Although humans use about 8% of the primary productivity of the oceans, that fraction increases to more than 25% for upwelling areas and to 35% for temperate continental shelf systems (Vitousek et al., 1997). For about one-sixth of the world's population (primarily developing nations), the oceans provide more than one-third of their animal protein (FAO, 1995). Many of the fisheries that depend upon the oceanic primary productivity are unsustainable. Although the primary causes for a decline in fish populations are predation and poor food supply for larvae, overfishing of adults, water temperature, pollution and disease (Holmes, 1994; Rothchild, 1996), exposure to increased UV-B radiation may contribute to that decline. The eggs and larvae of many fish are sensitive to UV-B exposure (Hunter et al., 1982; Little and Fabacher, 1994; Kouwenberg et al., in press b). However, imprecisely defined habitat characteristics and the unknown effect of small increases in UV-B exposure on the naturally high mortality rates of fish larvae are major barriers to a more accurate assessment of ozone depletion on marine fish populations.Actual in-lake experiments have demonstrated that ambient UV levels in the surface waters of temperate lakes are adequate to induce 100% mortality of yellow perch eggs in low DOC lakes but not in lakes with higher DOC levels (Williamson et al., 1997).
Amphibian populations are in serious decline in many areas of the world (Wake, 1991), and scientists are seeking explanations for this phenomenon (Hays et al., 1996; Blaustein and Kiesecker, 1997). Worrest and Kimeldorf (1976) noted several adverse effects of increased exposure to UV-B radiation on the systemic development of boreal toad (Bufo boreas boreas) tadpoles in the laboratory. They questioned whether an increased exposure to UV-B radiation in nature could have an adverse impact on amphibian development. Vetter and colleagues (submitted), using a newly developed chemiluminescent immunoblot assay capable of measuring thymine-thymine pyrimidine dimers (TT dimers) in DNA, have investigated DNA damage and repair in pelagic fish eggs and larvae. Since the typical method of thymine dimer repair is photoenzymatic repair, the observed amount of DNA damage at any time of day is the net result of damage rates and repair rates. They find that over a day the typical diel pattern of DNA damage, at least for northern anchovy, resembles a dose-rate meter rather than a cumulative dose meter, i.e. DNA damage increases as the sun rises, reaches a peak level of damage near solar noon, and is followed by a period of rapid repair in the afternoon when UV-B is decreasing but the visible light utilized for repair is still abundant. An understanding of this diel cycle of damage and repair is essential for the correct interpretation of relationships between solar irradiance and levels of DNA damage in field samples.
As reported by several authors (Blaustein et al., 1997; Licht and Grant, 1997; Ovaska et al., 1997; Corn, 1998; Ankley et al., in press), field studies in which amphibian embryos were exposed to natural sunlight or to sunlight with UV-B radiation removed have shown conflicting results. Some studies resulted in increased embryonic mortality after UV-B exposure; whereas others show that current levels of UV-B radiation are not detrimental. Abiotic factors, such as water depth, water color, and dissolved organic content at the egg-laying sites, effectively reduce UV-B penetration through the water and reduce exposure to UV-B radiation at all life history stages. Biotic factors, such as jelly capsules around eggs, melanin pigmentation of eggs, and color of larvae and metamorphosed forms, further reduce the effectiveness of UV-B penetration.
Most amphibian population declines
are probably due to habitat destruction or habitat alteration. Some declines
are probably the result of natural population fluctuations. Other explanations
for the population declines and reductions in range include disease, pollution,
atmospheric changes and introduced competitors and predators. UV-B radiation
is one agent that may act in conjunction with other stresses to adversely
affect amphibian populations.