166 Guidelines
Recommendation
Recommendation: Daily sun protection in the
prevention of chronic UV-induced skin damage
Peter Elsner, Erhard Hölzle, Thomas Diepgen, S. Grether-Beck, Herbert Hönigsmann, Jean Krutmann,
Karin Scharffetter-Kochanek, Thomas Schwarz, Thomas Luger
Preamble
Guidelines are systematically derived rec-
ommendations intended to aid the clini-
cian or practitioner in making choices
for the appropriate care of patients in
specific clinical situations. Guidelines
apply to “standard situations” and take
into account all current scientific knowl-
edge available on the particular question.
Guidelines require continuous review
and perhaps revision based on the state
of scientific knowledge and practicability
in day-to-day practice. Guidelines
should not limit the methodical freedom
of the physician. Following guidelines
does not guarantee diagnostic and thera-
peutic success. Guidelines make no claim
to being comprehensive. The decision as
to the appropriateness of the measure to
be taken is made by the physician in light
of the individual problem.
Goal
Educating the population about individ-
ual risks and the resulting need for a rea-
sonable and moderate exposition to sun-
light is a public health priority considering
the dramatic increase in UV-induced
damage. This guideline gives suggestion
for correct everyday sun protection to
avoid chronic solar damage, especially
skin aging and skin cancer.
1 UV radiation
The natural source of UV radiation in
our environment is the sun. The electro-
magnetic radiation originating from the
sun and reaching the earth’s surface is
known as the optical spectrum. It ranges
from 290 to 4,000 nm. This optical
spectrum is a part of the total electro-
JDDG | 2˙2007 (Band 5)
DOI: 10.1111/j.1610-0387.2007.06099.
magnetic spectrum which encompasses
extremely short-wave cosmic radiation,
gamma rays, x-rays, ultraviolet radiation
(UV radiation), visible light, infrared
radiation up to microwaves and radio
waves (Table 1, Figure 2). UV radiation
is only a small segment of the electro-
magnetic spectrum. International con-
vention divides UV radiation into short-
wave UVC (200–280 nm), middle-wave
UVB (280–320 nm) and long-wave
UVA (320–400 nm).
The electromagnetic radiation emitted
by the sun is greatly modified during
passing of earth’s atmosphere through
absorption by oxygen, water vapor, ozone
and carbon dioxide. Solar radiation
reaching the earth’s surface at a defined
point at a defined time is known as
global radiation. It is quantitatively and
qualitatively modified during the passage
through the earth’s atmosphere. In addi-
tion to atmospheric conditions such as
ozone layer and air pollution, factors
such as latitude, altitude, season, time of
day, cloud cover and effects of indirect
radiation due to scattering in the atmos-
phere and reflection by the ground play a
role in modifying global radiation into
biologically active radiation (Figure 2).
The distribution of radiation on the body
surface varies with the angle of incidence
and the positioning of the body. Cumula-
tive UV exposure is mainly determined by
outdoor occupation or recreation and is
supplemented by use of tanning parlors or
phototherapeutic measures.
1.1 Light exposure of the skin
Studies on the anatomic distribution of
sunlight on the body surface show that
Dt. Dermatologische Gesellschaft. Journal • compilation © Blackwell Verlag GmbH • JDDG •1610-0379/2007/0502-0166
Section Editor
Prof. Dr. Hans Christian Korting,
München
the highest dose is measured on the
crown of the head. The shoulders, largely
independent of the type of bodily activ-
ity, receive about two-thirds of the total
dose; the hands, 30 to 50 %; the back,
40 to 60 %; the chest, 25 to 70 %; the
thighs, 25 to 33 %; and the calves about
25 % [1–4]. The distribution of inten-
sity on the face is, dependent on bodily
activity, for the forehead and nose 20 to
65 % of the value of the crown of the
head; for the cheeks ,15 to 40 %; for the
chin 20 to 35 %; and for the nape, 20 to
35 %.
