de Laat A, van der Leun J C, de Gruijl F R
Department of Dermatology, University Hospital Utrecht, Utrecht University, The Netherlands.
Carcinogenesis. 1997 May;18(5):1013-20. doi: 10.1093/carcin/18.5.1013.
Although ultraviolet B (UVB wavelengths 280-315 nm) dominates the carcinogenic effect of sunlight, ultraviolet A (UVA 315-400 nm) is estimated to contribute 10-20% to the carcinogenic dose; a substantial background that is not affected by a depletion of the ozone layer. Furthermore, certain high-power modern tanning lamps emit mainly long wave UVA (UVA1; 340-400 nm). For a proper risk estimate of UVA exposure its carcinogenicity relative to that of UVB exposure needs to be determined more accurately. To this end we determined the dose-time relationship for skin tumor induction in hairless mice that were irradiated daily with custom-made Philips 365-nm sources. Irradiation of the group exposed to the highest of the four daily doses (430, 240, 140 and 75 kJ/m2) had to be discontinued because severe scratching set in after 3 months (no tumors). In the lower dose-groups the prevalence curves for skin carcinomas (percentage of tumor-bearing mice versus logarithm of time) ran virtually parallel, and were similar to those found with daily UVB exposure. However, the relationship between the daily dose (D) and the median tumor induction time (t50) appeared to differ: with UVB we found that t50 D(r) = constant, with r = 0.6, whereas with UVA1 we found r approximately 0.4. This would imply that 365-nm carcinogenesis shows less of a dose-dependency than UVB carcinogenesis, and that 365-nm radiation becomes more carcinogenic, relative to UVB, as the daily doses are lowered. This relative shift at low doses complicates extrapolation of UVB to UVA risks in humans. Based on the t50 from the lowest dose-group we found that the carcinogenicity at 365 nm (per J/m2) is 0.9 x 10(-4) times that at 293 nm, the wavelength of maximum carcinogenicity in hairless mice. This result for 365-nm carcinogenicity falls well within the margins of error of the wavelength dependency that was estimated earlier from experiments with broadband UV sources.
尽管紫外线B（UVB波长280 - 315纳米）在阳光致癌效应中占主导地位，但据估计紫外线A（UVA 315 - 400纳米）对致癌剂量的贡献为10% - 20%；这是一个不受臭氧层损耗影响的相当大的背景因素。此外，某些高功率现代晒黑灯主要发射长波UVA（UVA1；340 - 400纳米）。为了对UVA暴露进行恰当的风险评估，需要更准确地确定其相对于UVB暴露的致癌性。为此，我们确定了用定制的飞利浦365纳米光源每日照射的无毛小鼠皮肤肿瘤诱导的剂量 - 时间关系。暴露于四个每日剂量中最高剂量（430、240、140和75 kJ/m²）的组在3个月后因出现严重抓挠（无肿瘤）而不得不停止照射。在较低剂量组中，皮肤癌的患病率曲线（荷瘤小鼠百分比与时间对数）几乎平行，并且与每日UVB照射时发现的曲线相似。然而，每日剂量（D）与肿瘤诱导中位时间（t50）之间的关系似乎有所不同：对于UVB，我们发现t50 D(r) =常数，r = 0.6，而对于UVA1，我们发现r约为0.4。这意味着365纳米致癌作用的剂量依赖性比UVB致癌作用小，并且随着每日剂量降低，相对于UVB，365纳米辐射变得更具致癌性。低剂量下的这种相对变化使在人类中从UVB风险推断UVA风险变得复杂。基于最低剂量组的t50，我们发现365纳米处（每J/m²）的致癌性是293纳米处（无毛小鼠中致癌性最高的波长）的0.9×10⁻⁴倍。365纳米致癌性的这一结果完全落在早期用宽带紫外线源实验估计的波长依赖性误差范围内。
