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PG Corner: SUNSCREENS in Dermatology



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Dr Shail Aggarwal Post Graduate II MAMC New Delhi

 Sun is like a dancing partner you may have the pleasure of holding him in your arm but he may step on your toes as well. Similarly from time immemorial, sun is known to provide light and warmth to mankind but is responsible for the development of several photosensitivity disorders. Sunscreens have an important role in prevention of these disorders so they are important. They are active against different components of sunlight, so it is important to know about various components of sunlight.

   Spectrum of sunlight:  Sunlight comprises of a spectrum of electro-magnetic waves like ultraviolet, visible and infrared rays. Ultraviolet rays are further divided into 3 components depending on there wavelengths, UVA (320-400nm), UVB (290-320), UVC (100-290). 90-95% of the UV rays are UVA and because penetration in the skin is directly proportional to the wavelength UVA penetrates deeply in the dermis. It causes both immediate and delayed tanning with or without erythema and has also been implicated in photo-aging, photosensitization and immuno-supression.

                    UVB (290-320nm) comprises of 5-10% of UV rays reaching earth’s surface. It is more potent, erythemogenic and harmful as compared to UVA.

                    UVC(100-290)rays are most dangerous of the UV rays but thankfully absorbed by the ozone layer so don’t reach earth’s surface but at places where there is a defect in the ozone layer(due to chemicals like chlorofluorocarbons)this layer  gets depleted and UVC rays can reach earth’s causing potentially dangerous side effects like mutations and skin cancers.                                  

              Sunlight is very important for persistence of life on earth and among the beneficial effects of sunlight vit-D synthesis, warmth, vision and killing of pathogens are important.                                                                                                                            


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Harmful effects of sunlight: The effects of sunlight are not same in every person. It varies from person to person depending on the skin photo-type, race, occupation, lifestyle, geographic factors (like altitude and latitude), age, genetic make up of the person and any metabolic disorder (like Hartnup’s disease). Therefore the effect of same amount, duration and type of exposure will be different in every individual and so should the treatment.    

                     Among the harmful effects of sunlight sunburn is important which is characterized by erythema, pain, warmth and swelling. The amount of UV rays required to produce visible and uniform erythema with clearly demarcated borders (Minimal erythemal dose). MED of UVB is 1000 times less as compared to UVA so it is much more erythemogenic.                                       

                     UV rays can also cause tanning which can be of two types – (a) IPD (Immediate pigment darkening) or Meirowsky phenomenon which is due to photo-oxidative darkening and cellular redistribution of epidermal melanin.

(b) delayed tanning which appears after 48-72 hrs and because of neo-melanogenesis, increased tyrosinase activation, increase in size of melanocytes and activation of quiescent melanocytes.           

                    Another property of UV rays making them very harmful is there capacity to cause immunological changes like altering epidermal langerhan’s cell morphology & function, increase in non-langerhan’s antigen presenting cells & circulatory suppressor T cells. These changes modify antigen presentation, causes enhanced immunological suppression, mainly delayed type hypersensitivity and also increase risk of skin cancer.

                     Regular exposure to UVA for weeks to months can cause cutaneous blistering, increased fragility & superficial atrophic scarring. Long term recurrent sun exposure can cause cumulative DNA damage causing deterioration of skin structure and function. As a result skin becomes atrophic, wrinkled, scaly, inelastic, and leathery with a yellowish hue, mottled pigmentation, telangiectasias, comedones and freckles. All these changes contribute to photoaging.

    Photodermatoses: Chronic UVA, UVB exposure may cause DNA damage and mutation in p53 gene which is a tumor suppressor gene which can cause increase in risk of melanomas and non melanoma skin cancers. Photodermatoses are defined by their clinical features which result from exposure to UV radiation or visible light. Photodermatoses can be acquired, idiopathic like Polymorphic light eruption (PMLE), actinic prurigo, hydroa vacciforme, solar urticaria and chronic actinic dermatitis. It can also occur in DNA repair defect syndromes like Xeroderma pigmentosa, Cockayne’s syndrome, Trichothiodystrophy, Bloom’s syndrome and Rothmund-Thomson syndrome. Photosensitization can also occur by exogenous chemicals or drugs

e.g. seen in porphyrias, phototoxic and photo allergic reactions which can be caused by drugs like griseofulvin,  fluoroquinolones, phenothiazines, NSAIDS, psoralen, fragrances, sunscreens, thiazides and plants of Compositae family etc. Besides that there is a group of dermatoses which are exacerbated by UV radiations e.g. Lichen planus actinicus, Seborrheic dermatitis, Acne aestivalis, Lupus erythematosus, DLE, Mycosis fungoidis, Pellagra and Pemphigus erythematosus.                                                                                                                                                                          Most of the photodermatoses are common in females as compared to males except few like Hydroa vacciniforme. Usually in these photodermatoses patient is sensitive to different types of UV rays or visible light or both depending upon the type of photodermatoses. So a correct diagnosis and proper sensitivity pattern of irradiations in a particular photodermatoses is important for effective treatment. As far as the treatment of photodermatoses is concerned the best treatment is to avoid sun exposure completely but that is practically impossible. Here comes the role of sun blocking tools e.g. clothes, caps and umbrella but they are not very effective and reliable.                                                                                                                  Sunscreens : Sunscreens have been used for photodermatoses since long time. They are defined as physical or chemical substances designed to protect structure and function of human skin from actinic damage.                                    

