Topical Sunscreens: A Narrative Review for Contact Sensitivity, Potential Allergens, Clinical Evaluation, and Management for their Optimal Use in Clinical Practice

Abstract

Topical sunscreens decrease the quantity of ultraviolet (UV) light from the sun reaching the skin by either blocking or scattering it and help protect the skin from dyspigmentation, photoaging, DNA damage, and photocarcinogenesis, especially in photosensitive individuals. The significant role played by visible light and infrared light in skin pigmentation and photoaging has been recognized in recent years. The majority of broad-spectrum sunscreens protect against UV-B (290–320nm) and UV-A (320–400nm) radiation. Allergic reactions to sunscreens were relatively uncommon compared to their widespread use in the last more than four decades. With growing awareness of problems associated with excessive sunlight exposure, their use has increased exponentially, especially that of cosmetics and other personal grooming products containing UV filters. In recent years, sunscreen agents have been commonly identified as causing allergic contact dermatitis and photodermatitis. Thus, allergic contact dermatitis, photo-irritation, photo-allergenicity, and photo-toxicity (acute/subacute effects) are of immediate concern in the assessment of topical sunscreens for their optimal use. Sunscreen chemicals such as p-aminobenzoic acid (PABA) and PABA esters, the cinnamates, benzophenones, oxybenzone, and dibenzoylmethane that absorb UV radiation are common contact sensitizers capable of producing both allergic contact dermatitis and photodermatitis. The excipients in sunscreen formulations by themselves may also cause allergic reactions. Herein, we review potential allergens, clinical evaluation, and management aspects of topical sunscreen contact sensitivity for their optimal use in clinical practice.

Introduction

Topical sunscreens reduce the quantity of solar ultraviolet radiation (UVR) by blocking or scattering it and protecting the skin of photosensitive individuals. As melanin intrinsically protects skin from sunlight, its harmful effects occur earlier in persons with lighter skin. However, prolonged sun exposure eventually causes photodamage, photoaging, and skin cancer, warranting optimum photo protection with topical sunscreens. Although transient stinging, urticaria, and acne from topical sunscreens may happen immediately, sunscreens have been identified as a common cause of allergic contact dermatitis (ACD) and photoallergic contact dermatitis (PACD) from their increased usage, resulting from growing awareness about the hazards of excessive sunlight exposure.[1,2,3] Thus, photo-toxicity, photo-irritation, and photo-allergenicity (acute/subacute effects), photo-genotoxicity, and photo-carcinogenicity (chronic effects), along with allergic reactions from excipients, perfumes, and preservatives, remain major concerns for the assessment of sunscreen formulations.[4,5] Herein, we review potential allergens, clinical evaluation, and management aspects of topical sunscreen contact sensitivity for their optimal use in clinical practice.

Sunlight and Its Photobiologic Effects

It will be prudent to recapitulate the sunlight spectrum that consists of both visible and invisible light rays, the UVR. UVR is only 5% of the sunlight reaching the earth and is defined by wavelength and frequency. It comprises of UV-A (UV-A1, 340–400nm and UV-A2, 320–340nm), UV-B (280–320nm), and UV-C (200–280nm). UV-C of wavelengths ≤290nm is absorbed in the ozone layer of the atmosphere, UV-B gets strongly attenuated, and UV-A is transmitted almost unaffected. The UVR falling on earth is 90% UV-A and 10% UV-B, whereas ≈44% of sunlight is visible radiation.[6] Irradiance of UV-A is nearly 17 times higher than UV-B, irrespective of weather conditions. Clouds block only ≈20% of UVR. Window glass in buildings/automobiles filters out UV-B but not UV-A and can transmit nearly 0.1‒72% of UVR, depending on its type and thickness. A high prevalence of photodamage, actinic keratosis, melanoma in situ, and non-melanoma skin cancers is reported over skin exposed directly to UVR from automobile windows.[7,8,9] About 5% of UVR and visible radiation reaching the skin is diffusely reflected and the remaining gets transmitted, scattered, absorbed, or passed out. UVR penetrates skin 1.5‒90 μm deep in comparison to 90–750 μm for visible light.[6] Patients can be sensitive to the whole spectrum but mostly to UV-B, which manifests as erythema, sunburn, and photo-carcinogenesis.[6] The UV-A causes immediate tanning, photoaging, and wrinkling. Visible light produces immediate erythema in persons with Fitzpatrick’s skin type II and tanning and persistent pigmentation among those with skin types III–VI.[9,10,11] The infrared light and visible light, predominantly the high-energy blue light (380–455nm), have photodamaging and photoaging effects.[9] Although visible/blue light from computer/smartphone screens is 100‒1000 times less intense than sunlight, it may worsen melasma by interacting with potential photoallergens.[12] The synergistic effect of visible light and UV-A1 and their possible role in inducing melanogenesis and skin pigmentation too has been elucidated recently.[11,13,14]

