Roberts L K, Beasley D G, Learn D B, Giddens L D, Beard J, Stanfield J W
Schering-Plough HealthCare Products, Memphis, TN 38151, USA.
Photochem Photobiol. 1996 Jun;63(6):874-84. doi: 10.1111/j.1751-1097.1996.tb09645.x.
Acute exposure to UV radiation causes immunosuppression of contact hypersensitivity (CH) responses. Past studies conducted with unfiltered sunlamps emitting nonsolar spectrum UV power (wavelengths below 295 nm) or using excessive UV doses have suggested sunscreens may not prevent UV-induced immunosuppression in mice. This study was thus designed to evaluate critically the effects of different UV energy spectra on the immune protection capacity of sunscreen lotions. Minimum immune suppression doses (MISD), i.e. the lowest UV dose to cause approximately 50% suppression of the CH response to dinitrofluorobenzene in C3H mice, were established for three artificial UV sources. The MISD for each UV source was 0.25 kJ/m2 for unfiltered FS20 sunlamps (FS), 0.90 kJ/m2 for Kodacel-filtered FS20 sunlamps (KFS), which do not emit UV power at wavelengths < 290 nm, and 1.35 kJ/m2 for a 1000 W filtered xenon arc lamp solar simulator. Using MISD as baseline, sunscreens with labeled sun protection factors (SPF) of 4, 8, 15 and 30 were tested with each UV source to establish their relative immune protection factors. The immune protection factor of each sunscreen exceeded its labeled SPF in tests conducted with the solar simulator, which has a UV power spectrum (295-400 nm) similar to that of sunlight. Conversely, sunscreen immune protection factors were significantly less than the labeled SPF in tests conducted with FS and KFS. Comparison of the immunosuppression effectiveness spectra showed that relatively small amounts of nonsolar spectrum UV energy, i.e. UVC (200-290 nm) and/or shorter wavelength UVB (between 290 and 295 nm), produced by FS and KFS contributes significantly to the induction of immunosuppression. For example, 36.3% and 3.5% of the total immunosuppressive UV energy from FS and KFS, respectively, lies below 295 nm. Sunscreen absorption spectra showed that transmission of immunosuppressive UV energy below 295 nm for FS was at least eight-fold higher than that for KFS. Compared to the solar simulator UV spectrum the transmission of nonsolar immunosuppressive UV energy through sunscreens was > 15-fold higher for FS and > or = 1.5-fold higher for KFS. These data demonstrate that relevant evaluations of sunscreen immune protection can only be obtained when tests are conducted with UV sources that produce UV power spectra similar to that of sunlight and UV doses are employed that are based on established MISD.
急性暴露于紫外线辐射会导致接触性超敏反应（CH）的免疫抑制。过去使用发射非太阳光谱紫外线能量（波长低于295nm）的未过滤太阳灯或使用过量紫外线剂量进行的研究表明，防晒霜可能无法预防小鼠紫外线诱导的免疫抑制。因此，本研究旨在严格评估不同紫外线能谱对防晒乳液免疫保护能力的影响。为三种人工紫外线源确定了最小免疫抑制剂量（MISD），即导致C3H小鼠对二硝基氟苯的CH反应抑制约50%的最低紫外线剂量。对于未过滤的FS20太阳灯（FS），每种紫外线源的MISD为0.25kJ/m²；对于柯达塞尔过滤的FS20太阳灯（KFS），其在波长<290nm时不发射紫外线能量，MISD为0.90kJ/m²；对于1000W过滤氙弧灯太阳模拟器，MISD为1.35kJ/m²。以MISD为基线，对标签防晒系数（SPF）为4、8、15和30的防晒霜与每种紫外线源进行测试，以确定它们的相对免疫保护系数。在使用具有与太阳光相似紫外线功率谱（295 - 400nm）的太阳模拟器进行的测试中，每种防晒霜的免疫保护系数超过其标签SPF。相反，在使用FS和KFS进行的测试中，防晒霜免疫保护系数明显低于标签SPF。免疫抑制有效性光谱的比较表明，FS和KFS产生的相对少量非太阳光谱紫外线能量，即UVC（200 - 290nm）和/或较短波长的UVB（290至295nm之间），对免疫抑制的诱导有显著贡献。例如，来自FS和KFS的总免疫抑制紫外线能量分别有36.3%和3.5%低于295nm。防晒霜吸收光谱表明，FS在295nm以下的免疫抑制紫外线能量透过率至少比KFS高八倍。与太阳模拟器紫外线光谱相比，非太阳免疫抑制紫外线能量透过防晒霜的透过率对于FS高出>15倍，对于KFS高出>或 = 1.5倍。这些数据表明，只有当使用产生与太阳光相似紫外线功率谱的紫外线源并采用基于既定MISD的紫外线剂量进行测试时，才能获得对防晒霜免疫保护的相关评估。
