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Photochemistry and Photobiology, 2022, 98: 1264–1269

Invited Review
Visible Light and the Skin
Nneamaka Ezekwe1,2, Jalal Maghfour2 and Indermeet Kohli2,3*
1
Department of Dermatology, University of Colorado, Aurora, CO, USA
2
Photomedicine and Photobiology Unit, Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA
3
Department of Physics and Astronomy, Wayne State University, Detroit, MI, USA
Received 8 December 2021, accepted 31 March 2022, DOI: 10.1111/php.13634

ABSTRACT
Visible light (VL, 400–700 nm) was previously regarded as
nonsignificant with minimal to no photobiologic effects on the
skin. Recent studies have demonstrated that in dark-skinned
individuals (skin phototypes IV–VI), VL can induce more
intense and longer lasting pigmentation compared to ultravi-
olet A1 (UVA1, 340–400 nm). Additionally, long wavelength
UVA1 (370–400 nm) has been shown to potentiate these
effects of VL. The combination of VL and UVA1
(VL + UVA1, 370–700 nm) was also able to induce erythema
in light-skinned individuals (skin phototypes I–III), which is
a novel finding since the erythemogenic spectrum of sunlight
has primarily been attributed to ultraviolet B (UVB, 290–
320 nm) and short wavelength UVA2 (320–340 nm) only.
Although biologic effects of VL + UVA1 have been estab-
lished, there are no guidelines in any country to test for pho-
toprotection against this waveband. This invited perspective
aims to present the evolution of knowledge of photobiologic
effects of VL, associated phototesting methodologies, and cur-
rent position on VL photoprotection.
INTRODUCTION
Visible light (VL, 400–700 nm), which accounts for approxi-
mately 44% of the electromagnetic radiation (1), was previously
regarded as having minimal to no photobiologic effects on the
skin. However, exposure to VL has recently been shown to
induce oxidative stress with increases in epidermal reactive
oxidative species (ROS) in in vitro models, that results in the
release of inflammatory cytokines and upregulation of expression
matrix metalloproteinases (MMP) in human epidermal equiva-
lents (2). The downstream effect of these biologically active
agents can contribute to premature photoaging in skin. VL is also
known to be an action spectrum of some photodermatoses such
as urticaria and the cutaneous porphyrias (1,3–7).
Pigmentation induced by VL has been shown to be relatively
more persistent than that induced by ultraviolet A1 (UVA1, 340–
400 nm) (6). Additionally, synergistic effects of VL and long
wavelength UVA1 (VL + UVA1, 370–700 nm) in inducing ery-
thema in light skin and pigmentation and erythema in dark skin
*Corresponding author email: ikohli1@hfhs.org (Indermeet Kohli)
© 2022 The American Society for Photobiology.
phototypes have been established (4,8). While the initial phases
of VL + UVA1 induced pigmentation, immediate pigment dark-
ening (IPD, that occurs immediately after exposure and fades
within 20 min to 2 h), and persistent pigment darkening (PPD,
that occurs and persists from 2 to 24 h) have been suggested to
result from oxidation and redistribution of pre-existing melanin,
delayed tanning (DT, occurring 7–10 days after exposure and
lasting from weeks to months) has been attributed to synthesis of
new melanin (9–13).
Skin responses induced by VL and UVA1, and those by the
combination of VL and UVA1 have been reported in the litera-
ture; however, there is a lack of standardized VL phototesting
guidelines at this time (14). A number of studies have proposed
the use of in vitro methods in determining photoprotection
against VL (15,16,17,18,19,20). Although convenient for assess-
ing optical photoprotection, the evaluation of protective effects
of biologic agents, such as antioxidants, may be limited with
these in vitro methodologies. Herein, the focus of this article is
to provide an overview on the evolution of knowledge of in vivo
clinically relevant photobiologic effects of VL and UVA1 on
skin with an emphasis on associated phototesting methodologies.
The current in vivo VL phototesting methods including calcula-
tions for VL protection factor (VL-PF), and position on VL pho-
toprotection are also included.
