposure. In the UVB,
pigment formation always follows an erythema response (there is no pigtment without
erythema). in the case of UVA1 irradiation (Table 1.4), pigment appears immediately after
exposure without erythema. The histology and biology of these radiation-dependent events
are quite different.
SOLAR RADIATION AND ITS BIOLOGICAL EFFECTIVENESS
The spectrum of solar radiation is modified by the atmosphere of the earth; what reaches the
surface of the earth is a continuum composed of UVB, UVA, visible, and infrared radiation.
The major modifiers of the solar spectrum in the atmosphere are ozone and water. Water in
the atmosphere is responsible for attenuating the infrared component of the solar spectrum.
Stratospheric ozone, on the other hand, attenuates the short wavelengths of the UV.
The UV component of the solar radiation that reaches the surface of the carth is only 2-3% of
the total incident sunlight spectrum. The distribution of UV radiation on the earth surface is
given in Table 1.4.
It can be noted that the UVB band contributes approximately only 5% of the total UV
radiation; however, it constitutes more than 80% of the biologically effective radiation. The
biologically effective radiation is calculated by integrating over the appropriate wavelength
range the product of the intensity at each wavelength by the action spectrurn for erythema at
the same wavelength. While UVB is defined to include 280-320 nm, actually there is no solar
radiation with a wavelength shorter than 292 nm. The biological effectiveness of solar
radiation depends on the bological end point used; the end point that has been most precisely
determined so far is the minimal erythemal dose (MED). This does not mean that other end
points, for example, immunosuppression, are not important; erythema is the most familiar
response and is easy to assess. An action spectrum has been measured for minimum pigment
response in humans and for photocarcinogenesis (for the hairless mouse).
There has been a considerable effort to assess the changes induced in the skin by UVA
radiation, since UVA penetrates deeper into the skin targeting the structural matrix. It has
been shown that in photoaging the major changes are induced in the dermis. In view of these
results investigators should consider both the solar UVB, and the UVA by using a term
identified as biological effectiveness (BE). For this purpose, the solar UVB is integrated over
the range 280-320 nm and the solar UVA is integrated over the range 320-400 nm. The solar
irradiance at each wavelength is then multiplied by the erythema effectiveness at that

wavelength and integrated over the appropciate range. During daytime, BE in the UVB
ranges is maximal at about noon. Except at dusk, the contribution of UVA to BE is only about
20-25%. In other words, solar UVB is five times more effective than solar UVA for producing
a minimal sunburn reaction. When the UVB reactivity is less than four times that of UVA, it
would be practically impossible to get a sunburn. There are two components of solar
radiation, one direct and the other diffuse. The direct radiation is responsible for shadows and
may be attenuated by the use of an umbrella. Diffuse radiation comes from all directions
because the incoming radiation is scattered by particles and molecule,s in the atmosphere.
Scattering, is strongest in the UV. Therefore it is possible to get a sunburn staying under an
umbrella for a long time or staying outside on a cloudy day. The problem with clouds is that
some are very effective in attenuating solar UV, while others are not. Black clouds are always
effective absorbers, while a light cloud cover almost always passes enough solar UV to
produce sunburn. The intensity of diffuse sunlight remains essentially constant throughout the
year, while the intensity of direct sunlight is maximum in the summer months when the
average monthly intensity at solar noon is three times greater than in the winter. Therefore,
the diffuse component of sunlight plays a more important role in the winter months when it is
indistinguishable in intensity from the direct sunlight. A good estimate of need for protection
from solar UV radiation is to look at one's own shadow; if the shadow is longer than one's
height, there is no need for protection. If the shadow is shorter than ones height, protection is
necessary. Sunlight may also be reflected by ground cover, like white quartz sand and snow
contributing significantly to the ambient UV load. On the other hand, water is neither a good
reflector or a good attenuator (absorber) of solar UV radiation. People in boats are at risk
only from direct and diffuse sunlight, not because of the reflection by the surface of water. It
is possible to have a sunburn after swimming because the water does not attenuate sunlight.
There are no trees or buildings to cast shadows in the middle of the ocean; therefore solar
exposure is at a maximum.