Abstract
<h3>Background and Design:</h3> To date, studies of the effectiveness of sunscreens in preventing UVB-induced suppression of contact hypersensitivity in humans have not been published. Several studies in mice of the protection afforded by sunscreens from UVB-induced suppression of contact hypersensitivity and rejection of transplanted skin cancers have yielded dissimilar results, ranging from ''no'' to ''complete'' protection. We sought to determine whether the effect of preapplication of a sun protection factor (SPF) 29 sunscreen (containing octyl methoxycinnamate, oxybenzone, and octyl salicylate) could prevent local UVB-induced suppression of contact hypersensitivity to dinitrochlorobenzene (DNCB). Nineteen subjects received either three minimal erythema doses of UVB daily on three consecutive days (UVB group) or sunscreen followed by this same dose of UVB irradiation (sunscreen plus UVB group) to a 16-cm<sup>2</sup>area of the buttock. One day after completion of irradiation, DNCB was applied to this buttock site, and 2 weeks later, forearm challenge with four different concentrations of DNCB was performed. A control group of 10 subjects underwent DNCB testing as above, but with no prior exposure to UVB (no-UVB group). <h3>Results:</h3> The UVB group had a reduced response rate to all challenge doses of DNCB (3.125, 6.25, and 8.8 μg), except for the highest dose (12.5 μg) compared with the no-UVB control group (Fisher's Exact test, P≤.008), and compared with the sunscreen plus UVB group (P≤.02). The no-UVB and sunscreen plus UVB groups showed no significant differences in response rates to any of the doses of DNCB tested (P≥.53). <h3>Conclusions:</h3> These results indicate that application of a sunscreen with over ninefold greater protection than that needed to prevent erythema prior to localized UVB radiation prevents localized UVB-induced suppression of contact hypersensitivity. Further studies are needed to determine whether sunscreens providing less protection, yet still preventing erythema, adequately prevent suppression of contact hypersensitivity, a possible surrogate marker for skin cancer tumor antigen recognition and rejection. (Arch Dermatol. 1995;131:1128-1133)
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