PHOTOBIOLOGIC EFFECTS INDUCED BY VL
AND UVA1
VL was initially regarded as having no photobiologic effects;
however, early research revealed the potential impact of VL in
inducing skin pigmentation. In an in vivo experimental study
conducted by Kollias et al. (5), a polychromatic light source with
wavelengths ranging from 390 to 1700 nm was utilized to study
skin responses in individuals with skin phototypes (SPT) I–VI. It
was reported that irradiation with VL and infrared radiation
induced pigmentary changes which were spectroscopically differ-
ent from those induced by UVA. No erythema was reported to
be associated with this pigmentary change. A dose of
720 J cm 2 (2) was shown to cause delayed pigment darkening,
that persisted for up to 10 weeks. In another study conducted by
Rosen et al. (13), a xenon-mercury arc lamp was used to emit
select wavelengths (334, 365, 405, 435, 549 nm). The SPT
included ranged from III–V. It was demonstrated that, for the

1264

wavelengths investigated, the ability to induce IPD decreased
with increasing wavelengths. Extrapolation of spectroscopic data
indicated no measurable IPD observed for wavelengths greater
than 470 nm. However, higher intensities and delayed responses
were not investigated. Porges et al. (21) used a xenon-arc solar
simulator, with a spectral distribution between 385 nm and
700 nm, on subjects with SPT II-IV. It was demonstrated that
threshold dose for IPD ranged between 40 and 80 J cm 2 (2)
and that for delayed tanning between 80–120 J cm 2. In contrast
to other studies, Porges et al. (21), reported erythema that
resolved within 24 h. Although there were some variations in the
results among the above-mentioned studies, biologic effects of
VL were clearly demonstrated. The variations in the findings
could be attributed to the differences in the spectral distribution
of radiation source, SPT included and irradiance level used in
these studies.
VL-induced effects were shown to be more intense and persis-
tent compared to UVA1. In a clinical study, Mahmoud et al. (6)
evaluated the effects of visible light (98.3% VL (400–700 nm),
0.19% UVA1 (340–400 nm), and 1.5% IR (700–1800 nm)) on
cutaneous pigmentary alterations in individuals with SPT IV–VI
and compared to those induced by UVA1 (340–400 nm). Clini-
cal and instrumental assessment for pigmentation, erythema and
edema were performed from immediately after irradiation up to a
period of 2 weeks. The lowest dose to induce IPD was reported
to be 40 J cm 2 for VL, and 5 J cm 2 for UVA1. The skin
responses were dose dependent for both VL and UVA1, with
higher doses resulting in darker pigmentation. It was also shown
that VL-induced pigmentation had a sustained effect and was
observed up to 2 weeks, which was the completion of the study.
In contrast, UVA1-induced pigmentation was associated with a
lower intensity and progressively faded within 2 weeks. Finally,
erythema was noted immediately after VL irradiation, whereas
no erythema was induced by UVA1 at any time point after irra-
diation. Interestingly, no VL-induced pigmentation was seen in
SPT II. The clinical implications from this study further high-
lighted the importance of photoprotection beyond UV in
melanocompetent individuals, who have a high propensity to
develop hyperpigmentation on the skin such as melasma and
postinflammatory hyperpigmenation (6).
With sustained pigmentation resulting from VL being estab-
lished, knowledge on the contribution of the various wavelengths
within the VL spectrum began to emerge. Dutiel et al. (7), inves-
tigated the impact of different wavelengths within VL in a study
on human subjects with SPT III and IV. It was demonstrated that
irradiation with blue/violet (415 nm) light induced a dose depen-
dent hyperpigmentation response, while red light (630 nm)
induced no hyperpigmentation at any of the investigated doses
(maximum dose investigated 150 J cm 2) (7). In the same study,
it was shown that blue/violet-induced pigmentation was more
pronounced than that induced by UVB. In a subsequent ex vivo
study, with normal human melanocytes and abdominoplasty skin
from SPT IV, Regazzetti et al. (22), demonstrated that Opsin-3
was the key sensor in melanocytes causing hyperpigmentation
induced by shorter wavelengths of VL (415 and 465 nm). These
findings demonstrated that different wavelengths within the VL
waveband have different biologic effects. This catalyzed addi-
tional efforts in understanding the differences in skin responses
with variations of VL.
