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Spectral Dependencies of Killing, Mutation, and Transformation in Mammalian Cells and Their Relevance to Hazards Caused by Solar Ultraviolet Radiation¹

Mammalian Cell Biology Group, Division of Biological and Medical Research, Argonne National Laboratory, Argonne, Illinois 60439

Using germicidal lamps and Westinghouse sunlamps with and without filtration, the effectiveness of ultraviolet and nearultraviolet light in inducing molecular and cellular changes was measured. Cell survival and the induction of resistance to 6-thioguanine or to ouabain were measured with V79 Chinese hamster cells, cell survival and neoplastic transformation were measured with C3H mouse 10T cells, and the induction of pyrimidine dimers containing thymine was measured in both cell lines. The short-wavelength cutoff of the sunlamp emission was shifted from 290 nm (unfiltered) to 300 and 310 nm by appropriate filters. Although it was found that the efficiency with which all end points were induced progressively decreased as the short-wavelength cutoff was shifted to longer wavelengths, the rates of decrease differed appreciably. For example, doses of near-ultraviolet light longer than 300 nm that were effective in mutating or in transforming cells were ineffective in killing them. In respect to pyrimidine dimer induction, several but not all cellular end points were induced by dose ratios of sunlamp light (short-wavelength cutoff, 290 nm) to germicidal lamp light (254 nm) in fairly close accord with the doses required to produce equivalent proportions of dimers. However, for near-ultraviolet light having cutoffs at longer wavelengths, the biological action observed was appreciably greater than what would be predicted from the proportion of dimers induced. From the latter observation, it is inferred that increasing intensities of short-wavelength ultraviolet light, as would be expected from reductions in stratospheric ozone around the earth, would result in smaller increases in biological action, e.g., skin cancer, compared to current levels of action than would be predicted from an action spectrum completely corresponding to that of a pyrimidine dimer induction spectrum in DNA.

¹ Supported by the United States Department of Energy, Contract W-31-109-ENG-38, and the United States National Cancer Institute, Grant CA 26984. Presented in part at the 71st Annual Meeting of the American Association for Cancer Research, Inc., May 30, 1980, at San Diego, Calif. (11), and at the Eighth International Congress of Photobiology, July 20 to 25, 1980, at Strasbourg, France (18).

² On leave from Kanazawa University, Division of Radiation Biology, Kanazawa, Japan.

³ Present address: Biodynamics, Mettlers Road, East Millstone, N. J. 08873.

⁴ Present address: Radiation Biology Center, Kyoto University, Yoshida-Konoecho, Sakyo-ku, Kyoto 606, Japan.

⁵ To whom requests for reprints should be addressed.

Received 6/15/81. Accepted 8/13/81.