Several pieces of evidence suggest that UVB and UVA exposure results in pigmentation via distinct pathways. The character of the action spectrum suggests that DNA may be the chromophore in the UVB region, with a different target in the UVA region. The oxygen dependence of the response to UVA, but not UVB is consistent with this hypothesis. Peak et al [1984] have postulated two distinct mechanisms for certain cellular effects of UV, such as lethality and mutagenesis: a "UVC mechanism," which results from direct DNA photochemistry, with an action spectrum mainly in the UVC and UVB regions, and a "UVA mechanism" which results from oxygen-dependent effects, induced mainly by UVA; the two action spectra overlap in the short UVA region. At 333 nm, it was calculated that the two mechanisms contributed equally to mutagenesis. It is possible that an analogous process occurs for certain cutaneous responses and could account for some of the observed differences between the effects of different wavebands. This could also account for recent observations suggesting that the effects upon skin of different regions within the UVA spectrum differ qualitatively as well as quantitatively. In particular, the biological effects of "full spectrum UVA" (320-400 nm) appear to be different from those of UVA from which the wavelengths between 320-340 nm have been excluded. "Full spectrum UVA" appears to be more damaging with respect to connective tissue alteration [Kligman et al, 1985], Langerhans cell depletion [Aberer et al, 1981], and the ability to increase photocarcinogenesis by UVB [Staberg et al, 1983a; Staberg et al, 1983b]. An untested hypothesis is that this phenomenon is the result of overlapping "UVC mechanism" and "UVA mechanism" action spectra in the 320-340 nm region, with these wavelengths resulting in changes typical of both regions.