Sunscreens

Historically, the need for protection against sunlight has been felt since antiquity.[15,16,17] Modern sunscreens became commercially available in the 1930s, and several chemicals, either alone or in combinations, have been used in sunscreens since then. Sunscreens include two basic types: physical sunscreens and chemical sunscreens. Titanium dioxide, zinc oxide, and ferric oxide, the main mineral constituents in physical or inorganic (mineral) sunscreens, provide comprehensive sun protection by reflecting or scattering UVR and visible/blue light, improve hyperpigmenation, and prevent relapses in melasma more effectively than chemical sunscreens.[18] The exact ratio of each mineral determines the tint; darker shades have ferric oxide in a higher percentage.[6] Their current formulations containing nano sized (<100 nm) mineral constituents make them transparent and cosmetically pleasing. They act as physical barriers and are ideal for outdoor workers or those who need absolute sun protection. Zinc oxide and titanium dioxide are non-irritant/allergenic and do not cause phototoxicity/photoallergy but contact allergy from excipients such as parabens remains possible.[19]

The chemical sunscreens are practically transparent and cosmetically more acceptable. They offer protection from UV-B. But protection from UV-A and visible ranges is only partial. However, quantification of UV-A protection remains difficult in combination formulations. Chemical sunscreens have been used in Europe and the USA since the 1930, when sunbathing became fashionable. It is only in the last two decades that their use primarily for UV protection has increased rapidly worldwide for want of lighter skin and increasing awareness of the harms of sunlight. Consequently, ACD and PACD can occur frequently from many of the sunscreen ingredients.[20,21,22,23]

Epidemiology

The exact prevalence of sunscreen sensitivity in India remains understudied, and its actual prevalence is generally considered low despite widespread use for sun protection or in personal care products. A low concentration of sunscreen chemicals used for patch testing to avoid irritant reactions is a frequently cited reason.[24] However, the photopatch test procedure itself may appear cumbersome for routine practice, discouraging confirmation of sunscreen photosensitivity. Moreover, many cases of sunscreen-induced photosensitivity and primary photodermatoses for which the sunscreen was used remain indistinguishable.[20] However, there are several reports of sunscreen-induced ACD and PACD. The prevalence of sensitivity from active sunscreen chemicals was 0.8% in a Canadian report from 2014, while the North American Contact Dermatitis Group (NACDG) reported about 1% positive patch test reactions among patients tested during 1998‒2004.[25,26,27,28] In a retrospective analysis of 23908 patients patch tested during 2001‒2010 by NACDG, 0.9% of positive reactions were from sunscreen chemicals, mainly benzophenone-3.[29] The prevalence of PACD from sunscreen agents also appears high. Of the 2715 patients evaluated for photosensitivity disorders during 1983‒1998, photoallergic reactions happened in 2.3%, and 65% of them were from sunscreen agents, while 68% of the other 49 patients had non-photoallergic reactions.[30] Schauder and Ippen[5] reported that 20% of 402 German patients with suspected photosensitivity were allergic to UV filters in sunscreens or cosmetics. Journe et al.[31] observed 15.4% positivity from sunscreens among 370 French patients evaluated for photodermatitis. A Singaporean study reported photodermatitis in 4.2% of 48 patients, and positive patch test reactions in 6.3% were from sunscreen chemicals.[32] Similar results were also reported in 19 Australian patients evaluated by photopatch testing.[33]

