UV light has been implicated in producing actinic (sun caused) damage, and causing skin cancers like basal and squamous cell carcinoma, cataract, dermatitis and morphologic changes of ageing. Among them the cancers are the most important. Particular increase in the incidence has been noticed in recent years. As outlined in the WHO-INCHEM, 1994 report, the “DNA is the most critical target for damage by UVB and UVC radiations”. UVR causes damage by an ionizing reaction which produces free radicals in the body.
UVR also activate latent viral infections like herpes, and HIV. DNA damage, and failure to conduct DNA repair is the hallmark of UVR injury. UVB is most implicated in causation of melanomas and other skin cancers. With increasing exposure to UVC, its role is also coming into the limelight. Acute effects of radiation cause a superficial burn or an erythematous reaction, which is self healing. Continued exposure will lead to more severe burns and secondary infections. UVA is probably least involved in this reaction.
Chronic skin changes due to UV consist of skin cancer (both melanoma and non-melanocytic), benign abnormalities of melanocytes (freckles, melanocytic naevi and solar or senile lentigines. In a unique condition known as xeroderma pigmentosa, where there is a congenital deficiency of DNA repair mechanism, there is a very high incidence of skin cancers, thus giving a direct proof of the tumorigenic potential of UVR. Cancers of the upper lip are also much more common than the lower lip due to increased exposure of the upper lip to sunlight.
This is also higher in the whites where the UVR pass deeper into the skin. ( INCHEM, 1994). As detailed in the WHO-INCHEM 1994 report there is strong epidemiologic proof of increased skin malignancy in people who work outdoors, and in areas where there is ‘ozone hole’ like Australia and Greenland. There is strong evidence of the protective role of dark skin in prevention of skin cancers. This is due to the absorption of UVR in the epidermis by the larger melanosomes, without giving a chance to the UVR to damage the dermis.