Environment and health: 3. Ozone depletion and ultraviolet radiation

Ultraviolet radiation from the sun is responsible for a variety of familiar photochemical reactions, including photochemical smog, bleaching of paints and decay of plastics. Conjugated bonds in organic molecules such as proteins and DNA absorb the LV radiation, which can damage these molecules. By a fortunate evolutionary event, the oxygen produced by photosynthesis forms a filter in the outer reaches of our atmosphere that absorbs the most energetic and harmful UV radiation, with wavelengths below 240 nm (in the WC band [wavelength 100-280 nm)). In the process, the oxygen molecules split up and recombine to form ozone (Fig. 1). This ratified ozone layer (spread out between 10 and SO km in the stratosphere but only 3 mm thick were it compressed at ground level) in turn efficiently absorbs UV radiation of higher wavelenghts (up to about 310 nm). A part of the LV radiation in the WB band (wavelength 280-315 nm) still reaches ground level and is absorbed in sufficient amounts to have deleterious effects on cells. The less energetic radiation in the WA band (wavelength 31 S-400 nm, bordering the visible band [wavelength 400-800 nm]) is not absorbed by ozone and reaches ground level without much attenuation through a clear atmosphere (i.e., no clouds, no air polution). Although not completely innocuous, the WA radiation in sunlight is much less photochemically active and therefore generally less harmful than WB radiation. UVB radiation is known to damage DNA at specific sites (neighbouring pyrimidines). Mutations in the p53 tumour suppressor gene in human skin carcinomas were found at precisely these sites.',e (The p53 protein plays an important role in the cellular response to DNA damage [cell cycle arrest to allow more time for DNA repair, and apoptosis if the cell is overly damaged]. Its dysfunction can cause genomic instability and thus lead to the dysfunction of other genes.) These point mutations in the p53 gene resembled those found in experiments with UV-irradiated cell cultures (mainly a cytosine substituted by a thymine, and sometimes even 2 neighbouring cytosines replaced by 2 thymines).',8 The high frequency and apparent selection of the p53 mutations in the tumours appears to constitute the most direct evidence that UVB radiation contributes to the formation of skin cancer. The risk of squamous cell carcinoma appears to increase with lifelong sun exposure, whereas accumulated exposure does not appear to contribute to the risk of basal cell carcinom