Although ACD from sunscreens in infants has been reported, sunscreen sensitivity in children is overall uncommon.[5,34,35] Among 157 children under photo-investigation, 6.4% had photoallergy. Sunscreen chemicals/cosmetics caused sensitivity in 5.7% of them, and benzophenone-3 was the commonest sensitizer.[36] Ferriol and Boniche[35] reported butyl-methoxydibenzoylmethane and octyl-methoxycinnamate contact sensitivity in a young girl. Benzophenone-3 and methoxycinnamate caused contact sensitivity in another child.[33] Octocrylene is another emerging cause of ACD in children.[37]

Risk Factors

The exposure is either from sunscreens used for recreational activity, such as at the beach or from the daily application of skin, lip, and hair cosmetics containing UV filters. Their recent use is also in paints, plastic and rubber products, clothing and the fabric industry, and post cosmetic procedures.[21] Although risk factors remain poorly defined, sunscreen contact sensitivity has become manifold with its increasing use in general. In a study of 80 patients with photodermatoses a high prevalence of 65% of women with ACD or PACD was attributed to their higher use of cosmetics/sunscreens.[5] Sunscreens used by individuals working outdoors for long hours or over previously damaged skin, as in atopic dermatitis or after cosmetic procedures are more likely to cause contact sensitivity.[3,20] Children with atopic dermatitis are particularly at high risk.[3]

Sunscreen Allergens

The contact sensitivity is almost exclusive to chemical sunscreens or their excipients. Table 1 lists common chemical agents in sunscreens.

Table 1.

Chemical sunscreens

Sunscreen chemicals	UV spectrum (nm)	Concentration in topical formulations (%)
PABA and PABA esters	UVB
• PABA	260–313	5–15
• Ethyl-dihydroxy-propyl-PABA	280–330	1–5
• Padimate-O (octyl dimethyl PABA)	290–315	1.4–8
• Glyceryl PABA	264–315	2–3
Cinnamates	UVB
• Cinoxate	27–328	1–3
• Ethyhexyl p-methoxy-cinnamate	290–320	2–7.5
• Octocrylene	250–360	7–10
• Octinoxate (octylmethoxy cinnamate)	290–320	7.5
Salicylates	UVB
• Octyl salicylate	280–320	3–5
• Ethyhexyl salicylate	280–320	3–5
• Homsalate	295–315	4–15
Benzophenones	UVA and UVB
• Oxybenzone (benzophenone 3, Eusolex 4360)	270–352	2–6
• Dioxybenzone	260–380	3
• Sulisobenzone (benzophenone 4)	320–350	5–10
Others	UVB
• Methyl anthranilate	260–380	3.5–5
• Digalloyl triolate	270–320	2–5
• Methylene-bis-benzotriazole tetra-methylbutylphenol (Tinsorb M)	320–350	5–10
• Bis-ethylhexyloxyphenol methoxy-phenol triazine (Tinsorb S)	305–360	1–5
• Drometrizole trisiloxane	311–313	10–15
• Octyl triazone	280–320	5
• Butyl-methoxy-dibenzoyl methane (Avobenzone, Parsol 1789)	UVA (320–400)	3–5
• Isopropyldibenzoylmethane (Eusolex 8020)*	–	–
• Anthranilates	320–400	5

*This has been removed from the list of sunscreen agents in 1993 due to high photosensitivity reactions

Para-aminobenzoic Acid (PABA), PABA-esters

PABA and PABA-esters, the earliest UV-B blockers commercialized in the USA, were identified to cause sensitivity as early as 1947. Transient stinging/burning from PABA-containing products is common but ACD and PACD are the main reasons for their declining use. Yet, their use in sunscreens is permitted up to a concentration of 5% in Europe and 10% in the USA.[22,38] PABA-esters include amyldimethyl-PABA (Padimate-A^®), ethylhexyl-dimethyl-PABA (Padimate-O^®), and glycerol-PABA. They are less commonly photoallergenic than PABA.[22] However, only Padimate-O^® is used despite the risk of photoallergy.[39] The photoallergenicity of PABA is attributed to quinine amines, products of its oxidation from photoactivation or photodegradation.[20]

