Sunscreen Allergy: A Review of Epidemiology, Clinical Characteristics, and Responsible Allergens

Elyse Scheuer; Erin Warshaw


Dermatitis. 2006;17(1):3-11. 

In This Article

Abstract and Introduction

Although allergy to sunscreen represents a small proportion (< 1%) of allergic contact dermatitis reactions in North America, it is one of the most common causes of photoallergy. The epidemiology and clinical characteristics of sunscreen allergy are summarized in this review. In addition, a detailed discussion of specific chemical sunscreen allergens is provided.

Sunscreens have traditionally been divided into chemical absorbers and physical blockers.[1] Chemical sunscreens absorb ultraviolet (UV) radiation and incorporate its energy into the structure of the sunscreen molecule itself, exciting the molecule to a higher energy state. This in turn converts the ultraviolet energy into less dangerous wavelengths. Chemical sunscreens can absorb in the ultraviolet B (UVB) (290-320 nm), ultraviolet A II (UVA II) (321-340 nm), and ultraviolet A I (UVA I) (341-400 nm) ranges.[2] By contrast, physical blockers reflect and scatter UV radiation and dissipate the energy into the surrounding environment.[1]

Although chemical sunscreens were first introduced in the 1930s, widespread use of these products has occurred only in the last 20 years as the photocarcinogenic and photoaging properties of UV radiation have been increasingly recognized by the general population.[3]Consequently, in the United States, allergic reactions to sunscreens have also become more common. Allergic and photoallergic reactions have been reported with several chemical sunscreen families.[4,5]

Photoallergic contact dermatitis is a T-cell-mediated delayed-type hypersensitivity reaction. It occurs in response to a photoallergen or antigen in a person previously sensitized to the same substance or to a cross-reacting substance. It occurs in response to both UV (most commonly UVA) and visible light.[6,7] The mechanism by which UV light contributes to photoantigen formation is not well understood. Two mechanisms have been proposed. The skin has several endogenous chromophores (including keratin proteins, porphyrins, lipoproteins, hemoglobin, melanin, and amino acids) that can absorb UV radiation.[7] These chromophores may be transduced to an excited state after exposure to UV radiation and, upon reversion to the ground state, may conjugate with a carrier. Alternatively, UV radiation may induce a stable photoproduct that serves as a hapten. The hapten would then conjugate with a carrier protein to serve as a complete antigen.[6] Once complete antigen formation occurs, the pathophysiology of photoallergic contact dermatitis is identical to that of allergic contact dermatitis.[6,7,8]

In addition to reacting to active sunscreens, patients may demonstrate allergy or photocontact allergy to inactive ingredients in sunscreen formulations. Most significant among these are fragrances, formaldehyde releasers, preservatives, and lanolin alcohol.[9,10] A full discussion of inactive sunscreen allergens is beyond the scope of this review; the purpose of this discussion is to present a comprehensive overview of the epidemiology and clinical characteristics of allergic and photoallergic contact dermatitis from active sunscreen agents and to provide a detailed description of each allergen.