It has been suggested that ultraviolet light induces free radical formation in skin, leading to photoaging and cancer. We have demonstrated by electron paramagnetic resonance that the ascorbate free radical is naturally present in unexposed skin at a very low steady state level. When a section of SKH‐1 hairless mouse skin in an EPR cavity is exposed to UV light (4,500 J m−2−1, Xe lamp, 305 nm cutoff and IR filters), the ascorbate free radical signal intensity increases. These results indicate that UV light increases free radical oxidative stress, consistent with ascorbate's role as the terminal, small‐molecule antioxidant. The initial radicals produced by UV light would have very short lifetimes at room temperature; thus, we have applied EPR spin trapping techniques to detect these radicals. Using α‐[4‐pyridyl 1‐oxide]‐N‐tert‐butyl nitrone (POBN), we have for the first time spin trapped a UV light‐produced carbon‐centered free radical from intact skin. The EPR spectra exhibited hyperfine splittings that are characteristic of POBN/alkyl radicals, aN= 15.56 G and aH= 2.70 G, possibly generated from membrane lipids as a result of β‐scission of lipid alkoxyl radicals. Iron can act as a catalyst for free radical oxidative reactions; chronic exposure of skin to UV radiation causes increased iron deposition. Using our spin trapping system, we have shown that topical application of the iron‐chelator, Desferal, to a section of skin reduces the UV light‐induced POBN adduct radical signal. These results provide direct evidence for free radical generation and a role for iron in UV light‐induced dermatopathology. We suggest that iron chelators can serve as photoprotective agen