The knowledge about impact of narrow wavebands within VL
is important; however, impact of broadband VL is more
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Photochemistry and Photobiology, 2022, 98 1265
meaningful in the field of photoprotection with this being rela-
tively more similar to outdoor sun exposure. Considering this
and the knowledge, shorter wavelengths of VL being relatively
more biologically effective in terms of hyperpigmentation, Kohli
et al. (4) investigated the biologic effects induced by small
changes in the spectral output of VL sources by including trace
amounts (< 0.5%) of UVA1 in one of the VL sources. A dose of
480 J cm 2 was administered with two light sources, pure VL
(400–700 nm with 0.004% UVA1, 97.9% VL, and 2.05% IR)
and VL + UVA1 (370–700 nm with 0.44% UVA1, 99.4%VL,
and 0.15% IR) on opposite sides of the back of subjects with
SPT IV-VI. The UVA1 waveband of 370–400 nm was purpose-
fully selected as 370 nm corresponded to the critical wavelength
for broad-spectrum photoprotection, and protection offered by
broad-spectrum products reduces rapidly beyond this wavelength.
It was thus important to study potential effects caused by this
waveband. Along with variation in spectral composition, the
impact of irradiance was also investigated by administering the
dose at different irradiance levels (rate of delivery) ranging from
100 to 250 mW cm 2. Skin responses, pigmentation and ery-
thema, were evaluated for a period of 2 weeks. Both clinical and
instrumental data indicated stronger and more persistent pigmen-
tation of all phases: IPD, PPD, DT and persistence of DT,
induced with VL + UVA1 compared to pure VL. Additionally,
clinical erythema was observed only at the VL + UVA1 side for
the higher irradiances, but only subclinical erythema observed
for the pure VL side for all irradiance levels investigated. Pig-
mentary responses to pure VL did not change with change in
irradiance, whereas those to VL + UVA1 did with responses to
irradiances greater than 200 mW cm 2 being significantly stron-
ger than those below this level. As such, reciprocity, irradiance
independence or skin response only being dose dependent, was
followed for pure VL but not for VL + UVA1. The minimal
threshold doses for UVA (320–400 nm)-induced IPD, PPD and
DT to a single exposure, as demonstrated in a previous study,
were 0.7  0.3, 11.0  3.4, and 18.2  4.1 J cm 2, respec-
tively (8). As such, the UVA1 dose used in this study (approx.
2.4 J cm 2), with the VL + UVA1 light source, would have
been insufficient to induce PPD or DT. Altogether, this study
yielded several important findings. First, potentiation of pigmen-
tation by VL + UVA1, compared to pure VL, with such low
dose of UVA1 was suggestive of the synergistic relationship
between the two: VL and long wavelength UVA1. Second, ery-
thema induced by VL + UVA1 and the absence of clinical ery-
thema with pure VL at similar irradiances again pointed toward
synergism between the two. Third, reciprocity failure for
VL + UVA1 irradiation suggested caution for selecting parame-
ters for VL + UVA1 phototesting as failure to do so may pro-
vide results that could not be accurately generalized to outdoor
sun exposure. Lastly, the need for photoprotection beyond
370 nm and standardization of VL phototesting methodologies.
