Photochemistry and Photobiology, 2008, 84: 450–462
Review
Effects of Visible Light on the Skin†
Bassel H. Mahmoud, Camile L. Hexsel, Iltefat H. Hamzavi
and Henry W. Lim*
Multicultural Dermatology Center, Department of Dermatology, Henry Ford Hospital,
Detroit, MI
Received 1 October 2007, accepted 5 December 2007, DOI: 10.1111 ⁄ j.1751-1097.2007.00286.x
ABSTRACT
Electromagnetic radiation has vast and diverse effects on
human skin. Although photobiologic studies of sunlight date
back to Sir Isaac Newton in 1671, most available studies
focus on the UV radiation part of the spectrum. The effects of
visible light and infrared radiation have not been, until
recently, clearly elucidated. The goal of this review is to
highlight the effects of visible light on the skin. As a result of
advances in the understanding of skin optics, and comprehen-
sive studies regarding the absorption spectrum of endogenous
and exogenous skin chromophores, various biologic effects
have been shown to be exerted by visible light radiation
including erythema, pigmentation, thermal damage and free
radical production. It has also been shown that visible light
can induce indirect DNA damage through the generation of
reactive oxygen species. Furthermore, a number of photoder-
matoses have an action spectrum in the visible light range,
even though most of the currently available sunscreens offer, if
any, weak protection against visible light. Conversely, because
of its cutaneous biologic effects, visible light is used for the
treatment of a variety of skin diseases and esthetic conditions
in the form of lasers, intense pulsed light and photodynamic
therapy.
INTRODUCTION
Studies in photodermatology have focused mainly on the
UV part of the electromagnetic radiation spectrum. It is
known that UV radiation contains sufficient energy that
produces biologic effects in the skin. Until recently, visible
light (400–700 nm) has been regarded to have no significant
cutaneous photobiologic effect. Recent developments in
photodynamic and laser therapy have led to further inves-
tigations to be conducted on the cutaneous effect of visible
light; yet, until recently, technologies in the incoherent,
nonlaser light sources have had great difficulty in fraction-
ating light to produce pure visible spectrum without a UV
†This paper is part of a special issue dedicated to Professor Hasan Mukhtar on
the occasion of his 60th birthday.
*Corresponding author email: hlim1@hfhs.org (Henry W. Lim)
 2008 The Authors. Journal Compilation. The American Society of Photobiology 0031-8655/08
450
or infrared components. This review will focus on the effects
of visible light on the skin.
HISTORY
The earliest study on photobiology was reported in 1671 by Sir
Isaac Newton, who fractionated sunlight into different colors
of the rainbow using a prism (1). Radiation outside of the
visible light spectrum was discovered 125 years later by Sir
William Herschel and by Johann Ritter. In 1800, Herschel (2)
found that a thermometer registered a higher temperature
beyond the visible red end of the spectrum than within it, a
spectrum now known as infrared radiation. In 1801, Ritter
showed a stronger chemical action on silver chloride beyond
the visible violet end of the spectrum (3), hence the term UV
spectrum.
In 1798, Robert Willan described sensitivity to sunlight
under the term eczema solare (4), a condition which was also
reported by Rayer (5). Sir Everard Home’s (6) experimental
observation in 1820 in England reported that some compo-
nents of sunlight, other than heat, affected the skin, which was
confirmed in 1829 by Davy (7), who investigated whether
different rays of the solar spectrum produce different effects.
Since ancient times, it has been known that electromagnetic
radiation has injurious as well as useful effects; however, the
science of photobiology only started to fully develop in the
past few decades. As the ability to produce specific wave-
lengths was developed, the biologic implications of these
wavelengths were identified.
BIOLOGIC EFFECTS OF LIGHT
Electromagnetic radiation is classified based on wavelength.
Visible light (400–760 nm) is the wavelength range of general
illumination. Other regions of this spectrum include radio
waves, microwaves, infrared radiation (heat), UV, X-rays and
gamma radiation.
Definition of visible radiation
The visible spectrum is the portion of electromagnetic radiation
visible to the human eye, which responds to wavelengths from
400 to 700 nm; some individuals can perceive wavelengths from

380 to 780 nm. A photopic eye, namely the eye that has been
exposed to a relatively high intensity light which permits
photochemical changes in the retina and constriction of the
pupil, has its maximum sensitivity at 555 nm, the green region
of the optical spectrum. The frequently used term, UV light, is
technically incorrect. The term ‘‘light’’ is best used for
wavelengths of radiation that results in a sensation of vision.
Hence, the preferred term is UV radiation (8).
Skin optics
Once photons enter the skin one of two processes may occur.
The first process that takes place when UV and visible photons
enter the skin is absorption, which initiates chemical changes in
the cells. When absorbed, the energy of the photon is
transferred to the chromophore and the photon no longer
exists; hence the depth of penetration of radiation is affected by
position and absorption spectrum of the chromophore in the
skin. The second process to occur is scattering, which is
dependent on the wavelength of the photon, which affects the
depth of penetration of radiation into the skin (8). Absorption
spectrum is the probability of absorption of photons against
the wavelength. A number of chromophores only absorb UVB
and UVA, and others absorb throughout the UV and visible
wavebands. b-carotene has absorption maxima at 465 and
490 nm in the visible spectrum, but also absorbs in the UV
range. Protoporphyrin IX has an absorption maximum at
405 nm but absorbs UVA strongly; the other major absorption
bands include 410, 504, 538, 576 and 630 nm. Other endoge-
nous chromophores which absorb visible light include melanin,
water, riboflavin, hemoglobin and bilirubin. In photodynamic
therapy (PDT), the photosensitizing dyes absorb longer visible
wavelengths (>650 nm), while 5-aminolaevulinic acid (ALA)
PDT results in endogenous protoporphyrin IX production
which absorbs light in the aforementioned spectra. Exception-
ally, melanin absorbs throughout the UVB, UVA and visible
wavebands (8). Figure 1 illustrates absorption spectra of some
of the chromophores in the skin.
Erythema
UVB can penetrate through the epidermis to the upper dermis.
It exerts its biologic effects, in part, via mediators released by
epidermal cells (9,10). Erythema and sunburn are mainly
caused by UVB radiation, although UVA and visible light can
also cause skin erythema, requiring much higher doses than
Figure 1. Skin chromophore absorption spectra.