1.2 Depth of penetration in
human skin
The depth of penetration of UV radia-
tion in human skin is of great impor-
tance for the development of various
pathological changes. While UVC (only
from artificial UV sources) hardly pene-
trates into the epidermis, UVB can reach
the superficial dermis and UVA even the
deep dermis (Figure 3).
1.3 Cumulative UV exposure
The development of chronic UV damage
is dependent on the genetics of the indi-
vidual, especially on his skin type, and
on the cumulative UV dose. This en-
compasses natural UV exposition by the
sun as well as exposition to artificial UV
sources. Important factors are outdoor
work, recreational activity, use of tan-
ning parlors and phototherapy. The
main cumulative UV burden in Europe
for people without an outdoor occupa-
tion is caused by weekend and vacation
activities and affects mainly the dorsa of
the hands, the forearms and the face.

Table 1: The electromagnetic spectrum.
Term
Electric waves (microwaves)
Infrared radiation
Visible radiation
Ultraviolet radiation
X-rays
Nuclear radiation
2 Effects of chronic UV exposure on
the skin
2.1 Photocarcinogenesis
2.1.1 Basal cell carcinoma and squamous
cell carcinoma
Non-melanoma skin cancers constitute
more than one-third of malignant tu-
mors in the white population. One can
truly speak of a global epidemic [5]
About 75–80 % of cutaneous malignan-
cies are basal cell carcinomas occurring
mostly on chronically sun-exposed skin,
especially on the head and nape. Never-
theless, about 20 % of basal cell carcino-
mas occur at sites only intermittently
exposed to the sun [6, 7]. Basal cell carci-
nomas grow slowly and practically never
metastasize. Left untreated, they can grow
destructively into bone or other tissue.
Squamous cell carcinomas comprise
about 15 % of cutaneous malignancies.
In contrast to basal cell carcinoma, they
are much more aggressive, invade under-
lying structures more quickly and can
lead to lymph node or distant metas-
tases. Typically, squamous cell carcinoma
develops in chronically sun-exposed ar-
Figure 1: Complete electromagnetic spectrum with subdivision of UV spectrum.
Wavelength spectrum Frequency spectrum
107-10-3 m 101-1011 Hz
10-3-8  10-7 m 1011-4  1014 Hz
8  10-7-4  10-7 m 4  1014-8x1014 Hz
4  10-7-1  10-7 m 8  1014-3  1015 Hz
5  10 -1  10
-8 -13
m 6  1015-3  1021 Hz
1  10 -1  10
-13 -16
m 3  10 -3  10 Hz
21 24
eas such as face, ear, nape, lips and dorsa
of hands. Actinic or solar keratoses are
precursors of squamous cell carcinoma
and considered squamous cell carcinoma
in situ.
The pathogenic role of sunlight in car-
cinogenesis can only be demonstrated
indirectly by a variety of observations.
Certain phenotypic characteristics are
more common in patients with epithelial
tumors. These include a pale complexion
with little or no ability to tan (skin types
I and II) with those exhibiting light-col-
ored eyes, red hair and freckles (“Celtic
skin type”) being particularly at risk.
Skin cancer is extremely rare in the dark-
skinned and black, presumably due to
strong pigment protection. Albinos of all
races have high incidences of tumors.
There is a significant correlation between
regular (usually occupational) outdoor
activity over years and the occurrence of
squamous cell carcinomas. The slow ac-
cumulation of the total dose leads to in-
creased risk with increasing age. Skin
cancers occur primarily on chronically
light-exposed sites, with sub-erythe-
mogenic doses appearing sufficient. In
Guidelines 167
Source
Oscillation circles
Thermal radiators
Thermal excitation,
electron impulse
Electron impulse
Internal atomic electrons
Nuclear reactions
basal cell carcinoma this correlation is
not quite as clear, as they appear less of-
ten on strongly sun-exposed sites but on
lightly shaded ones (canthus, upper lip).
