title: Analysis of effects of ultraviolet B radiation on induction of primary allergic reactions.
abstract: Acute, low-dose exposure to UVB light reveals a genetic polymorphism in humans with respect to the ability of irradiated skin to support the induction of contact hypersensitivity (CH) to dinitrochlorobenzene (DNCB). In healthy adult caucasians, as well as in humans with deeply pigmented skin, approximately 45% fail to develop CH when DNCB is painted on UVB-irradiated skin; these individuals are termed "UVB susceptible" (UVB-S), whereas those who develop CH at the challenge site are termed "UVB resistant" (UVB-R). The UVB-S trait is characteristic of virtually all patients with biopsy-proved basal/squamous cell cancer, and may therefore be a risk factor for this disease. We have investigated the effects of UVB on expression of primary allergic reactions (PAR) in healthy caucasian and black-skinned adults, as well as patients with skin cancer. Among UVB-R caucasians, very few (less than 25%) developed PAR at site exposed to UVB, whereas among black-skinned UVB-R subjects, all displayed a PAR at the UVB irradiated site. To determine whether the lack of PAR in UVB-R caucasian subjects was systemic or local in origin, DNCB was applied to UVB-exposed buttock skin, and each individual was then challenged with dilute DNCB on forearm skin twice: 11 and 30 d thereafter. When inflammatory responses were evaluated at the original hapten application site, as well as both challenge sites, complete concordance was observed between positive challenge reactions at 30 d (UVB-R) and positive challenge reactions at 11 d, whereas only one caucasian subject displayed a PAR at 12 d. Thus, UVB-R caucasians can display CH as early as 11 d following hapten application to UVB-treated skin, indicating that their failure to display PAR is a local, rather than a systemic, effect of UVB. Because UVB-induced phototoxicity was significantly greater in caucasian than in deeply pigmented skin, it is anticipated that phototoxicity leads to rapid hapten "washout" from UVB-exposed caucasian skin. We propose that PAR usually do not occur in UVB-treated caucasian skin because insufficient hapten remains at the site to trigger a spontaneous inflammation when systemic hapten-specific immunity emerges.
authors.affiliation: Department of Microbiology and Immunology, University of Miami School of Medicine, FL 33101.
authors.forename: C
authors.initials: C
authors.lastname: Tseng
authors.forename: B
authors.initials: B
authors.lastname: Hoffman
authors.forename: I
authors.initials: I
authors.lastname: Kurimoto
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: G J
authors.initials: GJ
authors.lastname: Schmieder
authors.forename: J R
authors.initials: JR
authors.lastname: Taylor
authors.forename: J W
authors.initials: JW
authors.lastname: Streilein
mesh_terms: D000328:Adult; D000367:Age Factors; D003877:Dermatitis, Contact / Q000209:etiology* / Q000276:immunology; D004137:Dinitrochlorobenzene / Q000276:immunology; D006801:Humans; D008875:Middle Aged; D011446:Prospective Studies; D011836:Radiation Tolerance; D012867:Skin / Q000276:immunology / Q000528:radiation effects; D012878:Skin Neoplasms / Q000276:immunology; D012880:Skin Pigmentation; D014466:Ultraviolet Rays; D044465:White People
chemical_list: D004137:Dinitrochlorobenzene