Environmental Effects of Ozone Depletion 1998 Assessment
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Socioeconomic
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Environmental Effects of Ozone Depletion 1998 Assessment |
The future projections of ozone depleting substances in the atmosphere made in recent years have invited scenario studies on future ozone density and corresponding levels of ambient UVR. These in turn are now being translated into assessments of the risks to the biosphere in order to assess the importance of such atmospheric changes. It cannot be over-emphasized (see Chapter 1), however, that these scenario studies should not be taken as genuine forecasts. They are, at best, idealized computations on the effects of the changes in a small subset of factors leaving all other relevant modifying factors undisturbed. In the real world many of the other relevant factors may change and diminish or aggravate the effects (e.g. increased or decreased cloudiness). Nevertheless, these scenario studies serve the purpose of quantifying and comparing the potential effects of certain policies.
As indicated above it is not currently possible to develop quantitative risk assessments for all of the health effects expected from ozone depletion. Presented below, therefore, is a mixture of quantitative and qualitative information that assesses to the extent possible, the likely impacts of ozone depletion on human health.
Analysis of available knowledge leads to the conclusion that sunburns will not appreciably increase under a decreasing ozone layer; this is due to a powerful adaptation of the skin (van der Leun and de Gruijl, 1993). A gradual thinning of the ozone layer would, for instance, lead to 20 percent more UV-B in 10 years' time. The skin is equipped with an adaptation that can even cope with the changes in UV-B with the seasons. These are much more drastic; in mid-latitudes, the UV-B irradiance in summer is typically 10 times larger than in winter.
Fig. 2.6 Cataract risk estimates based on various scenarios.
Experience with phototherapy of skin diseases shows that one UV-B exposure, sufficient to cause a slight reddening, decreases the sensitivity of the skin by about 20 percent. In a series of exposures, this can be repeated many times. That is how the skin adapts to the UV-B changes with the seasons. A calculation shows that adaptation from winter to summer irradiance requires 13 such steps of 20 percent each. This will not change much under a UV-B irradiance increased by 20 percent due to ozone depletion. It will in fact become a bit easier, as the winter irradiance increases more than that in summer, so that the difference becomes a bit smaller.
It is certainly possible to think of situations where adaptation cannot work in this way. For instance, if a totally unadapted skin is suddenly exposed to full sunlight, more UV-B in the sunlight will increase the likelihood of sunburn. Persons going on an expedition to the Antarctic ozone hole have reported experiences in this line. But such conditions are quite exceptional. By far the most sunburns arise from lack of care in going through the adaptation process. Such sunburns will not increase.
Recent risk assessment efforts with a quantitative model that incorporate ozone depletion scenarios from the Scientific Assessment Panel, provides estimates of the additional cancer risks in populations annually based on the estimated changes in UV-B over time (Slaper et al. 1996; Arnold et al. 1998). It should be noted, however, that such efforts are not just a matter of including information on the changing concentration of ozone (and UV-B) with time. There are also a number of issues that need to be addressed with regard to the assumptions chosen for the dose-response models used to approximate the relationship between exposure and effect. The process of disease development has to be dissected in phases (steps) that are either UV-driven or not, and it should be known at which stage in the development (early or late, or both) UV is important. From experimental data and epidemiology, it can be inferred that chronic accumulation of UV exposures is important throughout the development of SCC. In contrast, for BCC and CM, acute intense exposures, particularly those acquired in childhood, may be the critical dose metric, although as discussed above, this may be true in the case of CM only if adulthood exposures are also substantial (Autier and Doré, 1998).
Several groups are developing risk estimates using such scenario-based approaches; unpublished data from two of them developed for this assessment are presented here. Given below in Fig. 2.7 is a summary graphic from the Dutch group (Slaper et al., 1996) Calculations for skin cancer risks are performed for five scenarios applying the UV-chain methodology developed by Slaper et al. 1996, and assuming full worldwide compliance with the agreed protocols within the Vienna Convention.
Fig. 2.7 All cancer risk estimates based on various scenarios
The calculations are based on the production and depletion scenarios used in the WMO/UNEP scientific assessment of ozone depletion (WMO, 1998). Skin cancer risks are calculated for the zonal average ozone depletion observed at 45 degrees N (as reported in the 1998 ozone assessment), assuming a population with the sensitivity and age distribution as in the USA (risk in 1980 estimated at 2000 skin cancer cases per million per year). Excess cases refer to additional cases due to ozone depletion. The majority of the excess cases are nonmelanoma, and the lethality is approximately 2% of the incidence. The risks are probably conservative estimates, because:
In developing animal models for the effects of UV radiation on infections, investigators have been measuring changes in fundamental immune reactions that are associated with the course of the infection and that may also be measured in humans. Thus, the aim is to predict UV-induced effects on human resistance to infection by measuring the relevant changes in basic immune responses after UV exposure (Goettsch et al.,1998), a so-called 'parallelogram' approach. This approach is in its infancy and requires a thorough and detailed knowledge of the immunological responses that play a role in any particular infection under consideration, in order to identify the relevant measurements. This approach also has certain limitations in that the outcome of such analysis only evaluates host resistance and does not provide complete information on the spread and course of an infection in a population.
The first conjectural calculations
demonstrate that physiologically relevant exposures to solar UV radiation
(e.g. 90 minutes around noon in July at 40o N) may significant
hamper cellular immunity against a bacterial infection (Listeria monocytogenes)
in the 5 % most sensitive individuals in a population of white Caucasians.
This result is in reasonable agreement with direct measurements of the
UV-induced suppression immune reactions against simple chemicals (Yosikawa
et al., 1990; Cooper et al., 1992), where UVB exposures of the same order
of magnitude as those calculated were found to affect a high percentage
of people. In spite of these promising developments in indirect methods
for assessing UV-related risks of infection, a more direct quantitative
assessment of UV-induced enhanced infection remains desirable. A reliable
assessment of the magnitude and breadth of effects of current ambient UV
levels on infections and on success rates of vaccinations appears to be
a long way off, and an expansion to include the effects of an ozone depletion
delves even deeper into realm of human ignorance.
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