Cinnamates

Cinnamates, the oil-soluble UV-B blockers, have been popularized for water-resistant sunscreens and are often used in combination with benzophenones. They infrequently cause ACD but are the third most common cause of PACD after oxybenzone and avobenzone (4-tert-butyl-4-methoxydibenzoylmethane/ Parsol-1789).[40,41] Octylmethylcinnamate (ethylhexyl-p- methoxycinnamate/Parsol MCX), the most used cinnamate, is negligibly irritant and less photoallergenic.[41,42] Schauder and Ippen[5] reported ACD in seven and photoallergy in 14 of 402 patients from octylmethylcinnamate and infrequently used isoamyl-p-methoxycinnamate (cinoxate, Neo Heliopan).

Octocrylene, a sunscreen agent chemically related to cinnamates with water-resistant properties, was introduced to substitute highly sensitizing oxybenzone. It is photostable and a photostabilizer for other cinnamates and butyl-methoxydibenzoylmethane. Most high-sun protection factor (SPF) sunscreens today contain octocrylene, which has broad spectrum UVR absorption within the UV-B to UV-A2 range. It has been associated with the rising prevalence of ACD and PACD in adults and contact urticaria and ACD in children, notably reported from France, Belgium, Spain, and Italy.[3,43,44,45,46] It is a strong allergen and not recommended for children and individuals sensitive to other cross-reacting agents (vide infra).[22]

Salicylates

Salicylates, weak UV-B absorbers, are water-insoluble and used in high concentrations or incorporated into other cosmetics. ACD from salicylates is uncommon, and even high concentrations are considered safe. Presently, octylsalicylate (2-ethyl-hexyl-salicylate) is commonly used and perhaps an emerging contact sensitizer.[45] Octylsalicylate has been reported to cause both ACD and PACD.[47]

Other UV-B blockers include drometrizole trisiloxane, octyltriazone, and methylene-bis-benzotriazolyl tetramethylbutylphenol (MBBT or Tinosorb M^®), a phenolic benzotriazole that stabilizes other UV absorbers. These are new UV-B and UV-A filters, and infrequently cause ACD and PACD.[48,49,50] Phenylbenzimidazole sulfonic acid and 3,4’- methylbenzylidene camphor (Parsol 5000/Eusolex 6300), presently authorized in Europe, are rare causes of ACD and PACD when used in combination with another strong allergen (coupling allergy).[51]

Benzophenones

Benzophenone-1 to benzophenone-10 are primarily UV-B filters and absorb UV-B to UV-A2 (321-340nm) spectrum.[52] They are commonly incorporated in cosmetics (shower gels, nail varnish, and daily moisturizers) and as preservatives in textiles, paints, plastics, and rubber products to prevent photo-discoloration. They are slightly irritating, non-sensitizing, and phototoxic in human and animal studies.[4] Benzophenone was the commonest allergen in up to 0.6% of positive reactions, and benzophenone-3 was a relevant allergen in 70% of positive reactions during 2003‒2004.[28] Contact sensitivity has been increasing proportionately with their growing use, and they were even named the “allergen of the year” for 2014.[52] Benzophenone-3 (syn. oxybenzone, Eusolex 4360, methanone, Uvinul M40, and diphenylketone), an emerging environmental contaminant, is a commonly used sunblocker. It causes the highest incidence of PACD, accounting for 12‒21% of positive photopatch tests across studies where the exposure was mainly from daily moisturizers.[5,28,41,42,53] Benzophenone-3 has been reported to cause erythema multiforme-like rash, PACD, contact/photocontact urticaria, and anaphylaxis with a positive skin-prick test.[54,55,56,57,58,59] However, at 1‒6% concentration, it was not a significant sensitizer/irritant.[60] Benzophenone-4 (sulisobenzone) has elicited positive reactions in 2.3% of 1693 patients patch-tested with a cosmetic series and was the third most common allergen among other UV filters including benzophenone-3.[23] Benzophenone-3, benzophenone-8, and benzophenone-10 had reportedly caused painful, pruritic, and edematous eruptions and anaphylactoid reactions with recurrence during patch testing.[61]

