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 Table of Contents  
Year : 2018  |  Volume : 5  |  Issue : 2  |  Page : 78-82

Sunscreens: Time to think beyond UV rays

1 Department of Dermatology, JNIMS, Porompat, India
2 Medical Officer, State Health Service, Manipur, India
3 Department of Dermatology, MAMC, Delhi, India

Date of Web Publication14-Dec-2018

Correspondence Address:
Dr. Chitralekha Keisham
Department of Dermatology, Jawahar Lal Nehru Institute of Medical Sciences, Imphal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/Pigmentinternational.Pigmentinternational_

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It has been known to us that solar radiation contributes to photoaging. Until recently, it was thought to be due to ultraviolet rays alone. However, a growing number of evidence confirms that visible and infrared (IR) rays also contribute to extrinsic aging. Visible and IR rays account for 50% and 45% of the solar radiation reaching the earth. Ultraviolet A induces retrograde mitochondrial signal, thus leading to induction of matrix metalloproteinase. Ultraviolet B and IRC cause heat-related generation of free radicals and destruction of collagen and elastin. Exposure to visible light induces cytokines, free-radical formation, and pigmentary changes in human skin. The end result of solar radiation is generation of free radicals and ultimately oxidative damage, photoaging, and photocarcinogenesis. The present broad spectrum sunscreen does not provide complete protection of the human skin from oxidative insult. So, a combination of a sun protection factor active component along with an antioxidant is the ideal way of photoprotection. Till date, a number of antioxidants have been tried in human and animals which have shown to be an effective photoprotective agent, though few studies have failed to prove the same. Even with conflicting reports, effect of antioxidants on human skin needs to be explored more. A good study design with a large sample size in humans must be conducted as visible light and IR rays contribute significantly to photodamage.

Keywords: antioxidants, infrared, sunscreens, UV rays, visible light

How to cite this article:
Keisham C, Elangbam N, Sarkar R. Sunscreens: Time to think beyond UV rays. Pigment Int 2018;5:78-82

How to cite this URL:
Keisham C, Elangbam N, Sarkar R. Sunscreens: Time to think beyond UV rays. Pigment Int [serial online] 2018 [cited 2023 Mar 30];5:78-82. Available from: https://www.pigmentinternational.com/text.asp?2018/5/2/78/247502

  Introduction Top

Sunscreens are a group of chemicals used for protection of human skin from various acute and chronic side effects of sun exposure. Acute exposure to sun rays causes sunburn and delayed tanning. Chronic sun exposure is associated with photoaging, actinic keratosis, and squamous cell carcinoma. Intermittent sun exposure is associated with basal cell carcinoma and melanoma. The first ultraviolet (UV)B filter para-aminobenzoic acid (PABA) was patented in 1943 and the first UVA filter benzophenone was introduced in 1962. In 1982, Lorraine Klingman supported the role for infrared (IR) radiation (760–4000 nm) in premature skin aging.[1] Haywood[2] showed that visible light (400–700 nm) also contributed to skin damage via induction of radical formation. Although initially used mainly for protection against UV wavelength, in the past decade, it has come to the knowledge that wavelength beyond UV rays, that is, visible and IR rays, also contribute to skin damage and photoaging in particular. And since then, this has prompted the development of novel products for photoprotection.

Ours was an evidence-based review. Study data were searched in PubMed for articles related to the use of sunscreens and newer agents for photoprotection that would include protection against visible light and IR rays. There was no limit in the search timeframe. Keywords used were sunscreens update, polyphenols, and antioxidants. The search was further extended to the keywords solar protection, IR radiation, visible rays, ectoin, oxothiazolidine, and Uvinul A plus (BASF, Ludwigshafen, Germany).