Photochemistry and Photobiology, 2008, 84 451
UVB. Mediators released under the effect of visible light and
action spectrum of erythema in the visible range are not yet
fully studied. A 1960 study (11) described the erythema caused
by UV radiation and visible light. It found that the UV
erythema caused by 250 and 297 nm is the result of capillary
dilatation, and such wavelengths penetrate only very superfi-
cially into the upper dermis. On the other hand, as the long-
wave UV (366 nm) and visible light (405 and 436 nm)
penetrate much deeper into the dermis, it is suggested that
the erythema caused by these longer wavelengths radiation is
the result of dilatation of the vessels of the subpapillary plexus.
Radical production
Ascorbate is a nonenzymatic antioxidant, which contains
oxidative products including ascorbate free radical (12). A
2006 study (13) of ex vivo irradiation of human skin with solar-
simulated radiation, showed that the ascorbate radical signal
was directly proportional to the irradiance. Radical produc-
tion in the substratum corneum by UV and visible light
components were approximately 67% and 33%, respectively.
This study indicated that visible light contribution to radical
production, which has obvious implications in the design of
organic sunscreens and the prevention of free-radical, induces
damage.
Pigmentation
Limited information is available regarding the role of visible
light on pigmentation. As a result, most information is
extrapolated from UVA wavelengths upon pigmentation. Skin
pigmentation induced by radiation occurs in three
phases—immediate pigment darkening (IPD), persistent pig-
ment darkening (PPD) and delayed tanning (DT) (14). IPD
occurs as a response to low doses of UVA (1–5 J cm)2),
appears immediately after exposure, and fades within 20 min
to 2 h (15). IPD results from oxidation and redistribution of
pre-existing melanin (14). At higher UVA doses (>10 J cm)2),
PPD occurs and persists from 2 to 24 h (15). PPD also results
from oxidation and redistribution of pre-existing melanin (14).
In contrast to IPD and PPD, DT, occurring days after
exposure, is associated with the synthesis of new melanin. Both
UVB and UVA are capable of inducing DT, However, DT
induced by UVA is preceded by IPD and PPD without
noticeable redness, while that induced by UVB is always
preceded by erythema. UVB is more efficient than UVA in
inducing erythema and DT (16).
In 1983, Kollias and Baqer (17) conducted an in vivo study
on the changes in pigmentation induced by visible and near-
infrared light using a polychromatic light source of 390–
1700 nm, which simulates the solar spectrum without the UV
part, with powers of up to 0.35 W cm)2. Their aim was to
determine the changes in color occurring during irradiation and
to also record them using remittance spectroscopy. They found
that pigmentation could occur without any UV component,
and that there were no erythema or temperature changes
greater than 0.4C, even after 3 h of irradiation, associated with
the pigmentary change. They objectively defined detectable
erythema as changes in the remittance at 542 and 575 nm of
more than 5%. IPD was observed with energy greater than
720 J cm)2, and the pigmentation lasted for up to 10 weeks.
452 Bassel H. Mahmoud et al.
Other studies showed that exposure of normal skin to
visible light can result in the induction of IPD, immediate
erythema and DT. Porges et al. (18) exposed 20 healthy
individuals with skin Types II, III and IV to visible light source
of a compact 150 W xenon-arc solar simulator, with a spectral
distribution between 385 and 690 nm. Both IPD and imme-
diate erythema faded over a 24-h period; whether these
represent thermal effects is unclear. The residual tanning
response remained unchanged for the remaining 10-day
observation period. The threshold dose for IPD with visible
light was between 40 and 80 J cm)2, while the threshold dose
for DT was closer to 80–120 J cm)2.
Because of lack of standardization pertaining to the
spectrum of visible light producing sources in the aforemen-
tioned studies by Kollias and Porges, it is hard to compare
their results. The filter used in the latter study was a 3-mm
Schott GG385, which should remove most of the short
wavelength UV radiation; however, a part of the long UVA
spectrum, from 385 to 400, together with the visible light, is
still emitted by this filtered light source.
While currently there is no standardized visible light source
used consistently in all studies, there are several ways of
obtaining visible light radiation. Broadband visible light could
be produced by filtering out the UV and infrared energy in
most broadband light sources. For example, the solar simu-
lator could be used with proper filters to attenuate the UVA,
UVB and IR radiation. Long-pass glass filters could be used to
attenuate UVA and UVB radiation and heat-absorbing hot
mirrors could be used to block the infrared energy. A low-cost
option is to use an incandescent lamp with a Plexiglas that
blocks most of the UV component. The more expensive option
is to use a xenon-arc lamp with modern high-throughput
interference filters (Semrock, Inc., Rochester, MN) to obtain
the broadband visible light (400–700 nm) while efficiently
blocking the UV radiation as much as 6 orders of magnitude.
To minimize the effect of heat resulting from infrared
radiation, the ideal choice could be a water filter (Y. Liu,
personal communication). In the future, it would be ideal to
use an identical type of light source in all studies.
Kollias et al. (19) reported the development of erythema
and melanogenesis in skin Type V individuals following
exposure to 295, 305, 315 and 365 nm monochromatic
radiation, and then compared erythema and melanogenesis
observed in individuals with skin Types I and II. The ratio of
values for the minimum erythema dose between skin Type V
and skin Types I and II was 2.29 ± 0.8 (mean ± SD), which
is close to the ratio of constitutional pigment in these skin
types, as measured by diffuse reflectance spectroscopy in the
visible range. Interestingly, the minimum melanogenic dose at
295, 315 and 365 nm was independent of skin type.
It would be interesting to correlate the above data presented
by Kollias and colleagues with future studies in the longer
visible light spectrum aiming at determining the minimal
erythema dose and minimum melanogenic dose at different
wavelengths.
CELLULAR AND MOLECULAR
PHOTOBIOLOGY
Radiation has a variety of biologic effects on human skin,
depending on the wavelength. The effects of UVB (290–
320 nm) on the skin are mediated predominantly by direct
DNA damage, while the effects of UVA (320–400 nm) are
dominated by indirect damage caused by reactive oxygen
species (ROS) such as singlet oxygen. UVA has been divided
into UVA1 (340–400 nm) and UVA2 (320–340 nm), with
UVA2 inducing damages similar to that of UVB (20). UVB
dominates the carcinogenic effects of sunlight; however, UVA
has been estimated to contribute around 10–20% to the
carcinogenicity of sunlight (21).