The frequency of both tumors in the
white population increases with decreas-
ing latitude. All these observations impli-
cate that the development of epithelial
skin tumors directly correlates with the
cumulative dose of photons reaching the
germinative layer. In animal models skin
cancers (excluding basal cell carcinoma)
can be provoked by UV irradiation over
several months. Carcinogenicity of each
wave-length parallels the ability to pro-
duce erythema. Older experiments al-
ready showed that the UVB range
(280–320 nm) was most potent in ani-
mal models [8]. Because of these studies,
the UVB fraction of sunlight was gener-
ally held for the responsible action spec-
trum in causing basal cell carcinomas
and squamous cell carcinomas. Recent
studies prove that UVA (320–400 nm)
also plays a significant role [9, 10].
Irradiation of human skin with natural
of artificial UV sources leads directly to
changes in DNA, the primary target of
carcinogenic effects. DNA absorbs radia-
tion especially well in the UVB spec-
trum, explaining its carcinogenic poten-
tial. UV radiation causes various DNA
lesions, of which cyclobutane-pyrimi-
dine dimers and (6-4) photoproducts
play a major role. Both UVB and UVA
can indirectly damage DNA by generat-
ing reactive oxygen radicals that can lead
to DNA adducts. Oxidative DNA dam-
age leading to mutations are presumably
responsible for UVA-induced tumors.
Situations increasing UVA contribution
to tumor formation could include the
use of sunscreen protecting solely from
JDDG | 2˙2007 (Band 5)
168 Guidelines

UVB and irradiation with high intensity

UVA sources (tanning parlors).
Various repair mechanisms which can
eliminate these lesions exist. Not all repair
mechanisms always guarantee error-free,
correct restoration of genetic material.
Further, the most important error-free
mechanism, excision repair, is quickly
saturated when large numbers of dimers
are formed [11]. When damage goes un-
recognized and is not repaired, perma-
nent mutations in the DNA base se-
quences develop during cell division.
The vital role of repair systems is best ap-
preciated by studying diseases in which
repair defects occur, such as xeroderma
pigmentosum.

2.1.2 Melanoma
The most aggressive skin cancer is
melanoma, which comprised 4–5 % of
all cutaneous malignancies. The inci-
dence has climbed dramatically in the
last decades. Melanoma also displays a
south-north gradient in the USA with a
significantly higher incidence in the white
population. In Australia, the numbers are
3 to 4 times higher than in Europe.
Despite epidemiologic similarities to ep-
ithelial skin tumors, there are differences
in the history of sun exposure in
melanoma patients, so that the correla-
tion between UV exposure and develop-
ment of melanoma has repeatedly been
questioned [12, 13]. Development and
frequency of melanoma suggest that not
chronic continuous irradiation but in-
stead acute, intensive intermittent irra-
diation, mainly during leisure activity
with sunburn reactions, constitutes a
prime risk factor with the absolute UV
dose possibly playing only a secondary
role. The latency period is shorter than
in epithelial tumors [14–16]. Figure 2: Factors influencing global radiation.
This might explain why melanoma occurs
more commonly in people spending their
time mainly indoors with sun exposure ous studies suggest that this trend corre- 2.2 Immunosuppressive effects
only on vacation or during leisure time ac- sponds to altered leisure activities. Immunosuppressive effects of UV radia-
tivities. This hypothesis is supported by As sunburn is mainly elicited by UVB, tion are of great biological and clinical
preferential occurrence on body sites ex- UVB has long been suspected of being relevance, as they contribute to photo-
posed mainly during leisure time activity the sole pathogenetic factor, even though carcinogenesis. UV radiation suppresses
and not protected by pigmentation or excessive solar irradiation leads to exces- the immune system in many ways. It in-
thickened stratum corneum, two protec- sive UVA exposition. The role of UVA hibits antigen presentation, stimulates
tive mechanisms developing during has not been studied sufficiently and the release of immunosuppressive cy-
chronic sun exposure. Sites covered by controversy exists as to the importance of tokines and induces T lymphocytes of
bathing apparel such as bathing trunks or UVA in causing melanoma. It has defi- the regulatory type. A prime molecular
the female breast are often spared. nitely been proved that UVA radiation target in UV-induced immunosuppres-
Incidence and mortality of melanoma induces DNA damage and is immuno- sion is UV-induced DNA damage.
