Depletion of the stratospheric ozone layer has led to increased solar UV-B radiation (280-315 nm) at the surface of the Earth. This change is likely to have had an impact on human exposure to UV-B radiation with consequential detrimental and beneficial effects on health, although behavioural changes in society over the past 60 years or so with regard to sun exposure are of considerable importance. The present report concentrates on information published since our previous report in 2007. The adverse effects of UV radiation are primarily on the eye and the skin. While solar UV radiation is a recognised risk factor for some types of cataract and for pterygium, the evidence is less strong, although increasing, for ocular melanoma, and is equivocal at present for age-related macular degeneration. For the skin, the most common harmful outcome is skin cancer, including melanoma and the non-melanoma skin cancers, basal cell carcinoma and squamous cell carcinoma. The incidence of all three of these tumours has risen significantly over the past five decades, particularly in people with fair skin, and is projected to continue to increase, thus posing a significant world-wide health burden. Overexposure to the sun is the major identified environmental risk factor in skin cancer, in association with various genetic risk factors and immune effects. Suppression of some aspects of immunity follows exposure to UV radiation and the consequences of this modulation for the immune control of infectious diseases, for vaccination and for tumours, are additional concerns. In a common sun allergy (polymorphic light eruption), there is an imbalance in the immune response to UV radiation, resulting in a sun-evoked rash. The major health benefit of exposure to solar UV-B radiation is the production of vitamin D. Vitamin D plays a crucial role in bone metabolism and is also implicated in protection against a wide range of diseases. Although there is some evidence supporting protective effects for a range of internal cancers, this is not yet conclusive, but strongest for colorectal cancer, at present. A role for vitamin D in protection against several autoimmune diseases has been studied, with the most convincing results to date for multiple sclerosis. Vitamin D is starting to be assessed for its protective properties against several infectious and coronary diseases. Current methods for protecting the eye and the skin from the adverse effects of solar UV radiation are evaluated, including seeking shade, wearing protective clothing and sunglasses, and using sunscreens. Newer possibilities are considered such as creams that repair UV-induced DNA damage, and substances applied topically to the skin or eaten in the diet that protect against some of the detrimental effects of sun exposure. It is difficult to provide easily understandable public health messages regarding "safe" sun exposure, so that the positive effects of vitamin D production are balanced against the negative effects of excessive exposure. The international response to ozone depl...
Ozone depletion leads to an increase in the ultraviolet-B (UV-B) component (280-315 nm) of solar ultraviolet radiation (UVR) reaching the surface of the Earth with important consequences for human health. Solar UVR has many harmful and some beneficial effects on individuals and, in this review, information mainly published since the previous report in 2003 (F. R. de Gruijl, J. Longstreth, M. Norval, A. P. Cullen, H. Slaper, M. L. Kripke, Y. Takizawa and J. C. van der Leun, Photochem. Photobiol. Sci., 2003, 2, pp. 16-28) is discussed. The eye is exposed directly to sunlight and this can result in acute or long-term damage. Studying how UV-B interacts with the surface and internal structures of the eye has led to a further understanding of the location and pathogenesis of a number of ocular diseases, including pterygium and cataract. The skin is also exposed directly to solar UVR, and the development of skin cancer is the main adverse health outcome of excessive UVR exposure. Skin cancer is the most common form of malignancy amongst fair-skinned people, and its incidence has increased markedly in recent decades. Projections consistently indicate a further doubling in the next ten years. It is recognised that genetic factors in addition to those controlling pigment variation can modulate the response of an individual to UVR. Several of the genetic factors affecting susceptibility to the development of squamous cell carcinoma, basal cell carcinoma and melanoma have been identified. Exposure to solar UVR down-regulates immune responses, in the skin and systemically, by a combination of mechanisms including the generation of particularly potent subsets of T regulatory cells. Such immunosuppression is known to be a crucial factor in the generation of skin cancers. Apart from a detrimental effect on infections caused by some members of the herpesvirus and papillomavirus families, the impact of UV-induced immunosuppression on other microbial diseases and vaccination efficacy is not clear. One important beneficial effect of solar UV-B is its contribution to the cutaneous synthesis of vitamin D, recognised to be a crucial hormone for bone health and for other aspects of general health. There is accumulating evidence that UVR exposure, either directly or via stimulation of vitamin D production, has protective effects on the development of some autoimmune diseases, including multiple sclerosis and type 1 diabetes. Adequate vitamin D may also be protective for the development of several internal cancers and infections. Difficulties associated with balancing the positive effects of vitamin D with the negative effects of too much exposure to solar UV-B are considered. Various strategies that can be adopted by the individual to protect against excessive exposure of the eye or the skin to sunlight are suggested. Finally, possible interactions between ozone depletion and climate warming are outlined briefly, as well as how these might influence human behaviour with regard to sun exposure.