Having established that trace amounts of long wavelength
UVA1 (<0.5%) within VL + UVA1 potentiated VL-induced
effects, efforts were then made to investigate changes induced by
varying the UVA1 content while still keeping it low compared
to the corresponding waveband in sunlight. The effects of
VL + UVA1 [370–700 nm, 2.0% UVA1 (340–400 nm), 97.3%
VL (400–700 nm) and 0.7% infrared (700–1600 nm)] were eval-
uated in light-skinned individuals (SPT I-III) (8). Ten subjects of
SPT I-III were irradiated with a dose of 480 J cm 2. A statisti-
cally significant increase in erythema was observed immediately

1266 Nneamaka Ezekwe et al.
after irradiation compared with subjects’ baseline (nonirradiated
skin), and the erythema resolved within 24 h. This finding of
clinically perceptible erythema seen with VL + UVA1 was novel
in photomedicine, as previously the erythemogenic spectrum of
sunlight had only been attributed to UVB and short-wavelength
UVA2 (8). Evaluation of exposure to the same light source was
done in darker skin types (SPT IV-VI); intense pigmentation was
observed at lower doses than those reported previously (unpub-
lished data).
Studies have demonstrated efficacy of tinted sunscreens, oral,
and topical antioxidants against VL-induced effects (23–27).
However, irradiation and assessment methods vary. Commonly
used assessment methods include photography, clinical scoring,
spectroscopy, histology, and immunohistochemistry. Photography
ranges from standard to cross-polarized. Elimination of surface
reflectance resulting in improved visualization of sub-surface vas-
culature and pigmentary changes makes cross-polarized photog-
raphy more suitable for assessing VL + UVA1-induced effects,
especially in skin types V–VI. Clinical scoring scales are used
for pigmentation and erythema evaluation. Although useful, the
scales vary among studies and need to be validated and standard-
ized. Noninvasive spectroscopic techniques including colorimetry
and diffuse reflectance spectroscopy (DRS) are objective with
relatively less user dependence. Colorimetry measured changes
in L*a*b* parameters and individual typology angle (ITA), and
DRS measured changes in chromophore concentrations (melanin
and oxy-hemoglobin), and area under the curve (AUC, also ter-
med as relative dyschromia) of the absorption spectra have been
shown to be sensitive to changes in skin color
(4,7,23,24,26,27,28). Change in AUC, between 400 and 700 nm,
is a relatively novel assessment method and has been shown to
correlate well with clinical findings (4,24,27–29). This can in
part be explained by the fact that this shows a combined effect
of erythema and pigmentary changes that result in overall dark-
ness of the skin color. Oxy-hemoglobin and melanin changes
can be useful for early time points (immediate to 24 h) and
7 days and beyond, respectively, whereas AUC comparisons can
be made for all time points. VL + UVA1-induced histologic and
immunohistochemical changes in SPT IV–VI showed a signifi-
cant increase in inflammation and proliferation, as assessed by
cyclooxygenase-2 (COX-2) and cyclin D1, respectively, for sites
irradiated with 480 J cm 2 of VL + UVA1 compared to nonirra-
diated control skin (28). Interestingly, despite evidence of clinical
pigmentation, which was confirmed by spectroscopic measure-
ments, no changes in pigmentation were observed between irradi-
ated and nonirradiated skin with melanoma antigen recognized
by T cells (MART)-1 (23). This could be attributed to the cur-
rent lack of knowledge regarding optimal biopsy acquisition
timeline after exposure, choice of appropriate biomarkers specific
to VL, and the limitation of relative subjectivity of the assess-
ment of pigmentation, which relies on visual assessment of
change in the number of cells in high power fields and/or the
intensity of the staining. Altogether, this highlights the utility of
cross-polarized photography for visualization, and spectroscopic
methods in quantifying VL + UVA1-induced changes.
From the collective of the above-mentioned studies,
VL + UVA1 has been shown to induce erythema and persistent
pigmentation in melanocompetent (SPT IV–VI) and erythema in
light skinned (SPT I–III) individuals, with histologic evidence of
inflammation and proliferation. As most photoprotective mea-
sures to date only account for UV radiation, the discovery of the
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harmful photobiological effects of VL + UVA1 highlight the
importance of the development of means of photoprotection and
evaluation of associated efficacy with standardized protocols (in-
cluding irradiation and assessment methods) against this wave-
band. Additionally, there is a need to establish the action spectra
of long-wavelength UVA and VL.