has risen sharply in western industrial suppressive in laboratory animals and Immunosuppressed transplant patients
nations in the past two decades. Numer- humans [17–19]. possess a 250-fold risk of squamous cell

JDDG | 2˙2007 (Band 5)

170 Guidelines
Figure 3: Penetration of the individual wavelength ranges into the skin.
carcinoma on sun-exposed skin [20],
even patients on immunosuppressive
treatment for autoimmune diseases are at
greater risk. This suggests that the im-
mune system plays a vital role in skin
carcinogenesis. UV radiation suppresses
immunologic tumor surveillance. Thus,
UV radiation plays a double role: first,
induction of carcinogenesis through
DNA damage, and, second, suppression
of immunologic defenses against tumor.
2.3 Photoaging
Photoaged skin, whose general appear-
ance is termed solar elastosis, can be sub-
divided into classical elastosis and the
telangiectatic, atrophic phenotype. The
former variant is characterized by diffuse
yellowish discoloration, deep wrinkles,
laxity and leathery appearance with in-
creased vulnerability, propensity to blis-
tering and disturbed wound healing. On
the nape, deep furrows with a typical
rhomboidal pattern form cutis rhom-
boidalis nuchae. Favre-Racouchot syn-
drome is exemplified by actinic elastosis
with comedos and keratin cysts. The skin
in the atrophic variant displays notice-
able erythema and is traversed by strik-
ing telangiectasia, appears “cigarette-pa-
per”-like and atrophic.
Dysregulated gene expression with dis-
tinct shifts in the qualitative and quanti-
tative homeostasis of dermal connective
tissue results from UV radiation of the
skin. Elastin and tropoelastin synthesis is
JDDG | 2˙2007 (Band 5)
highly increased [21, 22]. Type I colla-
gen, the main structural protein of the
dermis with over 80 %, is drastically re-
duced in photoaged human and murine
skin [23, 24].
Following UVA and UVB radiation,
there is increased expression and activa-
tion of matrix metalloproteinases, serine
and other proteases responsible for the
degradation of dermal connective tissue
[25–27].
UV-induced reactive oxygen species di-
rectly influence collagen metabolism.
They damage collagen molecules, inacti-
vate physiologic tissue inhibitors of met-
alloproteinases (TIMP) and induce the
synthesis and activation of matrix-de-
grading metalloproteinases.
According to the mitochondrial theory of
aging, non-repaired DNA damage and
instability of the respiratory chain in the
mitochondria contribute to aging of the
organism [28]. The frequency of muta-
tions of mitochondrial DNA is 20 times
that of nuclear DNA. These mutations
impair mitochondrial functions. Singlet
oxygen generated by UV radiation causes
the “common deletion” mutation in mi-
tochondrial DNA found with great fre-
quency in photoaged skin [29].
3 Protecting skin from chronic UV
damage
Preeminent in light protection is pru-
dent behavior with avoidance of direct
and indirect UV exposition by natural
(sun) and artificial UV sources (tanning
parlors). Textile light protection (wear-
ing UV impermeable headgear with a
wide brim and UV impermeable textiles)
is next in importance. Sunscreens with a
sun protection factor of at least 15 and a
broad spectrum of protection in the
UVB as well as UVA range should be
used in addition to the above mentioned
primary protection strategies.
3.1 Sunscreens
The scientific data on the efficacy of sun-
screens in regard to avoiding acute pho-
todamage, photoaging of the skin, the
occurrence of UV-associated skin cancer
as well as UV-induced immunosuppres-
sion is divergent. As the efficacy of sun-
screens in humans in vivo is measured by
increases in the minimal erythema dose
(MED), the proof of protection from
sunburn under special test conditions is
by definition given.
