Wittenberg S
Am J Optom Physiol Opt. 1986 Aug;63(8):676-89.
Solar radiation has been implicated, with a variety of evidence, as a causative agent in photokeratoconjunctivitis, pinguecula and pterygium, nodular band keratopathies, epidermoid carcinoma, cataract, solar retinopathy, and macular degeneration. Much of the support for claims relating to chronic conditions having serious consequences and significant prevalence in the United States rests on investigations using animals and short-time exposures at high intensities. The direct applicability of these studies to humans in natural environments is uncertain, but they have been relied on because one cannot deliberately induce significant trauma in humans. The use of animal data is made difficult by the need to convert animal thresholds to human equivalents, to equate laboratory cycles and magnitudes of exposure to those in the natural environment, and to quantify the impact of avoidance and protective mechanisms. Risk can be assessed adequately only by epidemiological studies, but their potential has been only partially realized because of poorly controlled confounding variables. Epidemiologic evidence suggests that corneal trauma from ultraviolet radiation (UVR) is a risk of prolonged exposure in regions containing much ultraviolet (UV) or in highly reflective environments. The impact of UV-B on cataractogenesis has been investigated inadequately and no evidence exists for retinal trauma arising from routine exposure in even the brightest surroundings. However, there can be no question that enough solar energy reaches the earth to harm the eye if unattenuated. Damage to vision as a result of direct solar viewing demonstrates that unequivocally. The lack of clear evidence of radiation damage occurring other than in regions of high reflectivity and/or low horizons suggests that in normal surroundings there is little or no risk to the eye, although more careful epidemiological investigation is required before all concern can be ruled out completely. The major improvement required is the quantification of individual exposure histories. This step is necessary if we are to make significant progress toward better understanding the practical impact of solar radiation on the eye.
有各种证据表明，太阳辐射是引起光性角膜结膜炎、睑裂斑和翼状胬肉、结节性带状角膜病变、表皮样癌、白内障、日光性视网膜病变和黄斑变性的致病因素。在美国，许多关于慢性病具有严重后果且患病率高的说法的依据是对动物的研究以及高强度短时间暴露实验。这些研究在自然环境中对人类的直接适用性尚不确定，但由于无法在人类身上故意造成重大创伤，所以一直依赖这些研究。将动物阈值换算成人类等效值、使实验室周期和暴露强度与自然环境中的情况等同起来以及量化规避和保护机制的影响，这些都给使用动物数据带来了困难。只有通过流行病学研究才能充分评估风险，但由于混杂变量控制不佳，其潜力尚未得到充分发挥。流行病学证据表明，在紫外线（UV）含量高的地区或高反射环境中，紫外线辐射（UVR）造成的角膜损伤是长期暴露的一种风险。UV-B对白内障形成的影响尚未得到充分研究，而且即使在最明亮的环境中，也没有证据表明常规暴露会导致视网膜损伤。然而，如果不减弱，到达地球的太阳能足以伤害眼睛，这是毫无疑问的。直视太阳导致视力受损就明确证明了这一点。除了在高反射率和/或低地平线地区外，缺乏辐射损伤的明确证据，这表明在正常环境中，眼睛几乎没有或没有风险，不过在所有担忧完全消除之前，还需要更仔细的流行病学调查。主要需要改进的是对个人暴露史进行量化。如果我们要在更好地理解太阳辐射对眼睛的实际影响方面取得重大进展，这一步是必要的。
