Sunscreens

(Sunburn and Photosensitivity)

Ultraviolet (UV) solar radiation consists of:

• UVA (320-400 nanometres): causes skin aging (damage to collagen) and probably skin cancer

• UVB (290-320 nm): is 1000 times more active than UVA, acutely causes sunburn and tanning, and chronically skin cancer and skin aging

• UVC (200-290 nm) is prevented, at present, from reaching the earth at sea level by the stratospheric ozone layer, though it can cause skin injury at high altitude.

Protection of the skin

Protection from UV radiation is effected by:

Absorbent sunscreens. These organic chemicals absorb UVB and UVA at the surface of the skin (generally more effective for UVB).

UVB protection: aminobenzoic acid and aminobenzoates (padimate-O), cinnamates, salicylates, camphors.

UVA protection: benzophenones (mexenone, oxybenzone), dibenzoylmethanes.

Reflectant sunscreens. Inert minerals such as titanium dioxide, zinc oxide and calamine act as a physical barrier to UVB and UVA: they are cosmetically unattractive but the newer micronised preparations are more acceptable.

The performance of a sunscreen is expressed as the sun protective factor (SPF) which refers to UVB (UVA is more troublesome to measure and the protection is indicated by a star rating system with 4 stars providing the greatest). A SPF of 10 means that the dose of UVB required to cause erythema must be 10 times greater on protected than on unprotected skin. The SPF should be interpreted only as a rough guide; consumer use is more haphazard and less liberal amounts are applied to the skin in practice. Sunscreens should protect against both UVB and UVA. Absorbent and reflectant components are combined in some preparations. The washability of the preparation (including removal by sweat and swimming) is also relevant to efficacy and frequency of application; some penetrate the stratum corneum (padimate-O) and are more persistent than others.

Uses. Sun screens are no substitute for lightimpermeable clothing and sun avoidance. They are, however, beneficial in protecting those who are photosensitive due to drugs (below) or to disease, i.e. for photodermatoses such as photosensitivity dermatitis, polymorphic light eruption, cutaneous porphyrias and lupus erythematosus. Methodical use of sunscreens appears to reduce the incidence of squamous cell carcinoma in vulnerable individuals.

The lower lip receives a substantial dose of UV but may be neglected when a sunscreen is applied (specific lip-blocks are available). Sunscreens can cause allergic dermatitis or photodermatitis (but not titanium dioxide, though its vehicle may).

Treatment of mild sunburn is usually with a lotion such as oily calamine lotion. Severe cases are helped by topical corticosteroids. NSAIDs, e.g. indometacin, can help if given early, by preventing the formation of prostaglandins.

Photosensitivity

Drug photosensitivity means that an adverse effect occurs as a result of drug plus light, usually UVA; sometimes even the amount of ultraviolet radiation from fluorescent light tubes is sufficient.

Systemically taken drugs that can induce photosensitivity are many. Of the drug groups given below, those most commonly reported are:7 antimitotics: dacarbazine, vinblastine antimicrobials: demeclocycline, doxycycline, nalidixic acid, sulphonamides antipsychotics: chlorpromazine, prochlorperazine cardiac arrhythmic: amiodarone diuretics: frusemide (furosemide), chlorothiazide, hydrochlorothiazide fibric acid derivatives, e.g. fenofibrate hypoglycaemic: tolbutamide

7 Data from The Medical Letter 1995 37: 35.

nonsteroidal anti-inflammatory: piroxicam psoralens (see below).

Topically applied substances that can produce photosensitivity include:

para-aminobenzoic acid and its esters (used as sunscreens)

coal tar derivatives psoralens from juices of various plants (e.g. bergamot oil)

6-methylcoumarin (used in perfumes, shaving lotions, sunscreens).

There are two forms of photosensitivity:

Phototoxicity, like drug toxicity, is a normal effect of too high a dose of UV in a subject who has been exposed to the drug. The reaction is like severe sunburn. The threshold returns to normal when the drug is withdrawn. Some drugs, notably NSAIDs, induce a 'pseudoporphyria', clinically resembling porphyria cutanea tarda and presenting with skin fragility, blisters, and milia on sun-exposed areas, notably the backs of the hands.

Photoallergy, like drug allergy, is a cell-mediated immunological effect that occurs only in some people, and which may be severe with a small dose. Photoallergy due to drugs is the result of a photochemical reaction caused by UVA in which the drug combines with tissue protein to form an antigen. Reactions may persist for years after the drug is withdrawn; they are usually eczematous.

Systemic protection, as opposed to application of drug to exposed areas, should be considered when the topical measures fail. Antimalarials such as hydroxychloroquine may be effective for short periods in polymorphic light eruption and in cutaneous lupus erythematosus.

Psoralens (obtained from citrus fruits and other plants), e.g. methoxsalen, are used to induce photochemical reactions in the skin. After topical or systemic administration of the psoralen and subsequent exposure to UVA there is an erythematous reaction that goes deeper than ordinary sunburn and that may reach its maximum only after 48 h (sunburn maximum is 12-24 h). Melanocytes are activated and pigmentation occurs over the following week. This action is used to repigment areas of disfiguring depigmentation, e.g. vitiligo in black-skinned persons.

In the presence of UVA the psoralen interacts with DNA, forms thymine dimers, and inhibits DNA synthesis. Psoralen plus UVA (PUVA) treatment is used chiefly in severe psoriasis (a disease characterised by increased epidermal proliferation), and cutaneous T cell lymphoma.

Severe adverse reactions can occur with psoralens and ultraviolet radiation, including increased risk of skin cancer (due to mutagenicity inherent in their action), cancer of the male genitalia, cataracts and accelerated skin aging; the treatment is used only by specialists.

Chronic exposure to sunlight induces wrinkling and yellowing due to the changes in the dermal connective tissue. Topical retinoids are widely used in an attempt to reverse some of these tissue changes.

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