Except when sleeping, the cornea and interpalpebral conjunctiva are exposed to the ambient environment, both natural and man-made. Levels of solar ultraviolet irradiance reaching the eye may exceed the damage threshold under a number of circumstances. The consequences of overexposure may be acute after a latent period, sequelae to an acute exposure, or long-term chronic effects. Previously derived action spectra for photokeratitis and photoconjunctivitis due to incoherent ultraviolet are presented. These reveal interspecies similarities for the levels of radiant energy reaching each tissue. The initial in vivo (clinical) signs of photokeratitis are due to lost or damaged epithelial cells with other signs produced by this primary response. The conjunctival signs include injection and chemosis. Chronic exposure to solar ultraviolet is a factor in climatic droplet keratopathy and pterygium. Phototoxic compounds or their by-products potentially can reach the cornea from the air, via the tears or aqueous humor, or from the limbal capillaries. However, the human cornea appears to be much less susceptible to the influence of phototoxic agents than the skin.
Both eyes of female albino rabbits (1.9 kg) were exposed to a single dose of UV-B (300 +/- 9 nm; 0.125 J/cm2 total dose) between 13.30 and 15.00 h. The average irradiance was 209 +/- 4 microW/cm2 delivered over 612 +/- 13 s. At various time periods thereafter (every 12 h for 3 days, 6, 7, 14, 28, 42, 56, 112, 224 and 336 days post-irradiation), the animals were subjected to a full slit lamp examination to evaluate the status of the cornea and the anterior segment along with optical or ultrasonic pachometry of central corneal thickness. The results were compared with studies on age-matched rabbits over the same time period. In response to the UV-B irradiation, the corneas showed a modest edema (20% increase in central corneal thickness) that peaked at 48 h. Nearly normal central corneal thickness returned in 6 days and followed by a secondary very slight swelling (less than 5%) that resolved by 14 days. The edema was accompanied by keratitis over the same period. Thereafter, both control and UV-B irradiated corneas progressively increased in thickness with age. Biomicroscopy also revealed the appearance of granular opacities in the corneal epithelium that peaked at 72-96 h and resolved over 28 days. In addition, very small microdot opacities of the corneal epithelium were present in the UV-B irradiated corneas that reached maximum at 72 h but persisted to some degree throughout the evaluation period. Biomicroscopy also revealed a progressive disruption of the homogeneous nature of the corneal stroma by the appearance of large 'bread crumb'-like opacities that started at 72 h and was still present at the end of the evaluation period. These results suggest that long-term evaluation of the cornea is important after acute UV-B exposure and indicate that acute exposure to UV-R can produce corneal changes resembling those reported following chronic exposure to UV-R-rich environments.
One hundred pigmented rabbit eyes and ten primate eyes were exposed to infrared (IR) radiation in the 715 to 1,400 nm wavelength range and to the full spectrum output from a 5,000 W Xenon high-pressure source. The ocular exposures were evaluated independently with a slitlamp by two researchers and classified for ocular damage. The primary ocular lesions resulting from exposure to IR radiation were corneal, iritic, and lenticular. Corneal damage varied from epithelial haze to epithelial erosion but no endothelial damage was found. The iris showed stromal haze and swelling. Lenticular changes showed small white dots that, occur at the level of the anterior cortex. All lens damage depended on iris involvement. Ocular damage was related to the rate of delivery of the IR radiation since the data show that as the irradiance level increases, the radiant exposure threshold decreases. Exposures for the full spectrum were found to be additive for irradiance levels at 4 W.cm-2 and above. The threshold radiant exposures for the full spectrum of 750 J.cm-2 for the cornea, 1,000 J.cm-2 for the iris, and 2,000 J.cm-2 for the lens were essentially identical to the IR exposure thresholds for the same irradiance levels. The primate threshold radiant exposure was a factor of six above the respective rabbit thresholds.
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