Dibenzoylmethane Derivatives

Isopropyl-dibenzoylmethane (Eusolex 8020) and 4-tert-butyl-4-methoxydibenzoylmethane (avobenzone/Parsol 1789) are better UV-A blockers and not bereft of contact or photoallergy. Contact sensitivity and positive patch tests/photopatch tests have been reported from Germany, England, France, Italy, and the USA, making it the second most common allergen after benzophenone-3.[5,40,41,62]

Cross Reactions

Cross-reactions among sunscreen agents or with other structurally similar chemicals are not uncommon and necessitate the avoidance of sunscreen agents for individuals sensitive to either of them. Cross-reactions are common with PABA and p-phenylenediamine, benzocaine, sulfonamides, and azo dyes due to structural similarity. The significant feature of cinnamates is their cross-reactions with fragrances/flavoring agents (balsam of Peru, cinnamic aldehyde, and cinnamon oil). Octocrylene is distinct for frequent cross-reactions with ketoprofen, cis-3-hexenylsalicylate, benzophenone-3, and other cinnamates.[22,47] Cross-reactions within the benzophenone group are unproven. However, multiple contact allergies to benzophenone-3, benzophenone-4, and benzophenone-8 have occurred.[53,54]

Allergy to Excipients

Excipients in sunscreen products are important for efficacy, and most allergic/photoallergic reactions are from emollients (isohexadecane, isopropyl myristate, polyethylene glycol-7-hydrogenated castor oil), emulsifiers (wool alcohols, tetrahydroxypropyl ethylenediamine, triethanolamine, and pentylene glycol), surfactants (decyl glucoside, lauryl glucoside), preservatives (Euxyl K400, benzoic acid, ethylhexylglycerin), perfumes, and copolymers.[20,22] The frequency of patch test positivity from cinnamic aldehyde, a perfume, was 2.3% and 3.6% in two large studies.[20,28] Copolymers such as C30-38 olefin/isopropyl maleate/MA, polyvinylpyrrolidone (PVP)/hexadecane, PVP/eicosene, and PVP/1-triacontene added in sunscreens/cosmetics as skin conditioning, antistatic, emulsion-stabilizing, and film-forming agents to enhance water/sweat resistance may cause ACD.[63,64,65,66,67] Surfactant decyl glucoside, and xanthan gum, a thickening agent with skin hydrating, conditioning, and gel-forming effects, are common constituents of Tinosorb^®M sunscreen and causes of ACD.[68,69,70] Polycrylene (Polyester-8^®), a photostabilizer having structural similarities to octocrylene, in a sunscreen moisturizer too has caused ACD.[71] Aluminum in cosmetics and mineral sunscreens, added as an absorbent, pigment carrier, anticaking agent, and bulking agent for titanium dioxide to improve spreadability, has also caused ACD.[72,73]

Clinical Manifestations

The most common clinical presentation of sunscreen sensitivity is eczema of variable severity localized to sites exposed to sunlight and sunscreen application: the face, anterior neck, dorsal hands, and forearms. Acute eczema occurs more frequently, but it can be subacute or chronic and often simulates PACD. However, the non-sun-exposed skin (retroauricular skin, upper eyelids, upper lip, and submental region) remains spared in PACD. Unilateral dermatitis or dermatitis localized to a body site can occur where the sunscreen was applied or sun exposure has been prolonged. Contact dermatitis may occur from the passive transfer of a sensitizing sunscreen product with strong allergenic potential from one body site to another or from contact with another person who has applied it (consort dermatitis).

