CIESIN Reproduced, with permission, from: van der Leun, J. C. 1991. Effects of ozone depletion on human health. In Ozone depletion: Implications for the tropics, ed. M. Ilyas, 205-12. Papers initially presented at the International Conference on Tropical Ozone and Atmospheric Change, 20-23 February 1990, with support from the United Nations Environment Programme. Penang, Malaysia: University of Science Malaysia.



Mohammad Ilyas



J.C. van der Leun (The Netherlands)


A decrease of atmospheric ozone and a change of its vertical distribution will have many effects on man, animals, plants and materials. Decrease of ozone will have direct influences by an increase of the UV-B radiation penetrating to the earth's surface. This radiation has wavelengths between 290 and 320 nm and its effects are predominantly damaging. A change of the vertical distribution of ozone in the atmosphere is likely to induce changes of climate, and these in turn will influence the conditions for life.

The effects expected form the main reason for people and governments to be concerned about the ozone problem, much more so than the atmospheric processes which influence ozone. Yet, progress of research on effects is comparatively slow. Partly this is due to the complexity of the problems, such as in the case of climatic change. In the area of UV-B effects, however, the scientific tools are available, and progress depends strongly on the research effort invested (UNEP, 1986).


UV-B radiation has numerous influences on the human body. Some are positive, such as the formation of vitamin D3 in the skin, and the improvement of certain skin diseases. Many effects are damaging, such as sunburn, snowblindness, cataract, ageing of the skin and skin cancer. In the following survey, those effects will be discussed where there is reason to expect that increased UV-B irradiance may cause a considerable change.


Cataracts are opacities in the lens of the eye which impair vision. In developed countries, cataract operations prevent most cataracts from causing blindness. Nevertheless, in the U.S. cataract remains the third leading cause of legal blindness (Pitts et al, 1986). Worldwide senile cataract is responsible for significant visual impairment in 30 to 45 million people - of these perhaps 12 to 15 million are blind. Current treatment rates are not keeping pace with current incidence rates - thus the problem is growing (Maitchouk, 1985).

The exact mechanism of the formation of cataract is still unknown. Epidemiological studies, laboratory animal studies, and biochemical analysis support the belief that some cataracts are etiologically related to exposure to UV-B radiation (Pitts et al, 1986). The longer wavelength UV-A radiation and other causes, e.g., nutritional deficiency, may also contribute to cataract formation. Recent epidemiological studies of occupationally exposed individuals have indicated that the incidence of posterior subcapsular and cortical cataracts are directly related to cumulative exposure to UV-B (Maitchouk, 1985), thus changes in the amount of ambient UV-B radiation are likely to alter the incidence of cataracts. It has been estimated, on the basis of epidemiologic data, that for every one percent decrease in stratospheric ozone, there will be an increase in cataracts by about 0.6 percent (U.S. EPA, 1987). UV-B may also play a role in causing or exacerbating other eye disorders.


Non-melanoma skin cancers are the most common cancers occurring in white populations. The two major forms of non-melanoma skin tumours are basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Although the incidence of BCC is generally several times greater than the incidence of SCC, SCCs account for as much as four-fifths of all non-melanoma skin cancer deaths (NAS, 1984). Prolonged sunlight exposure is considered to be the dominant risk factor for non-melanoma skin tumours.

Quantitative projections depend on knowledge of the dose-effect relationship and the action spectrum. The dose-effect relationship has been known for some time (De Gruijl et al, 1983). An experimentally determined action spectrum for UV carcinogenesis in hairless albino mice became available recently (Sterenborg and van der Leun, 1987; Slaper, 1987) (Figure 1a,b). In its latest form (Slaper, 1987), it shows a more pronounced effectiveness for the longer wavelengths, in the UV-A, than was present in previously assumed action spectra. That makes it desirable to recalculate the radiation amplification factor, the percentage increase of carcinogenically effective UV-B irradiance with a one percent decrease of the total-column ozone. Preliminary calculations show that the new action spectrum leads to a radiation amplification factor of about 1.5 (Kelfkens and de Gruijl, 1988). Typical values for previously assumed action spectra were between 1.7 and 2.0.

Earlier projections can, therefore, be confirmed in general lines, but with slightly reduced numbers. Combined with biological amplification factors of 1.7 for BCC and 2.9 for SCC (Slaper et al, 1987; Scotto et al, 1981), the new data indicate that for every 1% depletion of ozone the incidence of BCC will ultimately increase by 2.5 percent and the incidence of SCC by 4.4 percent. In many registries, the non-melanoma skin cancers are still taken together. For a one percent depletion of ozone, the overall incidence of non-melanoma skin cancer will increase by about 3 percent. A similar conclusion was drawn in a recent analysis along quite different lines (U.S. EPA, 1987).


Cutaneous malignant melanoma (CMM) incidence rates throughout the world are rising at an alarming rate. During the decade from 1974 to 1983, CMM incidence has increased at an average yearly rate of between 3 and 4 percent (Sondik et al, 1985). For more than a decade, there has been serious concern that CMM is at least partially caused by UV-B radiation (NAS, 1987). However, several aspects of the scientific information about CMM have puzzled researchers and have contributed to uncertainty about the relationship of CMM to solar radiation, and in particular to the UV-B part of the spectrum. In the past several years, some progress has been made in understanding CMM and its possible relationship to solar radiation, and there now exists an array of evidence that indicates that exposure to solar radiation, and, in particular to UV-B, is a likely cause of CMM.

