Forbes P D, Davies R E, Urbach F, Berger D, Cole C
Cancer Res. 1982 Jul;42(7):2796-803.
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 lambda greater than 295 nm, is similar in shape to the mouse skin photocarcinogenesis action spectrum for lambda greater than 295 nm.
地球表面的太阳紫外线辐射是公认的皮肤癌致病因素。据推测,人为因素导致臭氧层厚度降低会使紫外线辐射量增加,进而预计会增加皮肤癌发生的风险。本研究以无毛(Skh:HR)小鼠作为动物模型来研究这种增加的风险。这些小鼠每周5天暴露于由五种不同厚度的肖特玻璃滤光片(WG320)衰减的氙弧灯发出的不同剂量的紫外线辐射下,以模拟不同的臭氧层厚度。使用罗伯逊 - 伯杰晒伤紫外线计作为剂量测定的一种方式。各种暴露处理的结果表示为出现肿瘤的动物百分比(发生率)与开始照射后的时间关系,以及累积肿瘤产量(每个存活动物的平均肿瘤数)与时间的关系。对于任何给定的滤光片,达到50%发生率的时间与罗伯逊 - 伯杰计单位中的日剂量成反比。通过不同滤光片厚度的可比罗伯逊 - 伯杰计剂量达到50%发生率的时间随着厚度增加而增加。这些结果表明,可根据罗伯逊 - 伯杰计剂量估算诱发皮肤癌的有效剂量,但罗伯逊 - 伯杰计响应光谱低估了较短波长的光致癌效力。累积肿瘤产量数据也与这些结论一致。用小鼠皮肤水肿的急性反应作用光谱对源光谱进行交替加权,使得单位剂量与肿瘤反应时间之间具有更好的相关性,而与源光谱分布无关。这表明,对于大于295 nm的波长,与人类皮肤红斑作用光谱无法区分的小鼠皮肤水肿作用光谱,其形状与大于295 nm的波长的小鼠皮肤光致癌作用光谱相似。