Solar ultraviolet radiation at the surface of the earth is a recognized cause of skin cancer. Postulated anthropogenic reductions in the thickness of the ozone layer would lead to an increased amount of ultraviolet radiation and hence would be expected to increase the risk of skin carcinogenesis. This study uses hairless (Skh:HR) mice as an animal model to study this increased risk. The mice were exposed 5 days/week to graded doses of ultraviolet radiation from a xenon arc lamp attenuated by five different thicknesses of Schott glass filters (WG320) to simulate various ozone layer thicknesses. A Robertson-Berger sunburning ultraviolet meter was used as one of the forms of dosimetry.

The results of the various exposure treatments are expressed as the percentage of animal with tumors (incidence) versus time after commencing irradiation and as cumulative tumor yield (average number of tumors per survivor) versus time. With any given filter, the time to 50% incidence is inversely related to daily dose in Robertson-Berger meter units. The time to 50% incidence for comparable Robertson-Berger meter doses through different filter thicknesses increases with increasing thickness. These results indicate that the effective dose for skin cancer induction may be estimated from the Robertson-Berger meter dose but that the Robertson-Berger meter response spectrum underestimates the photocarcinogenic effectiveness of the shorter wavelengths. The cumulative tumor yield data are also consistent with these conclusions.

Alternate weighting of the source spectra with the acute-response action spectrum for mouse skin edema gave a better correlation between unit dose and time to a tumor response, independent of the source spectral distribution. This suggests that the mouse skin edema action spectrum, indistinguishable from a human skin erythema action spectrum for λ >295 nm, is similar in shape to the mouse skin photocarcinogenesis action spectrum for λ >295 nm.

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Based in part on a Final Report for USPHS Contract NO1-CP43271.

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