IN VIVO VL PHOTOTESTING
METHODOLOGIES
Regulatory bodies throughout the world follow set methodolo-
gies for testing product efficacy against UVB and UVA; how-
ever, currently there are no such guidelines for VL in any
country. There are very limited published in vivo methods for
assessing VL protection. Duteil et al. (30) enrolled 20 healthy
subjects (SPT III-V) in a clinical study assessing VL protection.
Irradiation was performed with a modified solar simulator with
spectral output containing 0.1% of long UVA1 (360–400 nm),
95.1% VL (400–700 nm), and 4.8% of infrared radiation (700–
800 nm). A VL dose of 144 J cm 2 was administered for four
consecutive days. Assessment, performed on all 4 days and on
day 5, included clinical photography, erythema and pigmentation
scoring, and colorimetry. Visible light protection factor (VL-PF)
was proposed to be calculated as the ratio between untreated and
treated site based on the slope of the linear regression of col-
orimetry measured change in ITA between day 1 and day 5.
While multiple exposures are more physiological, this approach
involves product application for multiple days introducing addi-
tional variables. Multiple visits may also result in higher number
of subjects not willing or able to complete the evaluation. Addi-
tionally, 5 days may be insufficient to observe delayed pigmenta-
tion resulting from first exposure, and pigmentation observed at
all time points will be a mix of various phases of pigmentation
making it difficult to evaluate the actual efficacy against delayed
tanning.
Ruvolo and colleagues used VL doses ranging from 40 to
157 J cm 2 to induce pigmentation in healthy volunteers (SPT
IV-VI) (18). The VL source used included 0.002% UVA (320–
400 nm), 99.9% VL (400–700 nm), and 0.098% infrared radia-
tion (above 700 nm). The ratio of visually determined minimal
pigmentation dose, 2–3 h after irradiation, between protected and
unprotected skin was used to calculate the VL-PF. The 2–3 h
time point was used as the authors reported lack of consistent
delayed pigmentation responses after a single exposure. Of note,
although not used for VL-PF, in the same study authors reported
a delayed response after four consecutive VL exposures with
150 J cm 2.
Jo et al. (31) utilized a blue light device (peak emission at
456 nm, full width at half maximum 20 nm) to irradiate the back
of healthy subjects (SPT III–IV) with doses ranging from 45 to
270 J cm 2. Similar to Ruvolo et al., VL-PF was suggested to
be calculated as the ratio of visually determined minimal persis-
tent pigment darkening dose, 2–4 h after irradiation, between
treated and untreated skin.
The protocol developed by Kohli et al. (4,8,19,22–24)
involved the use of a single exposure with VL + UVA1 dose of
320 or 480 J cm 2 depending on SPT. The output of the light
source included <0.0001% below 370 nm, 0.5–4% long wave-
length UVA1 (370–400 nm), 96–99% VL (400–700 nm) and
(0–2%) IR. Clinical scoring, colorimetry, DRS and histology
were performed to assess the induced changes and subjects were

followed for a period of 1–2 weeks (4,8,24,27–29). For VL-PF
calculation, the ratio of the DRS measured change in AUC
between untreated and treated skin was proposed. The proposed
waveband, 370–700 nm, should be used in VL phototesting
because photoprotection from currently available broad-spectrum
products drops significantly beyond 370 nm exposing human
skin to these wavelengths even after application of broad-
spectrum sunscreens when outdoors. Additionally, because syner-
gistic effects between these long UVA1 wavelengths (370–
400 nm) and VL have been established.
While in vivo models are considered the standard for assess-
ing sunscreen protection against VL, variability in the methodol-
ogy and assessment techniques makes it challenging to compare
results across studies and translate the findings into clinical prac-
tice. This emphasizes the need for standardization of VL pho-
totesting.