Similar to the continuum of the biologic effects of UVB to
UVA2, because the division between UVA1 and visible light
is arbitrary, the photobiologic effects of UVA1 and visible
light may also be similar (22). The effects of UVA1 and
visible light on human skin have not been comprehensively
investigated, although it has been shown that UVA1 (365 nm)
induces squamous cell carcinomas (SCC) in hairless mice
which have been exposed to a daily radiation at three
different doses—240, 140 and 75 kJ m)2—for 620 days (23).
Due to the lack of in-depth investigations regarding the long-
term effects of visible light on skin, and as it is widely used in
laser and PDT, further studies on its long-term effects are
needed.
Edstrom et al. (22) studied the effects of repetitive low doses
of UVA1 on 12 healthy individuals, utilizing an output
spectrum between 340 and 400 nm, a peak emission at
365 nm, and visible light using an Osram xenon-arc lamp
with two filters (Schott KG 3 and GG 420), which gives a
transmission of only visible light. A segment of the buttock
was exposed to 20 J cm)2 UVA1 and another segment to
126 J cm)2 of visible light three times a week for 4 weeks.
Edstrom et al. observed a dispersed pattern of p53 (involved in
several cell-cycle checkpoints, in G1, G2 and at mitosis)
positive cells in the epidermis, which may be a reversible
reaction to both UVA1 and visible light. Ren et al. (24)
observed a compact pattern, which reflected a clonal multipli-
cation of keratinocytes with mutated p53; no expression of
p21WAF)1 (the p53 mediator responsible for the arrest in G1)
in keratinocytes was noted, which is in contrast to that
reported after UVA and UVB irradiation (25).
Interestingly, p53 was immunohistochemically detectable in
the biopsy specimens of healthy individuals after only few
irradiations with UVA1 in suberythemal doses. The increase
was observed even after the first UVA1 exposure, and there
were more positive cells after each consecutive irradiation. The
number of p53-positive cells tended to accumulate and
remained elevated 2 weeks after the last irradiation. An
increased expression of cyclin A and a preferential expression
of Ki67 was also observed, indicating proliferation of epider-
mal cells, which is a known effect of UVA1. These findings
suggest that there was an increase in epidermal cells in the G1
phase. p53 downregulates the bcl-2 gene, whose product acts as
an antiapoptotic agent. However, these investigators noted a
small increase in bcl-2 expression, the opposite of what was
expected, indicating that p53 may be mutated. Visible light
also caused an increase in p53-positive cells and proliferation
in the epidermis, but to a lesser degree than after irradiation
with UVA1 (22).
Kielbassa et al. (26) studied action spectrum for the
formation of dimers and oxidative DNA modification in
mammalian cells, using a monochromatic radiation. Oxidative
DNA damage formation was observed extending from the

UVA1 range into visible light, with a peak between 400 and
450 nm.
Similar to long-wave UVA, visible light produces DNA
damage indirectly through the generation of ROS. Hoffmann-
Dorr et al. (27) have analyzed the generation of micronuclei
associated with the induction of oxidative DNA damage by
visible light (>395 nm) in melanoma cells and primary
culture of human skin fibroblasts. Using cyclobutane pyrim-
idine dimers as a marker of the direct effect of electromag-
netic radiation, and the presence of modified DNA bases
sensitive to repair enzyme glycosylase as a marker of
electromagnetic radiation-induced oxidative damage, it was
concluded that indirectly generated oxidative DNA modifica-
tions can contribute significantly to the adverse effects
of visible light. Consequently, the wavelength dependence of
DNA mutation induction does not correlate with that of
pyrimidine dimer formation. The ratio of pyrimidine dimers
and oxidative DNA modifications at various wavelengths
depends on both the direct and indirect mechanisms which
have an impact on the assessment for the risk of mutation
related to solar irradiation. In addition to a peak at 313 nm,
DNA base modifications by solar radiation has a second peak
between 400 and 450 nm because of the excitation of
endogenous photosensitizers. Oxidative damage induced by
400–500 nm accounts for approximately 10% of the total
endonuclease-sensitive base damage in cells exposed to
sunlight (26).
In an in vivo study by Kvam and Tyrrell (28), the total
amount of oxidation of guanine induced by monochromatic
radiation ranging from a UVB wavelength (312 nm) up to
wavelengths in the near-visible (434 nm) range in dermal
fibroblasts was the same or greater than the amount of
cyclobutane pyrimidine (the major type of direct DNA
damage). The action spectra for oxidative damage in skin
fibroblasts were UVA (above 334 nm) and near-visible radi-
ations. In rapidly dividing lymphoblastoid cells, no oxidative
guanine damage was induced. However, in melanoma cells,
almost as much damage as in nongrowing fibroblasts (1.1 per
104 guanine bases after 1200 kJ m)2 UVA) were found. The
authors concluded that oxidative DNA base damage can most
likely contribute to the induction of both nonmelanoma and
melanoma skin cancer by sunlight.
ROLE OF ELECTROMAGNETIC
RADIATION IN THE PATHOGENESIS OF
PHOTODERMATOSES
UVB (290–320 nm) is the major spectrum responsible for
cutaneous erythema, whereas UVA (320–400 nm) is involved
in the majority of photodermatoses.
Photodermatoses are a broad group of skin disorders
primarily caused or exacerbated by exposure to UV or visible
light. Photodermatoses can be classified into five general
categories—idiopathic, most likely immune mediated; second-
ary to exogenous agents; secondary to endogenous agents;
photoexacerbated dermatoses; and genodermatoses (29).
Photodermatoses can have action spectrum in the UVB,
UVA and ⁄ or visible light range, with UVA being the most
common. Those with action spectrum in the visible light range,
solar urticaria, chronic actinic dermatitis (CAD) and cutane-
ous porphyrias will be discussed in the following section.
Photochemistry and Photobiology, 2008, 84 453
Solar urticaria
Solar urticaria is a rare photosensitivity disorder, most
commonly occurring in early adulthood, but with variable
age of onset. The disease has been well described from the
beginning of the 20th century. Hundreds of cases have been
reported worldwide. In 1988, Champion (30) reviewed 2310
cases of urticaria which his group had seen over a period of
30 years, of which nine (0.4%) developed solar urticaria. In a
recent survey of 390 patients with urticaria, only two cases
(0.5%) of solar urticaria were found. In a study conducted in a
photodermatology referral center, the percentage of patients
with solar urticaria in relation to other photodermatoses
ranged from 4% to 18% (31).