Types of Sunscreens : Sunscreens are divided into two categories- Physical and chemical. Physical sunscreens scatter the sunlight and are capable of blocking UVA, UVB and visible light and being chemically inert do not cause allergic reactions but are cosmetically unacceptable. While chemical sunscreens are generally aromatic compounds which have a property to absorb a specific wavelength of light and are divided into UVA and UVB blockers. Cosmetically they are better than physical sunscreens but being chemical in nature have a disadvantage of causing subjective irritation, photosensitivity, contact allergic dermatitis and comedogenicity.

UVA Blockers – Oxybenzone, Methyl anthranilate, Avobenzone.

UVB Blockers - Oxybenzone, Padimate –O, Cinnamates, Octyl salicylate, Phenyl bezamidazole sulphonic acid.

Physical sunscreens – Titanium dioxide, Magnesium oxide, Magnesium silicate and Zinc oxide. Now micronized forms of TiO2 and ZnO are also available which are more acceptable cosmetically.

Sun protection factor : The ability of a sunscreen to protect against sunburn is expressed in the form of  Sun Protection Factor(SPF) which is a measure of Minimal Erythemal Dose(MED) of solar simulated reaction before and after use of sunscreen( but the application of sunscreen should be 2 mg/ cm2). It is a very crude indicator of sun protection as it is just an indicator of UVB protection (sunburns)1. UV radiation exerts effects other than erythema such as DNA damage, immune suppression and consequent carcinogenesis which is because of cumulative exposure to UVA rays. Thus SPF does not necessarily reflect immune protection and no standard guidelines are available for testing protection against UVA rays.

Immune protection factor: A factor known as Immune Protection Factor (IPF) has been devised which is calculated as immune response with sunscreen divided by immune response without sunscreens 1. It is calculated by using two variables ID50 (an immune response that is 50% that of unirradiated controls) and MISD (Minimum Immunosupressive Dose). Another factor known as UVA Protection factor has been devised which is calculated on the basis of IPD(Immediate pigment darkening) and PPD(Persistent pigment darkening) 2.

Therefore two sunscreens can have same SPF but different UVA protection factor which is more reliable indicator of immune protection.

Another quality of sunscreens is to retain their SPF after immersion under water. A sunscreen which retains it’s effect (SPF) for 40 min. is known as “water resistant” and one which retains SPF for 80 min. as “very water resistant” or “water proof”.

Water resistance, efficacy and aesthetics of a sunscreen are vehicle dependant. Most common sunscreen vehicles are lotions and creams. Others are gels, sticks and aerosols. The amount and method of application of sunscreens is also important for it’s efficacy. Application of lesser amounts of sunscreen (less than 2mg/cm2) provides a lower protection than it’s SPF value.3

Protection achieved by a sunscreen is often less than expected as it depends on number of factors including application thickness, technique, type of sunscreen, water resistance and when reapplied4. So there is ample evidence that numerical measure of protection indicated on product pack is generally higher than achieved in practice. This may give patient a false sense of protection and may predispose to the harmful, cumulative effects of UVA rays.

Method of application: Sunscreens should be applied 15-30 min. over exposed sites before going out into the sun followed by reapplication 15-30 min. after the exposure begins 5. Further reapplication is necessary after vigorous activities that can remove sunscreen.

An ideal sunscreen should be inert, non-allergic, economical and cosmetically acceptable with capability of providing broad spectrum sun protection against both acute and long term actinic damage.

A higher SPF (30-60) should be used in photodermatoses such as polymorphic light eruption, actinic dermatitis, photosensitivity, porphyries, DLE, SLE, albinism and Xeroderma pigmentosum. In Indian skin type (mostly Fitzparick type 5) without any evidence of photosensitivity, sunscreen is often not required though for persons indulged in outdoor activities a sunscreen with SPF 15 is recommended.


  1. Baron ED, Steves SR. Sunscreens and immune protection. BJD 2002; 146 : 933-37.
  2. Seite S, Moyal D, Verdier MP. Photodermatol photoimmunol photomed. 2000 Feb ; 16(1) : 3.
  3. Lenane P, Murphy GM. Sunscreen and photodermatoses. J. Derm. Treat. 2001; 12: 53-57.
  4. Diffey BL. J. Photochem. Photobiol. 2001 Nov 15 ; 64: 105-108.
  5. Diffey BL. When should sunscreen be reapplied. JAAD 2001 Dec ; 45(6): 882-85.




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