Isoamyl-p-methoxycinnamate has been reported to cause polymorphic urticated and papular eruptions on sun-exposed skin sparing face and hands, as well as acrofacial photodermatitis with positive patch and photopatch reactions.[74,75] Contact urticaria with anaphylaxis from benzophenones and contact urticaria from octocrylene have occurred.[46,61] Allergic contact cheilitis is reported from benzophenone-3 in lip balm.[76] Pustular ACD in a child with pustular psoriasis in-remission occurred from triethanolamine, an emulsifier in her sunscreen.[77] Ethylhexyl salicylate and drometrizole trisiloxane containing sunscreens have caused ACD as well as frontal fibrosing alopecia.[48,78,79] Oxybenzone has caused erythema multiforme-like PACD.[56]

Diagnosis

A lack of clinical suspicion often delays the diagnosis, and the presence of dermatitis itself is not diagnostic. The common differentials include polymorphous light eruptions (PLE), persistent-light reactions, chronic actinic dermatitis (CAD), lupus erythematosus (LE), and porphyrias. Common clues to a sunscreen allergy include a poor therapeutic response or worsening of primary photodermatosis following sunscreen usage. Patients with suspected cosmetic dermatitis, particularly with photo-aggravation, photo-distributed dermatitis, and/or changing clinical patterns, especially in at-risk individuals (vide supra), need investigations for sunscreen allergy. Thus, a detailed medical history and clinical examination, along with patch/photopatch testing serially with a sunscreen series, baseline series, cosmetic series, and patient’s cosmetics, remain the preferred diagnostic approach. Evaluation by both standard patch testing and photopatch testing is warranted, as some cases of true sunscreen sensitivity can be missed if only patch testing is done.

Patch Testing and Photopatch Testing

Some cases of true sunscreen sensitivity can be missed if only patch testing is done, thus warranting evaluation by both standard patch testing and photopatch testing. Petrolatum remains a vehicle of choice for sunscreen antigens, but its utility may remain limited due to the bioavailability of test antigens; ethanol detects PABA sensitivity better.[20]

Sunscreen ACD may occur from hypersensitivity to the photoprotective chemical itself, excipients, or the vehicle. In suspected cosmetic dermatitis or photodermatitis, patch testing with a baseline cosmetic series including fragrances and preservatives should be done for screening and with a sunscreen series [Tables 2 and 3] along with the putative product(s) for confirmation. Sometimes, photoallergy can occur from benzophenones used in combination with cinnamates or avobenzone and not from an individual chemical.[80] This reflects that some “co-allergic” patients react to sunscreen agents in a specific combination and not to a single agent, necessitating additional testing with the patient’s own cosmetics.

Table 2.

Indian sunscreen series*

Patch test antigens	Conc. (w/w)	Veh.
p-tert-butyl-4-methoxy-dibenzoyl-methane	10%	pet
Homosalate	5%	pet
PABA	10%	pet
3-(4-methylbenzyliden) camphor	10%	pet
2-ethylhexyl-4-dimethyl-aminobenzoate	10%	pet
Benzophenone-3	10%	pet
2-ethyl hexyl-4-methoxycinnamate	10%	pet
2-hydroxy-4-methoxy-4-methyl-benzophenone	10%	pet
Phenyl benzimidazole sulfonic acid	10%	pet
Octyl triazone	10%	pet
Drometrizole trisiloxane	10%	pet
Octocrylene	10%	pet
Octyl salicylate	5%	pet
Ethylhexyltriazone	10%	pet
Isoamyl-p-methoxy cinnamate	10%	pet
Bis-ethylhexyloxyphenol methoxyphenyl triazine	10%	pet
Methylene bis-benzotriazolyl tetramethyl butyl phenol	10%	pet
2-(4-Diethylamino-2 hydroxybenzoyl) benzoic acid hexylester	10%	pet
Diethyl hexyl butamido triazone	10%	pet

*Approved by the Contact Dermatitis and Occupational Dermatoses Forum of India (CODFI)

Table 3.