Solar urticaria is considered to be a Type I immediate
hypersensitivity response, mediated by mast cells. It is char-
acterized by the onset of a pruritic, erythematous and
urticarial eruption on sun-exposed skin within minutes fol-
lowing sun exposure, and is usually resolved within 2 h, if
further exposure is avoided. Solar urticaria is usually more
marked on skin that is normally covered, with relative sparing
of the face and dorsa of the hands. Episodes may be
accompanied by systemic symptoms such as headache, nausea,
bronchospasm, faintness and syncope (32).
Action spectrum of solar urticaria. The activating wavelengths
responsible for solar urticaria vary from UVB to visible light.
Monochromator phototesting for solar urticaria was per-
formed by Stratigos et al. (33) in 23 patients, the majority
exhibiting induction of lesions with visible light. In a study by
Uetsu et al. (34), 24 patients (60%) were sensitive only to
visible light. On the other hand, patients with solar urticaria
seen in the UK and Europe have been reported to be activated
most frequently by UV radiation. The majority (77%) of
patients reported by Frain-Bell (35) reacted to a wide action
spectrum from UVB to visible light, and only 5 of 26 patients
responded to visible light alone. Ryckaert and Roelandts (36)
reported that from a series of 25 patients, 5 were sensitive only
to visible light. Figure 2 displays the results of the aforemen-
tioned studies in relation to the action spectrum of solar
urticaria.
In solar urticaria, a certain spectrum outside of the
activating wavelengths may affect wheal formation. An
inhibition spectrum was first demonstrated by Hasei and
Ichihashi (37) in a patient who developed urticaria in the 400–
500 nm range. Longer wavelengths inhibited wheal formation
when irradiation was performed immediately after exposure to
radiation at the action spectrum. The wavelengths of the
inhibition spectrum are commonly longer than those of the
action spectrum. However, in one of their patients and also in
a patient studied by Leenutaphong et al. (38), the urticarial
reaction to visible light was inhibited by pre-exposure and
postexposure to UVA, respectively. In addition, augmentation
spectrum has also been described in one patient with an action
spectrum in the 320–420 nm range; exposure to longer
wavelengths (450–500 nm) before exposure to 320–420 nm
enhanced wheal formation (34). In a study of 14 patients, an
augmentation spectrum was detected in four cases examined
(29%), while an inhibition spectrum was found in 68%. The
mechanisms and clinical relevance of inhibition and augmen-
tation spectra remain unknown (34).
454 Bassel H. Mahmoud et al.
Figure 2. Studies showing action spectrum of solar urticaria: (a)
Stratigos et al. (33). (b) Uetsu et al. (34). (c) Frain-Bell (35). (d)
Ryckaert and Roelandts (36).
Chronic actinic dermatitis
Chronic actinic dermatitis, a term originally proposed by
Hawk and Magnus (39), is a spectrum of clinical entity
covering conditions previously known as persistent light
reactivity, actinic reticuloid (40), photosensitive eczema (41)
and photosensitivity dermatitis (42). It affects most commonly
elderly males and manifests as a chronic eczematous photo-
distributed eruption (43). In several studies conducted in
photodermatology referral centers, the percentage of patients
with CAD in relation to other photodermatoses ranged from
5% to 17% (31).
Action spectrum of chronic actinic dermatitis. While the action
spectrum of CAD is primarily in the UVB or UVB and UVA
range, action spectrum at the visible light range has been
reported. Stratigos et al. (33) found that phototesting in
diagnosed cases of CAD showed abnormal erythemal reac-
tions to UVA (5 ⁄ 15, 33.3%), UVA and UVB (5 ⁄ 15, 33.3%),
UVB (2 ⁄ 15, 13.3%), and to UVA, UVB and visible light (2 ⁄ 15,
13.3%). Dawe and Ferguson (44) described a study involving
507 CAD patients investigated by monochromator phototest-
ing in the Dundee photobiology unit. UVB, UVA and visible
light induced lesions in 95%, 92% and 67% of cases,
respectively. Phototesting is always abnormal in moderate to
severe CAD, confirming the disorder. Papular or eczematous
lesions are commonly seen after exposure to the UVB
wavelengths, often also the UVA but rarely with visible light.
Occasional abnormalities have been reported to just the UVA,
and also very rarely to just 600 nm visible light (45).
Phototoxic and photoallergic skin reactions
Phototoxic reactions are significantly more common than
photoallergic reactions; they mimic exaggerated sunburn. Pho-
toallergic reactions are delayed hypersensitivity response
resembling allergic contact dermatitis on sun-exposed areas,
but may also extend into covered areas (46). Management
includes topical and systemic corticosteroids; avoidance of
precipitating agents is essential.
Porphyrias
Congenital erythropoietic porphyria was described using
different terminology such as pemphigus leprosus by Schultz
in 1874 (47) (who noticed the dark coloration of urine);
xeroderma pigmentosum by Gagey in 1896 (48); hydroa
vacciniforme by M’Call Anderson in 1898 (49) (who was the
first to recognize that the lesions were induced by light);
hereditary syphilis by Vollmer in 1903 (50); hydroa aestivale
by Ehrmann in 1905 (51) (who first suggested that the lesions
resulted from the sensitization of the skin to light exposure
by porphyrins); and also by Linser in 1906 (52); until
Günther described the condition, in 1911, as a porphyria. The
effect of porphyrins in leading to acute photosensitivity was
demonstrated by Meyer-Betz when, in 1912, he injected
himself with 200 mg hematoporphyrin and became acutely
photosensitive (53). The name porphyria cutanea tarda was
first used in 1937 by Waldenstrom (54), who also extensively
studied acute intermittent porphyria. The other porphyrias
were described later, some after World War II. In 1951,

erythropoietic protoporphyria was recognized. Variegate
porphyria was recognized in South Africa in the 1940s and
1950s (55).
Porphyrias are caused by accumulation of endogenous
phototoxic agents (porphyrins) because of enzyme defects in
heme biosynthesis. Characteristic porphyrin profiles in plasma,
erythrocytes, urine and stool allow for diagnosis. Porphyrin
molecules are tetrapyrrole ring structures which absorb visible
light, generating excited states. Exposure of porphyrins to
sunlight results in the generation of free radicals, which cause
lipid peroxidation and protein cross-linking leading to cell
membrane damage and death. The type of cellular damage
depends on the solubility and tissue distribution of porphyrins
(56).