Solar radiation and skin

The optical spectrum of sunlight consist of UV rays, visible, and IR rays which accounts for 5%, 50%, and 45% of the total spectrum.[3] Among the UV rays, UVC is filtered by the ozone layer. UVB rays are 5% of the solar UV radiation and are mainly responsible for a variety of skin diseases, including nonmelanoma and melanoma skin cancers. UVB (280–315 nm) is partially filtered by ozone layer, absorbed by melanin, and it penetrates up to the basal layer of the epidermis, producing reactive oxygen and nitrogen species (ROS and RNS). UVB rays are responsible for cutaneous inflammation, sunburn, aging, formation of cyclobutane pyrimidine dimers and photoadducts.[4] Accumulation of mutation in skin further due to excision repair failure leads to development of UV-associated cancers.[4] UVA comprises 90% to 95% of the solar UV spectrum, and it is considered as an aging ray. UVA (315–400 nm) is less energetic than UVB, but it is present is a larger amount. It is absorbed by melanin, riboflavin-containing flavin adenine dinucleotide, and flavin mononucleotide.[5] UVA reaches up to the dermis. It also generates ROS and RNS leading to oxidized deoxyribonucleic acid (DNA) base, hence causing premature aging and risks of cancer.[4],[6] Because UVA produces only a small number of pyrimidine dimers in skin, it is assumed that much of the mutagenic and carcinogenesis of UVA radiation is mediated through reactive oxygen species.[7]

Visible light accounts for 50% of the solar light. It penetrates into tissue, and 20% of it reaches the hypodermis.[8] Visible light is absorbed by it, schromophore which are hemoglobin, melanin, bilirubin, riboflavin, and porphyrins. This was followed by generation of ROS, inflammatory cytokines, and matrix metalloproteinase (MMP) enzymes in human epidermal equivalents.[9],[10] In ex vivo skin explants, ROS produced were 4% for UVB, 46% for UVA, and 50% for visible light.[9] Visible light produces DNA damage in the form of oxidized DNA.[11] Visible-light-induced pigmentation on skin types IV to VI was darker and lasted longer as compared to irradiation with long UVA.[12] Pigmentation with visible light was induced with 415-nm wavelength and not 630-nm radiation on skin types III and IV. The pigmentation lasted as long as 3 months.[13]

IR rays consist of IRA (700–1400 nm), IRB (1400–3000 nm), and IRC (3000 nm–1 mm). Of these IR rays, IRA penetrates skin deeply. IRA is 30% of all IR radiation and 65% of it reaches the dermis and 20% the hypodermis.[7] The action of IRA is mainly mediated through interaction with cytochrome C oxidase as a chromophore, leading to dysfunction of mitochondrial electron transport and production of ROS and triggering retrograde mitochondrial signaling. Retrograde signaling leads to modulation of genes involved in photo aging, that is, MMP-1 and type 1 procollagen.[14] IRA radiation directly stimulates dermal fibroblast to produce MMP-1, and this was not mediated through heat.[15] IRB and IRC induce MMP and cytokines production through heat-sensitive receptors.[16],[17] This leads to generation of ROS, an important step in tropoelastin expression. There is an imbalance with increased tropoelastin production and decreased fibrillin-1, leading to decreased tropoelastin deposition on microfibril causing abnormal elastic fiber formation. Moreover, MMP destroys newly formed tropoelastin and fibrillin.[18] As a result, IR rays cause degeneration of elastin and collagen leading to photodamage.

Sunscreen indices

Sunscreens-related indices have been formulated by various in vitro and in vivo methods to determine their efficacies. They are developed for both UVA and UVB spectrum. Various indices are described below.


It refers to the measurement of protection of skin from the harmful effects of UVB radiation. It is defined as the ratio of minimal erythema dose (MED) of photoprotected skin to MED of unprotected skin.

Grades of sun protection factor (SPF) are
  1. Low SPF: 2 to 15.
  2. Medium SPF: 15 to 30.
  3. High SPF: 30 to 50.
  4. Highest SPF: 50+.

