Atmospheric scientists were stunned in 1985 when a British Meteorological Survey team reported that concentrations of ozone over Antarctica had dropped by more than 40% during the early spring in the years between 1977 and 1984 from 1960 baseline levels.1 Although it has been understood that gases liberated from commercial processes could reduce the stratospheric ozone layer, which forms a shield protecting all living things from the damaging effects of the ultraviolet (UV) radiations from the sun, there was no suspicion that the effect would be so drastic or occur so soon. It was thought the effect would be distributed rather evenly throughout the stratosphere, and that perhaps in 100 years this might result in a worrisome thinning of the protective shield. The discovery of the ozone hole was the first definitive evidence that human activities are changing the global environment, and this totally unsuspected finding attests to the limits of our present understanding of global environmental changes. In the early spring of 1987 and 1989, other research teams found that the ozone over Antarctica had dropped to only 50% of the 1979 levels and had become larger in area than the Antarctic Continent itself---about twice the size of the United States.2, 3 In March 1988, a definite (but lesser) thinning of the ozone layer over the North Pole was also noted.4, 5 And satellite measurements during the first three months of 1993 of the ozone layer over the heavily populated mid latitudes of the Northern Hemisphere have demonstrated record low levels. 24
In the very cold, rarefied atmosphere of the stratosphere, some 20-50 kilometers above the surface, a molecule of oxygen (O2) is split by solar ultraviolet radiation into two reactive oxygen units:
O2 ---> O + O.
If one of these oxygen atoms encounters a molecule of O2 they may combine to form an ozone molecule:
O + O2 ---> O3.
It is this thin layer of ozone above us that absorbs incident ultraviolet radiation, protecting animal and plant life on earth from its toxic effects.
Ultraviolet radiation is the portion of the electromagnetic spectrum from 200 to 400 nanometers. This region is further divided arbitrarily into subregions termed UV-A, UV-B, and UV-C. The last includes wavelengths of 200-290 nm and is most destructive to life; fortunately, it is effectively blocked from reaching the earth's surface by the atmosphere. UV-B includes solar radiations from 290 to 320 nm; it is many times more effective in inducing erythema than UV-A, which is 320-400 nm in wavelength. DNA and aromatic amino acids absorb UV-C maximally, UV-B significantly, and UV-A minimally. The pathologic consequences of UV radiations seem chiefly attributable to their absorption by and disruption of DNA and proteins. The damaging effects of UV-B exposure are cumulative and are not dependent on the rate of exposure; a dose fractionated over several days can be as deleterious as the same does delivered all at once.
Chlorofluorocarbons (which are used in aerosols, refrigerants, and other industrial products) are remarkably inert and nonreactive. Indeed, it is because of these characteristics---specifically because they are nontoxic and nonflammable---that they were invented. But when they eventually rise into the stratosphere, they are decomposed by solar ultraviolet radiations into free chlorine atoms:
chlorofluorocarbon ---> Cl,
Cl + O3 ---> ClO + O2,
ClO + O ---> Cl + O2.
The chlorine atoms are recycled in these reactions, and are then free to attack other ozone molecules. A single chlorine atom, released by the action of UV radiation on chlorofluorocarbons, is capable of destroying catalytically tens of thousands of ozone molecules during its residence in the stratosphere.
The release of chlorofluorocarbons into the atmosphere has increased dramatically in the last 30 years. Tropospheric levels of two of the most widely used CFCs, CFC-11 and CFC-12, have tripled or more during this period. Public and governmental concerns about CFCs led to the Montreal Protocol of 1987, which in turn led to the Helsinki Meeting in late 1988, at which it was proposed that chlorofluorocarbons and other ozone-depleting chemicals, such as methyl chloroform, be completely phased out by the end of 1999. Some countries have proceeded to ban all production of chloroflurocarbons even before this date. However, because of their long atmospheric lifetimes, it will be at least 100 years before the effects on the ozone layer of the chlorofluorocarbons that have already been liberated into the atmosphere disappear, even after all further production and use of chlorofluorocarbons is stopped. The reduction in ozone concentration over Halley Bay in Antarctica and its relation to the increasing levels of two chlorofluorocarbons (CFC-11 and CFC-12) are shown in figure 1.