Most types of porphyrias are inherited in an autosomal
dominant manner with incomplete penetrance, but autosomal
recessive and more complex patterns of inheritance are also
seen in some. The genes coding for the enzymes have been
characterized and localized; mutations in them have been
identified in patients with porphyria. Individual porphyrias are
genetically heterogeneous but the clinical phenotype is uni-
form; the seven different porphyrias can be divided into two
subgroups—hepatic or erythropoietic—according to the organ
in which accumulation of porphyrins and their precursors
primarily appears (57). Porphyrias occur from the deficiencies
of seven enzymes in heme biosynthesis. Aminolevulinate
dehydratase deficiency porphyria and acute intermittent por-
phyria do not have cutaneous findings. Cutaneous findings in
the other porphyrias could be subdivided into acute photo-
toxicity and subacute phototoxicity (58). Prenatal diagnosis is
possible for congenital erythropoietic porphyria (59), and in
vitro gene therapy has been successfully performed for
hepatoerythropoietic porphyria, congenital erythropoietic por-
phyria and erythropoietic protoporphyria (60).
Pathogenesis of skin symptoms in hepatic porphyrias. Porphyria
cutanea tarda, hereditary coproporphyria and variegate por-
phyria have chronic manifestations usually days after sun
exposure. Blistering and scarring occur on the backs of the
hands. Hypertrichosis and hyperpigmentation arise on the
face. Skin symptoms are marked in summer after sun
exposure. Skin symptoms develop as a result of interaction
of solar radiation (around 400 nm) with high amounts of
circulating porphyrins, which originate from the liver and
accumulate in the skin (61). One of the properties of
porphyrins is their intense spectral absorption at about
400 nm. This is known as the Soret band, which is a very
strong absorption band in the blue region of the optical
absorption spectrum of porphyrin. It is intense and narrow
and is most well developed in acid solution; its position and
magnitude differ for each porphyrin (62). A study by Stolik
et al., on the kinetic of porphyrins in mice using photoacoustic
and fluorescence spectroscopies, showed that the highest
porphyrin concentration in skin, determined from the optical
absorption of the Soret band at 410 nm, occurred 2 h after
delta-aminolevulinic acid administration and corresponds to
porphyrin production in skin tissue. In addition, a first peak
was observed at 15 min, which possibly represents the por-
phyrin content in blood vessels within the skin (63). Skin
manifestations of porphyrias include two types—accumulation
of water-soluble uroporphyrins and coproporphyrins with
Photochemistry and Photobiology, 2008, 84 455
blister formation (which is the most commonly seen type of
cutaneous porphyrias) and accumulation of the lipophilic
protoporphyrin which is characterized by an immediate
burning sensation in the skin to exposure of light. This can
be followed by swelling, redness, purpura and sometimes
erosions. These clinical features occur more commonly in
erythropoietic protoporphyria (64).
PHOTOPROTECTION
Sunscreens
Sunscreens are the mainstay of treatment for photodermatoses.
In some cases, patients are sensitive to visible as well as UV
radiation or may be sensitive to isolated visible wavelengths,
particularly in the blue region. Unfortunately, currently avail-
able sunscreens are not effective for photodermatoses that
have action spectrum in the visible light range. Patients
taking systemic photosensitive drugs such as Photofrin for
PDT have photosensitivity in the visible light range for up to
6 weeks (65).
UV filters are divided into organic (also known as
chemical) and inorganic (also known as physical) filters;
currently there is no effective organic filter for visible light.
Chemical agents such as dibenzoylmethanes and camphor
derivatives have been used to provide extended protection
for the UVA region. The term ‘‘total sunblock’’ is imper-
fectly used to describe them. Only optically opaque filters
are able to absorb visible light; therefore, only optically
opaque inorganic filters can protect against visible light. The
two generally available inorganic sunscreen agents are zinc
oxide (ZnO) and titanium dioxide (TiO2) (66). When an
incident visible light enters particles of TiO2 and ZnO, it is
reflected by some facets of the particles in the direction of
our eyes and consequently it appears white (67). Absorption
range from visible to UVA to UVB depends on the particle
size. To enhance their cosmetic acceptability, inorganic
sunscreen agents are more commonly used in ‘‘micronized’’
or ‘‘microfine’’ form, and coated with dimethicone or silica
to maintain their effectiveness as sunscreen. Micronization
results in particle size of less than 50 nm in diameter, which
makes them much less visible on the skin; however, as the
pigment is micronized, absorption range shifts toward UVB,
especially with TiO2, which makes them poor absorbers of
visible light. Micronized ZnO has better UVA1 protection
and lower refractive index compared to microfine TiO2;
therefore it looks less white (66). Micronized forms of metal
oxides not only scatter and reflect light, but also absorb UV
as they are capable of mobilizing electrons within their
atomic structure. They are stable, nontoxic and safe in their
coated form (68).
Nano-sized formulations are able to enhance or reduce skin
penetration at a limited rate. Insoluble TiO2 or ZnO nano-
particles (NP) which are colorless do not penetrate into the
viable portion of human epidermis. In vitro cytotoxicity,
genotoxicity and photogenotoxicity studies on insoluble NP
which report uptake by cells, oxidative cell damage, or
genotoxicity should be interpreted with caution as these
toxicities may be secondary to phagocytosis of mammalian
cells exposed to high concentrations of insoluble particles.
Other NP may have characteristics enabling skin penetration.
456 Bassel H. Mahmoud et al.

There is little evidence that NP have greater effects on the skin fibroblasts. Pre-exposure incubation with this concentration
or produce toxicities relative to micro-sized materials. Current of EGCG also significantly reduced UVA ⁄ VIS-induced dam-
evidence suggests that nano materials such as nano-sized age in skin fibroblasts and epidermal keratinocytes. Data also
vesicles or TiO2 and ZnO NP (currently used in sunscreens) show that green tea polyphenols can exert a protective role
have no risk to human skin (69). through dietary supplementation (75).
In one study, diffuse spectral transmittance of various
thicknesses (7–260 lm) of opaque sunscreen formulations were
PHOTOTHERAPY USING VISIBLE LIGHT
measured in the 350–800 nm range using a spectrophotometer.