UVA indices

  1. Japanese standard (persistent pigment darkening): It is an in vivo method and calculated as UVA dose required to produce the effect with the sunscreen agent to that produced without an agent after 2 to 24 h.
  2. Australian/new standard: An 8-μm layer of the product should not transmit more than 10% of radiation of 320 to 360 nm or a 20-μm layer of the product should not transmit more than 1% of radiation of 320 to 360 nm.
  3. European Union guidelines: UVA protection factor (persistent pigment darkening) = 1/3 of SPF and critical wavelength = 370 nm.
  4. Boot star rating system: It is used in the United Kingdom and in an in vitro measurement of a product’s UVA (340–400 nm) absorbance over its UVB (290–320 nm) absorbance. Product with better UVA absorbance has higher Boot star rating.

Classification of sunscreen

Sunscreens have been mainly classified on the basis of blocking the UV radiation conventionally. There are reports of both visible light and IR radiation having detrimental effects on human skin.[19] The last food and drug administration (FDA) approval was given for 16 sunscreens in 1999.[20] There are three nomenclatures for sunscreen agents in the world. These are the International Nomenclature Cosmetic Ingredient name, US adopted name, and trade name.

Sunscreens consist of both organic and inorganic filters protecting against mainly UVA and UVB. But again the issues of stability, safety, and broader spectrum arose, and new agents having more photostability and broader spectrum covering both UVA and UVB were added. As of now considering all the factors, newer sunscreens are the need of the hour covering all the three spectrums, namely, UV radiation, visible light, and IR radiation. The agents protecting against the visible light and IR are at the experimental stage. The nonmicronized optically opaque zinc oxide, titanium dioxide, and iron oxide are able to block visible light.[21] The antioxidants, namely, grape seed extract including flavonoids, procyanidins, phenolic acids, etc., and extracts of Scutellaria baicalensis and Polygonum aviculare (high phenolic and flavonoid contents), may be able to act against the IR radiation.[22],[23],[24] Newer agents such as ectoin are also coming up with protection against UV rays and beyond.[25] A brief classification is proposed from the available data which is described in [Table 1].
Table 1: A newer classification proposed for sunscreen agents

Click here to view

Role of antioxidants in photoprotection

The end point of all different solar wavelength on human skin is the increased production of reactive molecule species and increased oxidative stress.[26] The present broad spectrum sunscreen does not protect human skin from 94.2% of solar radiation (comprised of visible and IR) or from heat accumulation damage. At present, only opaque filters such as nonmicronized form of zinc oxide, titanium dioxide, and iron oxide are able to block visible light.[21] Unfortunately, these compounds are matte white or red, water insoluble, and leave a tinted coating on the skin, which are cosmetically unacceptable to the patients. So, the need of the hour for sunscreen is an SPF active ingredient along with antioxidants.[26] The antioxidants must be stable to solar radiation, heat, and as well as highly potent in neutralizing ROS while promoting tissue repair.

There are numerous antioxidants that have shown efficacy in preventing photodamage. Among them, polyphenols have gained importance in the last decade. Polyphenols are a group of naturally occurring plant products that are widely distributed in plant foods including fruits, vegetable, nuts, seeds, flowers, and bark. Most of the natural polyphenols are pigments, typically yellow, red, or purple, and can absorb UV rays. They can absorb the entire UVB spectrum and part of UVC and UVA spectra. Antioxidants mainly polyphenols in oral and topical formulation, in both human and animal studies, have shown anti-inflammatory, antioxidant action against UV rays.[27],[28] Green tea polyphenols also have ability to repair photodamaged DNA as seen in epigallocatechin-3-gallate-induced DNA repair by nucleotide excision repair as shown by Meeran et al.[29] in human fibroblast. Various animal models have been able to show the antiphotocarcinogenic effects of polyphenols such as oral green tea polyphenols, topical epigallocatechin, oral proanthocyanidins, topical resveratrol, and silymarin.[30],[31],[32],[33] However, this studies are limited by their small sample size and poor study designs. Contradictory to this, a randomized, placebo controlled trials in 50 volunteers by Farrar et al.[34] using systemic green tea failed to demonstrate protection from UV-ray-induced sunburn. Similarly oral green tea in randomized controlled trial in 50 healthy adults did not provide protection from direct DNA damage induced by higher dose solar simulated radiation.[35]