International sunscreen series (updated in January 2014)*

Patch test antigens	Conc. (w/w)	Veh.
Butyl-methoxy-dibenzoyl methane (Parsol 1789, Eusolex 9020)	10.0%	pet
4-aminobenzoic acid (PABA)	10.0%	pet
Homosalate	5.0%	pet
4-methylbenzyliden camphor (Eusolex 6300)	10.0%	pet
Ethylhexyl dimethyl PABA	10.0%	pet
Benzophenone-3 (Eusolex 4360, Escalol 567, Oxybenzone)	10.0%	pet
Ethylhexyl methoxycinnamate (Parsol MCX, Escalol 55)	10.0%	pet
Benzophenone-10	10.0%	pet
Phenylbenzimidazol-sulfonic acid (Eusolex 232, Novantisol)	10.0%	pet
Benzophenone-4 (sulisobenzone, Uvinyl MS-40)	2.0%	pet
Drometrizole trisiloxane	10.0%	pet
Octocrylene	10.0%	pet
Ethylhexyl salicylate	5.0%	pet
Ethylhexyl triazone	10.0%	pet
Isoamyl-p-methoxycinnamate	10.0%	pet
Bis-ethylhexyloxyphenol methoxyphenyl triazine (Tinosorb S)	10.0%	pet
Methylene-bis-benzotriazolyl tetramethylbutylphenol (Tinosorb M)	10.0%	pet
2-(4-Diethylamino-2 hydroxybenzoyl) benzoic acid hexylester (Uvinul A+)	10.0%	pet
Diethylhexyl butamido triazone (Uvasorb HEB)	10.0%	pet
Disodium phenyl dibenzimidazole tetrasulfonate (Neo Heliopan AP)	10.0%	pet
Decyl glucoside	5.0%	pet

*This series is a selection of haptens (UV blockers) found in skincare products that protect against the sun and is authorized by the International Contact Dermatitis Research Group (ICDRG) for patch test/photopatch test and marketed by Chemotechnique MB Diagnostics AB, Vellinge, Sweden (www.chemotechnique.se)

Two sets of test allergens are placed over the back as in standard patch testing for photopatch testing. After 48 h of occlusion, one set of allergens is removed, and the site is irradiated with UV-A 5–10J/cm², depending on skin phototypes. However, apart from irritant reactions false-positive/-negative reactions are possible because of the improper selection of the UV-A dose. Some workers consider that the concentration of an allergen is more important for eliciting a photo response than the actual dose of UV-A and recommend to use of 5 J/cm² for photopatch testing.[81] A positive reaction from allergens on both sets reflects contact allergy with and without photo-aggravation, whereas photoallergy is confirmed when only the irradiated site shows a reaction. A careful interpretation of results is imperative in patients who develop positive responses from the UV-A dose alone (masked patch test).[20] For patients exhibiting negative/doubtful patch test results despite a strong suspicion of sunscreen sensitivity, a “usage test” or repeated open application test (ROAT) are useful diagnostic tools; the latter must be performed for 2‒3 weeks for weak allergens.

Treatment

Topical corticosteroids of mild to moderate potency, antihistamines for pruritus, and identification and avoidance of the culprit allergen(s) remain the first-line treatments for sunscreen ACD/PACD. Apprising patients of putative allergens, their synonyms, similar antigens, and available alternatives are crucial in long-term management. Patients must be made aware of sunscreen chemicals such as benzophenone added in personal care products primarily not meant for photoprotection (antiwrinkle/antiaging creams, face creams, skin whitening/anti-tanning creams, lip balms, daily moisturizing creams/lotions, shower gels, conditioners, and shampoos/hair care products). The new tinted/physical sunscreens, which are inert and cosmetically acceptable, can be prescribed when essential. Covering skin with apparel made of densely woven fabric of darker shades and using umbrellas/broad-brimmed hats as additional sun protection measures need emphasis, especially for children when outdoors.[82]

Guided Opinion for Optimal Use of Sunscreens

1. Sunlight sensitivity is traditionally assessed by Fitzpatrick’s skin types [Table 4], and recommendations for sunscreen usage in adults can be simplified by classifying photo-sensitive persons into one of the three groups [Table 5].