Transmission through 20% ZnO paste was high and decreased Intense pulsed light therapy
minimally despite large increases in the sunscreen layer
In 1976, Muhlbauer et al. (76) described the thermocoagula-
thickness (up to 260 lm). Adding another visible light
tion of capillary hemangiomas and port-wine stains by
absorber, iron oxide, substantially lowered transmittance
polychromatic infrared light. It was not until 1990 that
below that predicted by the product of the transmittances for
Goldman and Eckhouse developed new high-intensity flash-
each component alone. The addition of pigments greatly
lamps for treating vascular anomalies of the skin; and in 1994
enhances photoprotection and can produce a better match
the first intense pulsed light (IPL) technology was marketed.
with the patient’s skin color, which consequently increases
Theoretically, lasers are also a form of IPL; however, in
cosmetic acceptability (70).
clinical practice, the term IPL is commonly used to refer to a
Results of the study of Moseley et al. (71) confirmed the
high-intensity polychromatic incoherent light with a wave-
observation that pigmentary TiO2 plus ZnO exhibits relatively
length range from 515 to 1200 nm; by using different filters, a
uniform transmission in the UVB and UVA region, which
variety of wavelengths can be obtained with IPL devices (77).
extends protection into the visible region; this preparation has
The first law of photobiology, the Grotthus–Draper law,
been shown to provide protection for patients with sensitivity
states that light must be absorbed by tissue for a biologic effect
to the blue light region of the visible light.
to take place, whereas transmitted or reflected light has no
effect. The mechanism of action of light systems corresponds
Window glass to the selective photothermolysis that Anderson and Parrish
(78) described for the pulsed dye laser (PDL). The different
Standard glass filters out UVB, but transmits longer wave-
absorption maximums of the respective target structures allow
lengths radiation: UVA, visible light and infrared. Currently,
the right wavelengths to be selected for heating (>80C) and
filters are added for UVA and infrared radiation to provide
destruction to occur. Hemoglobin absorbs at a wavelength of
different levels of UV and infrared protection (72). Common
580 nm and melanin absorbs the entire visible spectral range
types of glass used in residential and commercial buildings are
(400–750 nm). The wavelength determines the absorption
summarized in Table 1.
behavior and the depth of penetration of light, which increases
with the wavelength. With different cutoff filters (515–
Antioxidants 755 nm), the optimal wavelength spectrum can be filtered
out to correspond to the depth of the target structure and to
Antioxidants are less potent than sunscreens in preventing
the patient’s skin type (77).
sunburn (73). The advantage of oral antioxidants is that they
protect the entire skin surface without being affected by
Advantages of IPL. The three main chromophores (hemoglo-
external factors such as washing, perspiration or rubbing.
bin, water and melanin) in human skin have broad absorption
Topical antioxidants diffuse poorly into the epidermis and are
peaks. Therefore laser monochromaticity is not a prerequisite
unstable (74). UVA ⁄ visible light (VIS) has been evaluated with
for selective heating (79). As a result, IPL can be a versatile
only ())-epigallocatechin-3-gallate (EGCG), which is the most
device to treat a variety of conditions in a cost-effective
effective chemopreventive component of green tea. Different
manner.
concentrations of EGCG were effective in preventing DNA
damage induced by UVR ⁄ VIS in cultured human lung
Disadvantages of IPL. Significant experience is needed when
working with IPL because of its wide range of wavelengths,
Table 1. Common types of glass used in residential and commercial
buildings. pulse durations and fluences. Because of lack of monochro-
maticity, the spectrum may not be consistent from pulse to
Transmission Transmission in pulse. The large handpieces and spot sizes used with IPL make
in the UV the visible light the device harder to maneuver than the laser, especially over
Glass types range (%)* range (%)†
irregular skin surfaces and discrete lesions (80). The decision to
Clear glass >72 >90 use an IPL or laser depends on the physician’s expertise with a
Tinted (heat-absorbing) glass 40 62 specific device and its availability.
Reflective glass 17 19
Low-emissivity glass 20 71
Laminated glass <1 79 Low-level light therapy
UV-blocking coated glass <1 80
Insulating glass <1 69 Low-level light therapy (LLLT) means to deliver doses lower
than the optimum value for a certain indication; this
Source: Modified from Tuchinda et al. (72). dose would produce a diminished therapeutic outcome. This
*Measured from 300 to 380 nm. †Measured from 400 to 780 nm. can be done using either coherent-light sources (lasers) or

noncoherent light sources (light-emitting diodes [LEDs]).
Whether the coherent monochromatic light of a laser is better
than noncoherent light in a defined wavelength range is still
controversial. LLLT is different from other types of laser by
having a low intensity, which causes low temperature changes;
still, it can induce biologic effects, with minimal discomfort to
the patient (81).
The mechanism of LLLT is absorption of red and near-
infrared light by chromophores present in the protein compo-
nents of the respiratory chain located in mitochondria, mainly
cytochrome c oxidase. This is followed by subsequent photo-
dissociation of inhibitory nitric oxide from cytochrome c
oxidase (82) leading to increased enzyme activity (83),
increased electron transport (84) and increased production of
ATP (85). In addition, LLLT stimulates the expression of
genes related to cellular migration and proliferation; it also
alters the production of growth factors and cytokines (86).
The currently two main indications for LLLT are wound
healing and stimulation of hair growth. A study by Demidova-
Rice et al. (81) suggested that LLLT stimulates mouse wound
healing by promoting contraction. They hypothesized that the
illumination delivered at 30 min postwounding induces fibro-
blast–myofibroblast transition and, hence, wound contraction.
They compared coherent monochromatic light from Helium ⁄
Neon laser (632.8 nm) and light from a broadband noncoher-
ent light source (635±15 nm) using the same spot size and the
same fluence rate. They observed improved wound healing
under both experimental conditions (He ⁄ Ne laser and
635±15 nm lamp) compared to controls; but the difference
between the light from different sources was not significant.
They also compared four different wavelength ranges of red
and near-infrared light centered at 635, 670, 720 and 820 nm.
The most pronounced stimulation of wound healing was
obtained with 820 nm delivered from the same noncoherent
polychromatic light source. Regarding fluences, 2 J cm)2 had
the largest positive effect, 1 and 10 J cm)2 improved healing to
a lesser extent while 50 J cm)2 had a negative effect on wound
healing. They concluded that the wavelength is the main
variable that defines the wound healing in response to light.
The other indication of LLLT is male and female pattern
hair loss. Bernstein (87) noticed thick terminal hair developed
in the treated area following 810 nm diode laser treatment. He
concluded that this phenomenon should be studied to better
understand hair growth cycles and to help develop more
effective treatments for hair loss and hair growth. There are
still no controlled trials to assess the efficacy of LLLT for hair
growth, that is why its clinical use remains controversial.