There are now reasons to expect that positive feedback will amplify the ozone-destroying action of stratospheric chlorine. The seasonal and regional occurrence of ozone depletion are dependent chiefly on the catalytic photochemical reactions on the surfaces of microcrystals of ice in the very frigid temperatures of the stratosphere above the polar regions, when the first solar radiations return to the poles after the long polar winters. This is why the nadir in ozone concentrations occur in October over Antarctica and in March over the Arctic.
The eruption of Mount Pinatubo in June 1991 spewed 15,000-30,000 tons of sulfur dioxide (SO2) into the stratosphere.7 This was converted in about a month to sulfuric acid (HlSO4), which in the stratosphere condenses into small particles called aerosols that are expected to remain in the atmosphere for 1-3 years. The atmospheric aerosol load was increased thereby some 10-100 times over that produced by biological and human sources. The aerosol particles, like the microcrystals of ice, provide surfaces in the lower stratosphere on which the catalytic photochemical reactions that destroy the ozone can occur. Figure 2 shows the results of computer modeling of stratospheric ozone reductions as they vary by season and by latitude.
Atmospheric scientists are monitoring these processes and measuring the increased incidence of UV-B reaching the earth's surface under the ozone holes. The World Meteorological Organization recently reported ozone levels over northern Europe, Russia, and Canada during the winter and spring of 1992 to have been 12% below the seasonal average--"an occurrence never before observed in more than 35 years of continuous ozone observations."8 Thus, the depletion of the stratospheric protective ozone shield, first noted over Antarctica less than 10 years ago, has now spread over the northern hemisphere as well---in fact, over the entire globe. The depletion remains most severe over Antarctica, where the human population is small; however, the oceans there are rich in phytoplankton, which are the beginning of the food chain for all aquatic creatures. UV-B can penetrate several meters into the surface of the oceans, where the phytoplankton obtain the sunlight that is essential for photosynthesis. Phytoplankton are highly vulnerable to damage by UV-B, 9, 10 so the potential for ecologic disaster is considerable.
The thinning of the stratospheric ozone shield and the resulting increase in UV-B radiation reaching the earth are expected to have direct health effects on humans. Exposure to the ultraviolet radiations in sunlight plays a major role in the premature appearance of aging of the skin. Dryness and wrinkles in the skin are brought on by solar exposure, and the preoccupation with acquiring a tan increases this cosmetic effect of sunlight.
The incidence of all kinds of skin cancer, which constitute the commonest form of cancer among white populations, will increase with more exposure to ultraviolet-B. 11 Skin cancer has been divided into two forms: nonmelanoma skin cancer, which affects the principal cell type of the skin (the keratinocyte), and cutaneous melanoma, which affects the pigment-producing cell (the melanocyte). Nonmelanoma skin cancers are of two kinds: basal-cell and squamous-cell carcinoma. Melanoma is the most dangerous form of skin cancer; it is estimated that in any year about 25% of the Americans who develop melanoma die from it. Basal-cell and squamous-cell cancers are much less dangerous, with a combined mortality of less than 1% (most of it due to squamous-cell carcinoma).
The incidence of melanomas has already been increasing in the United States; between 1982 and 1989 it rose by 83%. Unlike basal-cell and squamous-cell carcinomas, which seem to increase in proportion to total exposure to ultraviolet radiation, melanoma appears to be associated with an acute exposure such as a severe sunburn, which may serve as the initiating stress. Years or decades later, some other stress may serve to start the melanoma. Whether the second stress is also exposure to solar radiation is not known. The extent to which public education will offset this increase, by encouraging the wearing of hats and other protective clothing and the use of sunscreen lotions, is unpredictable. The U.S. Environmental Protection Agency estimates that if ozone depletion is allowed to continue until there is 40% depletion (estimated to occur in 2075), the increase in biologically active UV would result in an additional 154 million cases of skin cancer and an additional 3.4 million deaths. 11, 12 (This estimate was for individuals alive at the beginning of the assessment and born before 2075.)