Modern sunscreens consist of a base for-
mulation containing specific sunscreen-
ing agents, whose concentrations can
range from 4 % to 40 %. Active sun-
screening agents are either chemical or
physical UV filters. Chemical UV filters
protect by absorbing UV radiation con-
verting absorbed high energy radiation
into radiation of less energy. Physical fil-
ters (mineral pigments) reflect, scatter
and absorb UV radiation. Sunscreens of-
ten also contain substances that interfere
with other reactions following UV expo-
sure such as the formation of free radicals
or reactive oxygen species (antioxidants)
or mediators of inflammation. The effi-
cacy of sunscreens is rated in Europe on
humans in vivo by determining the skin
protection factor (SPF) according to the
COLIPA International Sun Protection
Factor Test Method (2003). This method
is based on measuring the rise of the
minimal erythema dose (MED) after
standardized application of the sun-
screens. By definition, SPF only denotes
protection from UVB radiation. No
worldwide accepted test for determining
protection in the UVA spectrum exists
yet. Since February 2005 a new German
industrial norm (DIN 67502) aids in
rating UVA protection. Using this DIN
method, UVA protection is measured
and placed in comparison to UVB pro-
tection (“UVA/UVB protection balance”).
This means that UVA protection is in-
creased with increasing UVB protection:
The ratio of UVA to UVB protection

remains constant. The method is based
on an in vitro transmission measurement
through a defined layer of the sunscreen.
Rare side effects of sunscreens are irrita-
tion, allergic and photoallergic reactions
[30]. Certain sunscreens display estro-
gen-like endocrine activity in animal
models; with appropriate use this is not
to be expected in humans. As a possible
side effect of continuous use of sun-
screens, a negative effect on serum levels
of vitamin D and consequently on cal-
cium metabolism has been discussed
[31, 32]. Prospective clinical studies on
long-term use of sunscreens show no
evidence for this [33, 34].
In several retrospective studies the use of
sunscreens was identified as a possible
risk factor for melanoma. This associa-
tion could not be confirmed in a meta-
analysis [35]. This can most readily be
explained by inappropriate sun exposure
by individuals using sunscreens. This
stresses the importance of primary sun
avoidance by means of behavior and
textiles
Chemically, four types of sunscreens can
be differentiated:
– polar oils (e.g. octinoxate, homosa-
late, octocrylene)
– lipid soluble crystalline solids (e.g.
avobenzone, benzophenone, Tino-
sorb S and M)
– water soluble salts (e.g. ensulizole,
mexoryl)
– insoluble solid particles (e.g. zinc
oxide, titanium dioxide).
Compliance in the use of sunscreens is
heavily dependent on their cosmetic
properties. The higher the sun protec-
tion factor, the higher the concentration
of sunscreening agents must be. This
leads to increased “substantivity” of the
formulation, that is, increasing residues
remain on the skin after application neg-
atively affecting cosmetic acceptance.
Sunscreens with a sun protection factor
of 15 can be produced with a sunscreen-
ing agent concentration under 10 %,
which is cosmetically acceptable and
leads to better compliance among users.
Such products are suitable for regular
use. To achieve higher sun protection
factors. Significantly higher concentra-
tions (often 25 % or more) of sun-
screening agents must be employed re-
ducing acceptance and compliance and
limiting their use to defined risk situa-
tions (extreme UV exposition, patients
at risk).
3.2 Efficacy of sunscreens in
preventing chronic UV-induced
skin damage
Reduction of photoaging of the skin
through use of sunscreens has been ex-
tensively documented in vitro [36, 37]
and in animal models [38–41]. Only few
clinical studies on humans exist that
demonstrate protection from photoag-
ing and show significant effects of sun-
screen on the parameters examined [42,
43]. Since the epidemiologic association
between cumulative UV exposition and
skin aging has been shown [44] and the
effects of even sub-erythematogenous
UV doses on skin aging in vitro [45, 46]
as well as in animal models [46–48] is
known, reduction of UV exposition even
at sub-erythematogenous doses by appli-
cation of sunscreens appears warranted.
Similar mechanistic and epidemiologic
considerations as for skin aging apply to
UV-induced skin tumors. Many experi-
mental studies have shown protection
from UV-induced skin tumors by sun-
screen [49]. A limited number of prospec-
tive clinical studies demonstrated a sig-
nificant reduction in the appearance of
solar keratoses [50, 51] and squamous
cell carcinoma [52] through daily applica-
tion of sunscreens with a sun protection
factor of 15 or more.