Topical use of ẞ-carotene (2 mg/cm2) was protective for human skin against IR radiation in a study by Darwin et al. on healthy volunteer. The in vivo cutaneous carotenoid concentration, measured by resonance Raman spectroscopy showed that free radicals produced due to IR radiation can be effectively neutralized by topically applied antioxidants. The relative degradation rate for a definite IR radiation dose was identical for all volunteers, independent of their initial carotenoid level. This means that individual living on a healthy diet rich in fruit and vegetable are better protected than those living on antioxidant poor nutrition and a stressed lifestyle.[36] Another study also showed the efficacy of a topical mixture of antioxidants (vitamin C, vitamin E, ubiquinone, and grape seed extract) in preventing IRA-induced MMP-1 expression in human skin.[19] Importantly when the above same mixture of antioxidants were added to a SPF 30 sunscreen, there was a significant reduction in MMP-1 messenger ribonucleic acid expression as compared to SPF 30 sunscreen alone in healthy volunteers.[37] However, data analysis of commercially available combined sunscreen and topical antioxidants available in market showed no antioxidant power or low power.[38] Contradictory to this, a study by McDaniel et al.[39] using a combination of sunscreen along with antioxidants demonstrated improvement in lines and wrinkle after 4 weeks of once daily use in patients of moderate-to-severe photodamage. Efficacy was also seen in vitro and ex vivo studies for the same. These results show the effect of antioxidants to repair the existing damage.[39] Although some data on topical sunscreen combined with antioxidants are conflicting, future prospect into such a formulation must be explored widely as it is much needed.The effectiveness of oral antioxidants depends on its metabolism and bioavailability. For topical formulation of antioxidants, it requires a suitable formulation for enhanced penetration to provide maximum action. For sunscreen to provide the mentioned protection, they have to be applied adequately. Unfortunately, sunscreens have been underapplied most of the time. This could be the reason why sunscreens with antioxidants fail to show results on actual human use. In addition, there is the issue of penetration and bioavailability of the active component of topical formulation of sunscreens and antioxidants.