Basal-cell cancers of the skin are very common today among fair-skinned individuals who imprudently expose themselves to excessive sunlight. These cancers do not metastasize to distant parts of the body or to internal organs, as do melanomas; they enlarge slowly and are cosmetically unsightly. Squamous-cell cancers are uncommon. They grow faster than basal-cell tumors and have the potential for metastasis. Individuals with dark skins are resistant to these solar-initiated cancers, and blacks are essentially immune. The dark melanin pigment in their chromophore cells within the skin absorbs the incident ultraviolet light, thus protecting the underlying skin cells from irradiation.
Cataracts may be a more widespread health effect of ultraviolet-B radiation than skin cancers, because all populations will be affected. A cataract occurs when the normally translucent lens of the eye becomes cloudy and scatters light so that vision is impaired. Cataracts account for half of the blindness in the world, 13 amounting to some 20 million cases. About 25 million cataract operations are performed annually in the United States, where cataracts currently represent the third-largest cause of preventable blindness.
Exactly how the ordered crystalline proteins of the lens become denatured, causing a cataract, is still uncertain. The lens proteins contain amino acids, such as tryptophane, which are susceptible to photo-oxidation by oxygen free radicals generated by UV-B. It is believed that the oxidized lens proteins become structurally altered.
Studies of fishermen and others engaged in gathering seafoods in Chesapeake Bay, who were exposed not only to direct solar radiation but also to its reflection from the ocean surface, showed a higher incidence of cataracts than did a control group who worked entirely indoors. Interestingly, wearing glasses or sunglasses is sufficient to block much of the ultraviolet radiation that causes cataracts. Plastic lenses, whether tinted or clear, reduce ocular exposure by more than 90%. Glass lenses afford only about 80% protection. Hats as well as protective eyewear provide major protection. Hugh R. Taylor and associates reported that people who worked indoors have a typical exposure of 4 units (Maryland Sun Years). 14 The typical waterman who worked outside without any ocular protection had an ocular exposure 18 times higher (72 units). If he wore a hat, his ocular exposure was cut almost in half to 47 units. If he wore glasses, it was cut to 17 units. Both a hat and glasses reduced his ocular exposure to only 8 units, only twice that of someone who was spending essentially all day inside. Furthermore, logistic regression analysis controlling for age showed a strong correlation between cumulative UV-B exposure and cataract. This analysis indicated that a doubling of UV-B exposure will increase the risk of developing cataracts by 60%. Conversely, if the ocular exposure to UV-B is halved, the risk is reduced by 40%. Those in the top quartile of annual ocular exposure had more than 3 times the risk of developing cortical cataract of those in the bottom quartile. There was no indication of any safe exposure or threshold for UV-B exposure, or of any safe period for exposure.
Epidemiologic studies have indicated that a diet rich in natural anti-oxidants. including vitamins C and E and beta carotene, reduces the incidence of cataracts. 15 This would support the hypothesis that oxygen free radicals play a causative role in cataract formation. To a considerable extent, the loss of vision due to cataract is correctable today, with surgery and the implantation of prosthetic lenses. But such operations are available to only a small percentage of those affected, particularly in the developing world.
Photokeratitis, or snowblindness, is another adverse effect of UV-B on the eye. Photokeratitis---literally sunburn of the cornea---results largely from UV-B exposure. 16 After undue exposure to bright sunlight, the afflicted individual develops red, inflamed, irritable, sore eyes. Photokeratitis clearly occurs with current UV-B levels, especially over bright snowy surfaces. It seems that we are very close to the threshold level for photo-keratitis during the summer months, especially at the beach. It is not known what level of depletion of stratospheric ozone and accompanying increase in ambient UV-B can be tolerated before photokeratitis becomes a much more widespread and common problem.