As UV radiation inhibits cellular immune
reactions on the one hand and cellular im-
munity is essential for cutaneous immune
surveillance against developing skin tu-
mors as well as infections on the other
hand, the question arises, if sunscreens
also protect against immunosuppression
[53]. Human experiments show that the
use of sunscreens with a high sun protec-
tion factor before UV exposition prevents
the UV-induced inhibition of certain cel-
lular immune reactions [53, 54].
Contradictory results in the literature can
be explained in terms of methodology with
differing light sources and sunscreens being
employed: Emission spectra and light
doses of the light sources, on the one hand,
and absorption spectra and concentrations
of the sunscreens, on the other, vary. For
the use of broad-spectrum sunscreens with
high sun protection factors, protection
from UV-induced immunosuppression
has definitely been shown [55].
4 Recommendations for daily
protection from UV radiation
To avoid acute and chronic damage by
ultraviolet radiation, particularly sun-
Guidelines 171
light, the following protective measures
in the order listed are recommended:
1. Avoid UV radiation from artificial
sources (tanning parlors) and avoid
the sun 2 hours before and after its
highest point especially in the sum-
mer months.
During this time UV irradiation on
the earth’s surface is greatest, while in
the morning or evening hours a rela-
tively larger proportion of long-
wavelength light is present. If tanning
parlors are visited, only those identi-
fied as “certified tanning parlor” ac-
cording to the recommendation of
the “Round Table on Tanning Par-
lors” (RTS) and meeting the stan-
dards of the Radiation Protection
Commission (www.bfs.de) should be
used.
2. Wear sun-protective textiles, hats
with broad brims and UV-ab-
sorbing sunglasses while exposed to
the sun.
3. On skin areas not covered by cloth-
ing, use a sunscreen with a sun
protection factor of at least 15 and
efficacy in the UVA spectrum also
on a daily basis.
Sunscreens with a sun protection
factor of 15 filter 93.3 % of UVB
radiation, while those with a SPF of
30 and 45 filter only marginally
more, 96.6 and 97.7 %, respec-
tively, and are cosmetically less ac-
ceptable. Sunscreens should be ap-
plied daily, as even minimal UV
exposure below the erythema thres-
hold contributes to UV damage.
For particularly UV-sensitive indi-
viduals and for especially risky sit-
uations (visit to the beach or moun-
tains) sunscreens with higher sun
protection factors are recommen-
ded. UVA radiation contributes
heavily to skin aging and possibly to
the development of skin cancer and
should be filtered in addition to
erythemogenic UVB.
People with a risk of vitamin D short-
age (e.g. strongly pigmented indivi-
duals, elderly in nursing homes etc.)
should use daily sunscreens only af-
ter consulting their physician. Con-
trols of vitamin D levels and bone
metabolism may be needed.
4. Apply sunscreens 30 minutes before
sun exposure.
5. Use water resistant sunscreens when
bathing.
JDDG | 2˙2007 (Band 5)
172 Guidelines
Procedure in creating consensus
Developed during the course of a con-
sensus conference on 20 Jan. 2005. Par-
ticipants: Prof. Dr. Peter Elsner, Prof.
Dr. Erhard Hölzle, Prof. Dr. Thomas
Diepgen, Dr. S. Grether-Beck, Prof. Dr.
Herbert Hönigsmann, Prof. Dr. Karin
Scharffetter-Kochanek, Prof. Dr. Jean
Krutmann, Prof. Dr. Thomas Schwarz,
Prof. Dr. Thomas Luger
Commission for Quality Assurance of
the German Society of Dermatology:
Chairman: Prof. Dr. H. C. Korting, De-
partment of Dermatology, University of
Munich, Frauenlobstr. 8–11, D-80337
Munich, Germany
Completed: November 2005
Last Revision:
Next revision planned: November
2007 <<<
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