Phototherapy for hyperbilirubinemia
Bilirubin alteration in the treatment of neonatal hyperbiliru-
binemia with phototherapy includes three different mecha-
nisms—photooxidation and photooxygenation to biliverdin,
maleimides and propentdyopents (88); photoaddition to pro-
tein-bound bilirubin (89); and constitutional, configurational
and structural photoisomerization. Production and excretion
of structural photoisomers through bile and urine is considered
to be the main mechanism (90).
Phototherapy lamps with output in the blue to green part of
the spectrum are most effective in lowering serum bilirubin
levels. At these wavelengths, light penetrates the skin well and
Photochemistry and Photobiology, 2008, 84 457
is absorbed strongly by bilirubin (91). Different light sources
exist for treatment of hyperbilirubinemia. Blue fluorescent
tubes, with an output in the blue spectrum (430–490 nm), are
an effective light source for lowering serum bilirubin (92).
LEDs provide high-intensity light in the blue portion of the
visible spectrum that emit light through a narrow wavelength
band with a peak emission between 450 and 470 nm. They do
not emit significant infrared or UV radiation and produce
minimal radiant heat; the latter must be taken into account
when administered to a naked infant (93).
Photodynamic therapy
While studying the influence of acridine orange on protozoa,
Oscar Raab, a medical student at the Department of Pharma-
cology at the University of Munich, Germany, was the first to
discover that the cell-killing effects of a drug were potentiated
by the presence of light. In 1904, von Tappeiner used the term
‘‘photodynamic reaction’’ (94).
Photodynamic therapy is a therapeutic technique based on
the delivery of a photosensitizer followed by irradiation with
visible light, as the light by itself is not sufficient to produce
significant photochemical reaction in the tissue. This reaction
activates molecular oxygen to generate ROS, such as singlet
oxygen, the hydroxyl radical, the superoxide anion and
hydrogen peroxide, which have a cytotoxic effect (95).
Depending on the amount and localization in the target tissue,
ROS either modifies cellular functions or induces cell death by
necrosis or apoptosis (96). Most of the currently approved
clinical photosensitizers belong to the porphyrin family.
Photosensitizers developed in the 1970s and early 1980s are
called first-generation photosensitizers (e.g. Photofrin). The
photosensitizers made since the late 1980s are called second-
generation photosensitizers such as ALA, which is the most
common photosensitizing agent used in dermatology, first
described by Kennedy and colleagues in 1990. New second-
generation photosensitizers (e.g. benzoporphyrin derivatives,
phthalocyanines and chlorins) were then developed; they have
the advantage of producing a photosensitivity that lasts for a
limited duration. Benzoporphyrin derivative has a delay before
irradiation of up to 2.5 h and duration of photosensitization of
up to 7 days. Third-generation photosensitizers refer to the
modifications such as biologic conjugates (e.g. antibody
conjugate, liposome conjugate) (97).
Photosensitizers. Topical sensitizers. Eosin red or erythrosine
were the first topical photosensitizers used to treat conditions
such as pityriasis versicolor, psoriasis, molluscum contagio-
sum, syphilis, lupus vulgaris and skin cancer (94). ALA is not a
photosensitizer by itself but it is metabolized to photosensitiz-
ing protoporphyrin IX (PpIX) through the intrinsic heme
pathway. It penetrates through the stratum corneum when
applied topically as a prodrug, and into dystrophic skin cells
and the sebaceous gland where it is transformed into a highly
photoactive porphyrin derivative, PpIX (98). ALA synthesis
and accumulation is higher in malignant and premalignant
cells than in their normal tissues. The ratio of PpIX accumu-
lation in epidermal tumors in comparison with surrounding
normal skin is 10:1 (99). The absorption spectrum of PpIX is
within the visible spectrum. Different light sources can be used
to activate it, including those that emit blue (410 nm), yellow
458 Bassel H. Mahmoud et al.
(595 nm) or red (630 nm) light. PpIX has a high absorption
peak corresponding to the Soret band at about 405 nm and
other absorption maxima, the Q-bands, at approximately 510,
545, 580 and 630 nm. Although the Q-bands are 10- to 20-fold
smaller than the peak in the Soret band, most clinical studies
have used 625–633 nm red light, which allows for a deeper
penetration into the skin (100).
Systemic sensitizers. Systemic photosensitizers are delivered
intravenously as they do not penetrate well into the skin.
Hematoporphyrin and Photofrin were the first photosensitiz-
ers to be studied, which have absorption spectra with a small
peak at 625–633 nm. Therefore, by using a red light source,
they would produce a biologic effect at a depth of 5–10 mm.
These photosensitizers also have an absorption peak in the
far red (660–700 nm) or near-infrared (700–850 nm) regions
where the depth of penetration into the tissues is up to
20 mm (100). In addition, near–infrared-absorbing photosen-
sitizers should allow for the treatment of highly pigmented
tumors, such as metastatic lesions of melanoma, which do
not respond in the visible range, but not above 850 nm.
Although wavelengths above 850 nm have good depth of
penetration in the tissue, they are not commonly used
because their photon energy is too low to trigger a photo-
chemical reaction (101).
Ideal photosensitizers. An ideal photosensitizer should be
available in the market with low toxicity without irradiation,
but powerful photocytotoxicity, selective toward target cells,
long-wavelength absorbing, rapid removal from the body and
easily administered through various routes (102).
Light sources. Light sources used for PDT belong to three
groups—broadband lamps, diode lamps and lasers. Their
activity depends on the emission spectrum, irradiance, spatial
distribution and constancy of the output. Broadband lamps
emit radiation in the visible and infrared ranges but with
insignificant UV emissions. LEDs have a high and reliable
emission in a narrow bandwidth of 20–50 nm without infrared
emission. Lasers produce high-energy monochromatic light of
a specific wavelength. They provide for the exact selection of
wavelengths matching the absorption peak of the photosensi-
tizer and a highly homogeneous light beam but with a limited
treatment field (101).
Applications of PDT in dermatology. Premalignant skin
lesions such as actinic keratosis became the first approved
dermatologic indication of PDT, and nonmelanoma skin
cancers, including Bowen’s disease, are amenable to treatment
using ALA-PDT. The exception is SCC, especially the nonsu-
perficial types, because of the high recurrence rates and
metastatic potential and lack of evidence to support its routine
treatment with ALA-PDT (103). A number of additional
nonmalignant conditions (e.g. psoriasis, viral warts and hair
removal) are currently under clinical investigation worldwide
(104,105). Studies of ALA-PDT have also been conducted on
basaloid follicular hamartomas and cutaneous T-cell lym-
phoma (106), also on both Mediterranean and HIV-related
Kaposi’s sarcomas, as it is effective, can be repeated and is not
associated with immunosuppression (107). PDT differs from
other cancer therapies in that the individual components of
drug and light are inert unless they are combined (108). Other
common dermatologic conditions treated include acne vulga-
ris, through accumulation of 5-ALA in the pilosebaceous unit,
particularly the sebaceous gland; rosacea, by selective occlu-
sion of abnormal dermal capillaries; sebaceous hyperplasia, as
5-ALA converts to PpIX in sebaceous glands; in photodamage
(dyspigmentation ⁄ poikiloderma), as ALA enhances the effec-
tiveness of laser and light treatment; and in actinic cheilitis
(109).