The effects of ultraviolet-B radiation on the skin, in addition to cancer formation, have been studied intensively in recent years. It is now recognized to have an important effect on the immune system. 17
There are two major arms to the body's defense against foreign antigens: a humoral and a cellular defense. The humoral immune system produces antibodies (immunoglobulins) that can react very specifically with and neutralize the harmful effects of foreign molecules that gain access into our bodies. The humoral immune system appears, however, to be unaffected by ultraviolet radiation. By contrast, the cellular immune system, which recognizes a cancer cell or a parasitic cell and mounts an immune attack, ultimately resulting in the killing and phagocytosis of the offensive foreign invader, is sensitive to ultraviolet radiation. The central player in the cellular immune system is the T-lymphocyte. Exposure to sunlight alters subsets of T-cells and induces suppressor T-cell activity in normal subjects. 18
As described above, ultraviolet radiation can cause the development of malignant skin tumors. In experimental animals it has been shown that cancer formation requires uniformly large doses of irradiation. When such tumors, induced by ultraviolet irradiation, are transplanted into normal genetically identical recipient animals, however, they are unable to grow. If the recipient animal is first exposed to a much smaller dose of ultraviolet radiation than that required to induce a skin tumor, the transplanted tumor is then not rejected. This clearly indicates that somehow the small exposure of the recipient animal to ultraviolet radiation has depressed the animal's immune system so that it will tolerate the growth of the cancer implant. Furthermore, this depression of the recipient animal's immune system must be a systemic effect, since the cancer implant will grow in the recipient even if transplanted to a site distant from that which was exposed to the ultraviolet radiation. Ultraviolet radiations are known to penetrate only the outermost layer of the skin.
All the details of how exposure to ultraviolet radiation may suppress the cellular immune responses are not yet elucidated. It is known that there are several cells of the immune system that are transiently resident in the skin but arise from tissues elsewhere. These include, beside the lymphocytes, macrophages and Langerhans cells that originate in the bone marrow. Both the Langerhans cells and the dermal macrophages are antigen-presenting cells, but they also secrete several chemical messengers that regulate other immune cells. Exposing normal skin to low doses of ultraviolet radiations results in a loss of recognizable Langerhans cells at the site of the ultraviolet exposure. Thus local suppression of cellular immunity can be explained.
The systemic suppression of the immune system appears to result chiefly from the altered production of chemical messengers arising from the effects of UV-B on the several important cells of the immune system that reside in the skin. These potent messenger molecules modulate the responses of the immune system throughout the body, and in consequence of exposure to UV-B they suppress the cellular immune responses. 19
Under conditions expected to prevail with global environmental changes, this suppression of the immune system acquires special significance. Since UV-B exposure can initiate skin cancers as described, a deficient cellular immune response to the presence of the cancer cells can only result in their more rapid proliferation and spread. More importantly, however, will be the impaired response of exposed individuals to infections, increasing the incidence of infections and making them more lethal. With the crowding due to population increases and to the displacement of people from submerged coastal and drought-stricken areas (secondary to global warming), with the mixing of immune and non-immune populations, with the possible spread of vector-borne diseases into new territories, with the contamination of water supplies, and with the increased prevalence of malnutrition and poverty, most kinds of infectious diseases will likely be increased. For people to have their immune systems suppressed under such conditions can only greatly aggravate the serious problems that will be posed by infectious diseases.
Closer to the ground, ozone, a major component of smog, is produced through chemical reactions involving hydrocarbons and nitrogen oxide emissions from automobiles and industrial processes. With reduction in the stratospheric ozone shield, more UV-B will penetrate down into the troposphere, where it will produce ozone from molecular oxygen just as it does in the stratosphere. It has been shown in laboratory animals and in humans that ozone is a respiratory irritant 20 that affects lung function in a manner similar to cigarette smoke, causing constriction of the small bronchial airways and a reduction in lung capacity. This causes increased predilection to respiratory infections, emphysema, and chronic pulmonary insufficiency.
Ozone plays two contrasting roles in the expected global environmental changes. In the stratosphere it provides a shield against harmful UV-B radiations, while in the troposphere it acts as a greenhouse gas and as a health hazard. So we are losing the ozone where it is beneficial and gaining it where it is deleterious to human health.
Of all the health effects of the anticipated global environmental changes, food shortages are likely to be the most devastating. UV-B radiations are toxic to most plants and will adversely affect agricultural productivity. As mentioned, phytoplankton, which are abundant in the cold polar oceans, are impaired by ultraviolet radiation. Since the phytoplankton form the beginning of the food chain on which all marine species depend, the possibility of ecologic catastrophe looms. Tropospheric ozone, an indirect result of depletion of stratospheric ozone, is also toxic to most plants. Levels of ozone over the eastern United States during summers are already high enough to cause damage to crops and vegetation. These effects of UV-B on agriculture will only add to the many other factors that will compromise food supplies for the world's burgeoning population, especially in the developing countries which already are faced with marginal supplies. 13
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