CURRENT POSITION VL
PHOTOPROTECTION-PROPOSED
HARMONIZATION
To reduce the heterogeneity of in vivo testing, Lim et al., proposed a
specific set of recommendations with the hope to create a standard-
ized methodology for the evaluation of VL photoprotection specific
to pigmentation. These include enrollment of a minimum number of
10 subjects with skin color ranging on colorimetry ITA scale from
10 to 40. These proposed cutoffs were suggested to aid standard-
ization of the study population and ensure clinical and spectroscopic
detection of pigmentary changes. The spectral output of VL sources
was suggested to include less than 0.0001% below 370 nm, 2–4%
UVA1 (370–400 nm), 94–98% VL (400–700 nm), and 0–2% IR
(above 700 nm). A single exposure with a dose of 480 J cm 2 was
recommended to be administered 30 min following test product
application. Anatomic areas including lower back and/or buttocks
were suggested as test sites. Primary efficacy endpoint for pigmen-
tation was suggested to be colorimetry assessed change in ITA with
VL-PF calculated as ratio of change in ITA between untreated and
treated skin at one time point, 7 days after irradiation.
CONCLUSION
Within photomedicine, VL is an evolving field and has clinical
implications in photoprotection. It has been recognized to have
photobiologic effects, including photoaging, clinical erythema
and pigmentation among others which are potentiated when com-
bined with long wavelength UVA1. There is a need for develop-
ment of means of protection against this waveband as well as for
standardization of in vivo testing methodologies including assess-
ment techniques and methods to determine VL-PF. The harmo-
nization work may lead to international standardization enabling
efficient comparisons among studies. This may also aid in pro-
viding data to establish adequate threshold for VL-PF.
Acknowledgements—We would like to acknowledge the Dermatology
Foundation for the salary support through the Research Career
Development Award.
CONFLICTS OF INTEREST
NE was a subinvestigator for La Roche Posay Dermatologique.
JM is a subinvestigator of Avita Medical, Incyte Corporation,
17511097, 2022, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/php.13634 by Nat Prov Indonesia, Wiley Online Library on [28/02/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Photochemistry and Photobiology, 2022, 98 1267
and Pfizer. IK has served as an investigator for Ferndale, Estee
Lauder, La Roche Posay Dermatologique, Unigen, Johnson and
Johnson, Allergan, Bayer and received support from American
Skin Association for a vitiligo project. IK has served as a consul-
tant for Pfizer, Johnson and Johnson, Beiersdorf (previously
known as Bayer) and ISDIN. IK has received salary support
from the Dermatology Foundation through a research career
development award.
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screens. Clin. Cosmetic Investigat. Dermatol. 12, 605–616. research fellow in the
21. Porges, S. B., K. H. Kaidbey and G. L. Grove (1988) Quantification Department of Dermatol-
of visible light-induced melanogenesis in human skin. Photo- ogy at Henry Ford Hospi-
Dermatology 5, 197–200. tal, Detroit, MI. She
22. Regazzetti, C., L. Sormani, D. Debayle, F. Bernerd, M. K. Tulic, G. completed her undergrad-
M. De Donatis, et al. (2018) Melanocytes sense blue light and regu- uate studies at Tougaloo
late pigmentation through Opsin-3. J. Investigat. Dermatol. 138, College, followed by her
171–178. medical school training at
23. Dumbuya, H., P. E. Grimes, S. Lynch, K. Ji, M. Brahmachary, Q. the University of Missis-
Zheng, et al. (2020) Impact of iron-oxide containing formulations sippi Medical Center. She
against visible light-induced skin pigmentation in skin of color indi- completed her transitional
viduals. J. Drugs Dermatol. 19, 712–717. year at the University of
24. Lyons, A. B., R. Zubair, I. Kohli, A. F. Nahhas, T. L. Braunberger, Texas Rio Grande Valley
M. Mokhtari, et al. (2022) Mitigating visible light and long wave- and is completing her
length UVA1-induced effects with topical antioxidants. Photochem. dermatology residency at
Photobiol. 98, 455–460. the University of Color-
25. Mann, T., K. Eggers, F. Rippke, M. Tesch, A. Buerger, M. E. Dar- ado Denver Department
vin, et al. (2020) High-energy visible light at ambient doses and of Dermatology. She is
intensities induces oxidative stress of skin-protective effects of the passionate about skin of
antioxidant and Nrf2 inducer Licochalcone a in vitro and in vivo. color dermatoses and
Photodermatol. Photoimmunol. Photomed. 36, 135–144. areas of research interests
26. Mohammad, T. F., I. Kohli, C. L. Nicholson, G. Treyger, S. include photomedicine,
Chaowattanapanit, A. F. Nahhas, et al. (2019) Oral polypodium Leu- lasers, hidradenitis suppu-
cotomos extract and its impact on visible light-induced pigmentation rativa, vitiligo, and alope-
in human subjects. J. Drugs Dermatol. 18, 1198–1203. cia.