  Conclusion Top

The harmful effect of solar radiation is not due to UV rays alone. Both visible light and IR rays are responsible for oxidative stress and aging. These have been proved by in vitro studies and clinical studies. So, a broad solar protection requires an SPF active component with a potent efficacious antioxidant. Moreover, well-designed human studies of topical as wells as oral antioxidants on a larger sample size must be undertaken. Presently, the combination of sunscreens with antioxidants has abundantly reached the consumer level. As of now, there are no well-defined criteria for the photoprotective effect given by antioxidants. Despite the emerging trend to use a novel sunscreen protecting against all components of the solar spectrum, the need to use protective clothing and shade seeking behavior have to be emphasized as sunscreens are incorrectly used most of the time.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Kligman LH. Intensification of ultraviolet induced dermal damage by infrared radiation. Arch Dermatol 1982;272:229-38.  Back to cited text no. 1
Haywood R. Relevance of sunscreen application method, visible light and sunlight intensity to free radical protection: A study of ex-vivo human skin. Photochem Photobiol 2006;82:1123-31.  Back to cited text no. 2
Svobodova A, Vostalova J. Solar radiation induces skin damage: Review of protective and preventive options. Int J Radiant Biol 2010;86:999-1030.  Back to cited text no. 3
Svobodova AR, Galandakova A, Sianska J, Dolezal D, Lichnovska R, Ulrichova J et al. DNA damage after acute exposure of mice skin to physiological does of UVB and UVA light. Arch Dermatol 2012;304:407-12.  Back to cited text no. 4
Baumler W, Regensburger J, Knak A, Felgentrager A, Maisch T. UVA and endogenous photosensitizers—The detection of singlet oxygen by its luminescence. Photochem Photobiol Sci 2012;11:107-17.  Back to cited text no. 5
Pfeifer GP, Besaratinia A. UV wavelength dependent DNA damage and human non melanoma and melanoma skin cancer. Photochem Photobiol Sci 2012;11:90-7.  Back to cited text no. 6
De Gruijl FR. Photocarcinogenesis: UVA vs UVB. Singlet oxygen, UVA, and ozone. Methods Enzymol 2003;319:359-66.  Back to cited text no. 7
Mckenzie RL, Aucamp PJ, Bais AF, Bjorn LO, Ilyas M, Madronich S. Ozone depletion and climate change: Impact on UV radiation. Photochem Photobiol Sci 2011;10:182-98.  Back to cited text no. 8
Zastrow L, Groth N, Klein F, Kockett D, Lademann J, Renneberg R et al. The missing link-light induced (280-1600 nm) free radical formation in human skin. Skin Pharmacol Physiol 2009;22:31-44.  Back to cited text no. 9
Leibel F, Kaur S, Ruvolo E, Kollias N, Southhall MD. Irradiation of skin with visible light induces reactive oxygen species and matrix degrading enzymes. J Invest Dermatol 2012;132:1901-7.  Back to cited text no. 10
Kielbassa C, Roza L, Epe B. Wavelenght dependence of oxidative DNA damage by UV and visible light. Carcinogenesis 1997;18:811-6.  Back to cited text no. 11
Mahmoud BH, Ruvolo E, Hexsel CL, Liu Y, Owen MR, Kollias N et al. Impact of long wavelength UVA and visible light on melanocompetent skin. J Invest Dermatol 2010;130:2092-7.  Back to cited text no. 12
Duteil L, Cardot-Leccia N, Queille-Roussel C, Maubert Y, Harmelin Y, Boukari F et al. Differences in visible light induced pigmentation according to wavelengths: A clinical and histological study in comparison with UVB exposure. Pigment Cell Melanoma Res 2014;27:822-6. s.  Back to cited text no. 13
Krutmann J, Morita A, Chung JH. Sun exposure what molecular photodermatology tells us about its good and bad side. J Invest Dermatol 2012;132:976-84.  Back to cited text no. 14
Schieke S, Stege H, Kurten V, Grether-Beck S, Seis H, Krutmann J. Infrared-A radiation induced matrix metalloproteinase 1 expression is mediated through extracellular signal kinase 1/2 activation in human dermal fibroblasts. J Invest Dermatol 2002;119:1323-9.  Back to cited text no. 15
Lee YM, Kim YK, Chung JH. Increased expression of TRPV1 channel intrinsically aged and photoged human skin in vivo. Exp Dermatol 2009;18:431-6.  Back to cited text no. 16
Park CH, Lee MJ, Ahn J, Kim S, Kim HH, Kim KH et al. Heat shock induced matrix metalloproteinase (MMP)-1 and MMP-3 are mediated through ERK and JNK activation and via an autocrine interleukin-6 loop. J Invest Dermatol 2004;123:1012-9.  Back to cited text no. 17