Fluorescence diagnosis. The selectivity of porphyrin follow-
ing topical application of ALA is used for diagnostic purposes
(through illumination of tissues with blue light at the Soret
band) to induce the emission of pink fluorescent light for
delineation of the tumor because of high ratio of porphyrin
content in the tumor against the surrounding tissue (110). The
dermatologist can then perform either a guided biopsy or a
complete resection of the tumor, sparing healthy tissue (111).
Laser emitting light in the visible range
The first laser was developed by Maiman (112) in 1959 using
a ruby crystal to produce red light with a 694 nm
wavelength. Cutaneous laser surgery was changed in the
1980s with the introduction of the theory of selective
photothermolysis by Anderson and Parrish, which was used
for the destruction of a target in the skin with minimal
thermal injury (78). Lasers emitting light in the visible range
are shown in Table 2. Once laser energy is absorbed into the
skin, three basic effects are possible—photothermal, photo-
mechanical or photochemical. Selective photothermolysis is
an example of photothermal damage, in which light of a
wavelength (which is absorbed by a target chromophore)
selectively destroys the chromophore if the fluence is high
enough and the pulse duration is less than or equal to the
thermal relaxation time (TRT). The TRT is the time taken
for the target to dissipate half of the incident thermal
energy. Photoaccoustic effect is another means by which a
laser can destroy a chromophore, in which extremely rapid
thermal expansion can lead to acoustic waves and subse-
quently photomechanical destruction of the absorbing tissue.
Laser-induced initiation of a chemical process is another
consequence of laser therapy. Photochemical effects serve as
the basis of PDT (113).
The main endogenous chromophores which absorb visible
light include melanin, oxyhemoglobin and dexohemoglobin.
The three primary absorption peaks of oxyhemoglobin are
within the visible range of the electromagnetic spectrum—418,
542 and 577 nm. Vascular lesions are commonly treated with
585 and 595 nm lasers which have the advantage of deeper
dermal penetration without significant loss of absorption
Table 2. Classification of lasers emitting light in the visible range
based on their wavelengths.
Lasers emitting light in the visible range Wavelength (nm)
Argon-pumped tunable dye 577 ⁄ 585 nm
Copper vapor laser 511 (green) ⁄ 578 (yellow)
fd Nd:YAG and KTP 532
PDL 585
Ruby 694
Alexandrite 755
Nd = neodymium; YAG = yttrium-aluminum-garnet; PDL =
pulsed dye laser; fd = frequency doubled; KTP = potassium-titanyl-
phosphate.

(114). Light penetrates the dermis to a depth of 1.2 mm and
photocoagulates vessels of up to 100 lm in diameter. PDL has
been reported as a successful treatment for viral warts, as it
photocoagulates the dermal vessels and compromises the
viability of the human papillomavirus-infected epidermis
(115). PDLs with longer wavelengths (585, 590, 595 and
600 nm) and extended pulse durations (1.5–40 ms) have been
recently developed, which have deeper tissue penetration
capability using large spot sizes while retaining vascular
specificity (116).
The potassium-titanyl-phosphate (KTP) laser uses a neo-
dymium:yttrium-aluminum-garnet (Nd:YAG) crystal
(1064 nm) to produce light that is passed through a KTP
crystal that frequency-doubles the wavelength to 532 nm. It
has the advantage, over PDL, in producing minimal ery-
thema and no purpura in patients with facial telangiectasia
(117). Q switched (QS) lasers have a very low pulse duration
expressed in nanoseconds, and are used for benign epidermal
and dermal pigmented lesions and tattoos. Superficially
located pigments are treated with shorter wavelength lasers
(e.g. 510 nm PDL, 532 nm frequency-doubled QS Nd:YAG),
while deeper pigments require longer wavelength (e.g. 694 nm
ruby, 755 nm alexandrite, 1064 nm QS Nd:YAG). The larger
the spot size used, the deeper the penetration of the laser
(118).
The target for selective photothermolysis in laser epilation
is melanin in the hair follicle, with a thermal relaxation time
of 40–100 ms (113). Melanin within the epidermis represents
a competing site for follicular melanin for laser energy
absorption. Cooling of the skin with refrigerated gels,
cryogenic sprays or contact cooling devices built into the
laser hand piece decreases epidermal injury mainly in darker
skin patients; it also allows delivery of higher fluences (119).
Ruby (694 nm), alexandrite (755 nm), diode (800 nm) and
Nd:YAG (1064 nm) lasers are all used for hair removal (113);
the selection of the appropriate device depends on both the
color and thickness of the hair follicle as well as the patient’s
skin type.
With the swift development of laser technology and the
better understanding of light–tissue interaction, cutaneous
laser treatment indications will continue to expand over the
coming years.
CONCLUSION
The visible light part of the spectrum has not been thoroughly
investigated for many years, compared to UV radiation,
regarding both effects and side effects. However, data are
enough that various biologic effects have been shown to be
exerted via visible light radiation including erythema, pigmen-
tation and radical production, as diverse endogenous and
exogenous chromophores have their absorption spectrum in
the visible light range. It has also been shown that visible light
can induce indirect DNA damage through generation of ROS.
The ability to fractionate visible light is a recent phenomenon.
As a result, advances have been made with respect to its
biologic activity on the skin but still a great deal is unknown. A
number of photodermatoses have an action spectrum in the
visible light range, even though most of the currently available
sunscreens offer, if any, weak protection against such relatively
longer wavelengths. Fortunately, because of its cutaneous
Photochemistry and Photobiology, 2008, 84 459
biologic effects, visible light is used for the treatment of many
dermatosis and for cosmetic purposes through its integration
in phototherapy devices such as IPL, lasers and in PDT.
Acknowledgement—Dr. Mahmoud has received a supporting grant
from Johnson and Johnson, Skillman, NJ.
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