27. Nnmeaka, E. (2021) Efficacy evaluation of topical sunscreens against
long wavelength ultraviolet a1 and visible light induced biological
effects: Preliminary findings. Ann Meet Photodermatol Virtual.
28. Kohli, I., T. L. Braunberger, A. F. Nahhas, F. N. Mirza, M. Mokh-
tari, A. B. Lyons, et al. (2020) Long-wavelength ultraviolet A1 and Jalal Maghfour MD is
visible light photoprotection: A multimodality assessment of dose currently a clinical
and response. Photochem. Photobiol. 96, 208–214. research fellow at the
29. Kohli, I., A. F. Nahhas, T. L. Braunberger, S. Chaowattanapanit, T. photomedicine photobiol-
F. Mohammad, C. L. Nicholson, et al. (2019) Spectral characteristics ogy research unit at
of visible light-induced pigmentation and visible light protection fac- Henry Ford Health Hospi-
tor. Photodermatol. Photoimmunol. Photomed. 35, 393–399. tal dermatology depart-
30. Duteil, L., J. Esdaile, Y. Maubert, A. C. Cathelineau, A. Bouloc, C. ment. He has completed
Queille-Roussel, et al. (2017) A method to assess the protective effi- his undergraduate degree
cacy of sunscreens against visible light-induced pigmentation. Photo- at the University of
dermatol. Photoimmunol. Photomed. 33, 260–266. Wisconsin-Stout. Subse-
31. Jo, H. L., Y. Jung, B.-F. Suh, E. Cho, K. Kim and E. Kim (2020) quently, he moved to
Clinical evaluation method for blue light (456 nm) protection of New Orleans, LA where
skin. J. Cosmet. Dermatol. 19, 2438–2443. he completed his Master’s
degree in biochemistry
and molecular biology as
well as his undergraduate
medical education. He
completed a preliminary
year in Internal Medicine
at Tulane University
School of Medicine. Inter-
ests include exploring and eradicating health disparities within dermatol-
ogy, community volunteerism and skin of color research. His current
research encompasses pigmentary skin disorders (e.g. post-inflammatory
hyperpigmentation), sunscreen, photoprotection, vitiligo and hidradenitis
suppurativa.
 17511097, 2022, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/php.13634 by Nat Prov Indonesia, Wiley Online Library on [28/02/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Photochemistry and Photobiology, 2022, 98 1269

Indermeet Kohli PhD

is an Associate scientist
in the Department of
Dermatology at Henry
Ford Hospital, Detroit,
MI. She joined Derma-
tology research at Henry
Ford in 2014 after grad-
uating with her PhD in
Physics from Wayne
State University. Her
research interests
include photoprotection,
vitiligo, hidradenitis
suppurativa, post inflam-
matory hyperpigmenta-
tion, and Basal cell
carcinoma. She serves
as the imaging commit-
tee chair for the Global
Vitiligo Foundation
(GVF) and as a member
of the board of directors
of the Photodermatology
Society. Dr. Kohli received the American Society for Photobiology
Young Investigator Award in 2020, and the Dermatology Foundation
Research Career-Development-Award in 2021.