2. Sunscreen usage is imperative for photosensitive disorders such as xeroderma pigmentosum or other DNA repair defects, porphyrias, albinism, LE, PLE, hydroa vacciniforme, actinic prurigo, CAD, solar urticaria, the intake of drugs with photosensitizing potential, and after cosmetic procedures as new skin is susceptible to photodamage.

3. A sunscreen that has both UV-A/UV-B and visible light blockers, easy spreadability, high substantivity, a non-oily feel, is photostable and sweat/water resistant (lasting for >40 min), is non-comedogenic, cosmetically elegant, and affordable is considered ideal. Antioxidants (vitamins E and C, niacinamide) in sunscreen(s) reportedly improve efficacy.[83,84,85] Current tinted sunscreens are non-allergenic and cosmetically elegant, and a formulation matching skin tone/undertone can be selected. They offer superior protection against both UV-A1 and visible/blue light compared to chemical sunscreens.[86,87,88] However, ACD from the excipient(s) remains possible.

4. At least 2mg/cm² of sunscreen should be applied to the face and uncovered skin 15‒30 min before going outdoors, even on cloudy days, while indoors, or traveling in cars. As some sunscreen chemicals degrade in sunlight or lose efficacy, reapplication every 2‒3h is recommended during continued sun exposure. A repeat application is also needed after swimming and sweating, as it usually gets washed away.[7,82]

5. The American Academy of Dermatology does not recommend sunscreen usage in children aged <6 months, but pregnancy is not a contraindication.[82,89] Since no sunscreen can filter out 100% of sunlight additional sun protection measures are recommended, which are also preferred for sun protection in children.

Table 4.

Fitzpatrick’s classification for sun-reactive skin types with special reference to the Indian population

Skin type	Skin Color	Reaction to UVA	Reaction to sun	Skin types applicable to Indian population
				Unexposed skin color	Approximate Population
Type I	Caucasian; blond or red hair, freckles, fair skin, blue eyes	Very sensitive	Always burns easily, never tans, very fair	-	0%
Type II	Caucasian; blond or red hair, freckles, fair skin, blue eyes or green eyes	Very sensitive	Usually burns easily, tans with difficulty, fair skin tone	Skin typeII and type III	5%
Type III	Darker Caucasian, light-skinned Asian	Sensitive	Burns moderately, tans gradually, fair to medium skin tone	Very fair-skinned	5-10%
Type IV	Mediterranean, Asian, Hispanic	Moderately sensitive	Rarely burns, always tans well, medium skin tone	Skin Type III and Type IV Fair-skinned	5%
Type V	Middle Eastern, Latin, light-skinned black, Indian	Minimally sensitive	Very rarely burns, tans very easily, olive or dark skin tone	Skin Type IV and Type V Wheatish to dark-skinned	90%
Type VI	Dark-skinned black	Least sensitive	Never burns, deeply pigmented, very dark skin tone	-	0%

Table 5.

Recommendations for sunscreen usage

Groups	Recommended Sun protection	Characteristics of individuals requiring sunscreen use
Group 1	Maximum	All individuals with
		• Skin type I
		• Skin types II and III involved in high outdoor activity; skiers, hikers, mountaineers, farmworkers, fishermen, lifeguards, sea surfers, and beach visitors, etc.
		• Photosensitivity disorders.
		• Previous history of skin cancer or precancerous changes.
		• Desirous of shielding from photoaging.
		• After cosmetic procedures (chemical peels, laser resurfacing, or dermabrasion).
Group 2	Moderate	All individuals with
		• Skin type II or III
		• Skin types III and IV involved in minimal outdoor activity
Group 3	Minimal	All individuals with
		• Skin types II–IV who choose to tan
		• Skin types V and VI

Notes:

Use of a broad-spectrum sunscreen having both UV-A/UV-B and visible light blockers, and an SPF* of at least 30 (SPF >50 offers no extra protection) is highly recommended.

*SPF, sun protection factor; defined as “the ratio of least amount of UVR energy needed to produce minimal erythema on unprotected skin and the same erythema on the skin protected by the sunscreen.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.