Evidence supporting a relationship between solar radiation and CMM includes:

  1. The fact that people who lack the protective pigmentation (which reduces penetration of solar radiation into the skin) have higher CMM incidence rates.

  2. A correlation, in well-designed ecologic epidemiological studies, of higher CMM incidence rates with decreasing latitude and increasing radiation (and in particular, UV-B) levels.

  3. The demonstration in several case-control studies of an association between freckling and nevus formation (risk factors for CMM) and solar exposure.

  4. Differences in CMM rates found between natives and immigrants to sunny climates.

  5. High rates of CMM in Xeroderma Pigmentosum (XP) patients who are genetically deficient at repairing DNA damage induced by UV-B.

  6. The indication, in case-control studies, that sun exposure at early ages and of an intermittent and severe nature (e.g., sunburn) results in higher CMM risks (Green et al, 1985; Holman et al, 1986).

The results of some studies have created uncertainty about the relationship between solar radiation and CMM: several ecologic studies failed to find latitude gradients for CMM (Crombie, 1979; Baker-Blocker, 1980); outdoor workers have been found to have lower CMM rates than indoor workers (but higher non-melanoma skin cancer rates) (Lee and Strickland, 1980; Holman et al, 1980); anatomic sites with lower cumulative sun exposure have high CMM rates, and there was until very recently no animal model for the induction of melanoma by UV-B (Holman et al, 1980b; Magnus, 1981). These uncertainties have made several scientists reluctant to venture any quantitative estimation of an influence of ozone depletion on the incidence of melanomas (van der Leun, 1988).

Recently the United States Environmental Protection Agency completed a review of the available data and literature to assess the relationship of CMM to UV-B exposure (Longstreth, 1987a). The salient conclusions of that review were that:

(a) The older literature, taken in conjunction with some very recent case-control epidemiologic studies, clearly indicated a role for sunlight in the etiology of CMM.

(b) The active portion of the solar spectrum was most likely to be in the UV-B region based on animal studies implicating UV-B in non-melanoma etiology and immunosuppression and on the sensitivity of XP-patients.

(c) The dose-response relationships for incidence and mortality were estimated to be such that for every one percent decrease in atmospheric ozone there would be up to a 2 percent increase in CMM incidence and between a 0.3 and 2 percent increase in CMM mortality.

Very recent evidence confirms the role of UV-B in CMM etiology, in that UV-B has now induced melanomas in two animal models, one in fish and one in marsupials (Setlow, 1988; Ley, 1988).


Ultraviolet radiation (UVR) has been found to alter, both locally (in the skin) and systemically, the immune response (ImR) to antigens administered via the skin in man and experimental animals (Kripke, 1986). The initial damage induced by UVR is inactivation of Langerhans cells - the principal antigen processing cell (APC) in the skin. APCs are required in the development of cell or antibody-mediated ImRs (Stingl et al, 1983). In man, loss of the Langerhans cells is accompanied by the migration into the skin of another type of APC which apparently has a predilection for interacting with a subset of T lymphocytes which suppress ImRs (suppressor T cells (Ts)) (Cooper, 1988). The Ts which arise in the skin as a result of UVR treatment are specific for antigen and prevent the development of ImRs. In a tumour bearing animal, this immunosuppression may result in the outgrowth of tumour cells which in normal animals would have been destroyed by the immune system (Kripke and Fisher, 1976). Although it is not certain that the damage to the Langerhans cells is entirely responsible for the immunosuppressive effect of UVR, it is clear that UV radiation of skin reduces the ImR in that skin (Kripke, 1986). Even more important, it is also clear that it is the UV-B portion of the UV spectrum that is responsible for the depression of the ImR (Longstreth, 1987b).

One important facet of this UVR-induced immunosuppression is the role it plays in UVB induced carcinogenesis; it affects the host's ability to respond to tumour-specific antigens present on the UVR-induced tumour cells thereby increasing the risk for tumour development in animal models, probably by allowing the tumour to escape the normal immune surveillance mechanisms (Kripke and Fisher, 1976). Thus the tumour cells are allowed to divide and establish a growing tumour in the host.

The immunosuppressive effects of UVR also are very likely to have a deleterious effect on the ImR to those infectious diseases that enter through the skin, especially if the initial ImR to the agent takes place in the skin. As yet, little research has been done in this area. Recently published reports indicate, however, that UV irradiation during a first cutaneous infection with two very different organisms, the parasite Leishmania sp. and Herpes simplex virus, may result in an impairment of the ImR of the host to subsequent infections (Giannini and De Fabo, 1987; Perna et al, 1990). In the case of leishmaniasis, this could lead to the development of the more lethal form of the disease, visceral leishmaniasis. There is also some very preliminary evidence that other systems, e.g., the ImR to malaria, may also be affected by UV-B irradiation (Taylor, 1988).

The effects of UV-B and solar radiation on the human immune system have not been studied in sufficient detail to allow estimation of dose-response relationships for these effects; in one case, in a study on UV-carcinogenesis in mice, the systemic effect induced by UV-B radiation was directly proportional to the UV-B dose given (van der Leun and Gruijl, 1988). It is known from animal studies that the doses of UV-B needed to induce immunosuppression are much lower than those required for carcinogenesis. This may mean that exposure to low doses of UVR, even doses that do not cause a sunburn, may decrease the ability of the human immune system to provide an effective defense against neoplastic skin cells or skin infections. In the quantitative projections of increasing skin cancer incidence, given in previous sections, such effects have been implicitly taken into account.


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