Chen Z, Seo JY, Kim YK, Lee SR, Kim KH, Cho KH et al. Heat modulation of tropoelastin, fibrillin-1, and matrix metalloproteinase-12 in human skin in vivo. J Invest Dermatol 2005;124:70-8.  Back to cited text no. 18
Schroeder P, Lademann J, Darvin ME, Stege H, Marks C, Brunhke S et al. Infrared radiation-induced matrix metalloproteinase in human skin: Implications for protection. J Invest Dermatol 2008;128:2491-7.  Back to cited text no. 19
Hexsel CL, Bangert SD, Hebert AA, Lim HW. Current sunscreen issues: 2007 Food and Drug Administration sunscreen labelling recommendations and combination sunscreen/insect repellent products. J Am Acad Dermatol 2008;59:316-23.  Back to cited text no. 20
Kaye ET, Levin JA, Blank IH, Arndt KA, Anderson RR. Efficiency of opaque photoprotective agents in the visible light range. Arch Dermatol 1991;127:351-5.  Back to cited text no. 21
Yilmaz Y, Toledo R. Health aspects of functional grape seed constituents. Trends Food Sci Technol 2004;15:422-33.  Back to cited text no. 22
Hsu CY. Antioxidant activity of extract from Polygonum aviculare L. Biol Res 2006;39:281-8.  Back to cited text no. 23
Zhao Q, Chen X-Y., Martin C. Scutellaria baicalensis, the golden herb from the garden of Chinese medicinal plants. Sci Bull 2016;61:1391-8.  Back to cited text no. 24
Buerger J, Driller H. Ectoin: An effective natural substance to prevent UVA induced premature photoaging. Skin Pharmacol Physiol 2004;17:232-7.  Back to cited text no. 25
Rai R, Shanmuga SC, Srinivas C. Update on photoprotection. Indian J Dermatol 2012;57:335-42.  Back to cited text no. 26
[PUBMED]  [Full text]  
Oresajo C, Pillai S, Manco M, Yatskayer M, McDaniel D. Antioxidants and the skin: Understanding formulation and efficacy. Dermatol Ther 2012;25:252-9.  Back to cited text no. 27
Nichols JA, Katiyar SK. Skin protection by natural polyphenols: Anti-inflammatory, anti-oxidant and DNA repair mechanisms. Arch Dermatol Res 2010;302:71.  Back to cited text no. 28
Meeran SM, Mantena SK, Katiyar SK. Prevention of ultraviolet radiation induced immunosuppression by(−)-epigallocatechin-3-gallate in mice is mediated through interleukin 12 dependent DNA repair. Clin Cancer Res 2006;12:2272-80.  Back to cited text no. 29
Mittal A, Piyathilake C, Hara Y, Katiyar SK. Exceptionally high protection of photocarcinogenesis by topical application of (−)-epigallocatechin-3-gallate in hydrophilic cream in SKH-1 hairless mouse model: Relationship to inhibition of UVB-induced global DNA hypomethylation. Neoplasia 2003;5:555-65.  Back to cited text no. 30
Mittal A, Elmets CA, Katiyar SK. Dietery feeding of proanthocyanidins from grape seeds prevents photocarcinogenesis in SKH-1 hairless mice: Relationship to decreased fat and lipid peroxidation. Carcinogenesis 2003;24:1379-88.  Back to cited text no. 31
Jang M, Cai L, Udeani GO, Slowing KV, Thomas CF, Beecher XX et al. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 1997;275:218-20.  Back to cited text no. 32
Katiyar SK, Korman NJ, Mukhtar H, Aggarwal R. Protective effects of silymarin against photocarcinogenesis in a mouse skin model. J Natl Cancer Inst 1997;89:556-66.  Back to cited text no. 33
Farrar MD, Nicolaou A, Clarke KA, Mason S, Massey KA, Dew TP et al. A randomized controlled trial of green tea catechins in protection against ultraviolet radiation induced cutaneous inflammation. Am J Clin Nutr 2015;102:608-15.  Back to cited text no. 34
Farrar MD, Huq R, Mason S, Nicolaou A, Clarke KA, Dew TP et al. Oral green tea catechins do not provide photoprotection from direct DNA damage induced by higher dose solar simulated radiation. A randomised controlled trial. J Am Acad Dermatol 2018;78:414-6.  Back to cited text no. 35
Darwin ME, Fluhr JW, Meinke MC, Zastrow L, Sterry W, Lademann J. Topical beta-carotene protects against infrared light induced free radicals. Exp Dermatol 2011;20:125-9.  Back to cited text no. 36
Grether-Beck S, Marini A, Jaenicke T, Krutmann J. Photoprotection of human skin beyond ultraviolet radiation. Photodermatol Photoimmunol Photomed 2014;30:167-74.  Back to cited text no. 37
Wang SQ, Osterwalder U, Jung K. Ex vivo evaluation of radical sun protection factor in popular sunscreens with antioxidants. J Am Acad Dermatol 2011;65:525-30.  Back to cited text no. 38
McDaniel MD, Hamzavi IH, Zeichner JA, Fabi SG, Bucay VW, Harper JC et al. Total defense + repair. A novel concept in solar protection and skin rejuvenation. J Drugs Dermatol 2015;14:s3-11.  Back to cited text no. 39


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