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Farmers Warn of Worldwide Water Loss and Deadly UV Radiation?


Ultraviolet radiation was surveyed in a mixed deciduous forest in Maryland, USA, using a Robertson-Berger meter. A smaller number of comparable measurements were made in closed-canopy forests in Chile, Panama, and Washington State, USA, and under two canopies recently disturbed by hurricanes, in Virginia, USA, and Mexico. Simultaneous measurements of photosynthetically active radiation were also made. As sunlight and radiation nearest the forest floor was generally low compared to hi UV radiation incidents on the outer canopy, and had a positively skewed frequency distribution. Under closed canopies, mean UV-B transmittance was only 2% of incident radiation; under disturbed canopies, between 8-17%. In Maryland, mean UV-B transmittance increased to 30% during the leafless season.


Gaps received larger UV-B exposures over time than shaded locations. Thus UV-B transmittance depends strongly on canopy structure. UV-B transmittance did not, however, have a detectable dependence on solar elevation or time of day and heat from the sun. The vertical extinction of UV-B through a closed canopy was rapid: in Maryland, about 40-70% of incident UV-B was absorbed by the top 25% of the canopy. The space and time variation in UV-B within the canopy were qualitatively similar. However, UV-B varied less dramatically than PAR, and the two wavebands also had different patterns of variation in canopy space.


These differences were probably due to the greater diffuse component meaning, levels of shade. In Panama and the two disturbed sites, UV-B transmittance was significantly greater than PAR transmittance; in the other sites no significant differences were found. These results were combined with a published model of the atmospheric transmission of UV-B to estimate present and future UV-B exposures in the Maryland forest, factoring the current rate of decline in the stratospheric ozone. The greatest increases in UV-B exposure should come in the summertime in the upper canopy, and in the spring in the lower canopy. UV radiation has been recognized as a direct driver of litter decomposition by photodegrading organic matter in dryland ecosystems. This is basically fuel for forest fires on the forest floor couple that with the drying of the inner core of branches and you have a recipe for extreme forest fires.


Plants are highly sensitive to UV-B radiation because of their sessile nature. In plants, UV-B radiation damages cell membranes and all organelles within the cell, including the chloroplasts, mitochondria, and deoxyribonucleic acid (DNA) within the nucleus. Damage to these cell organelles directly or indirectly affects basic plant metabolic processes, such as photosynthesis, respiration, growth, and reproduction. Consequently, UV-B damage harms forests and crops. However, the effect of UV-B radiation varies with intensity and duration of irradiation and stage of plant development. In addition, sensitivity to UV-B radiation varies widely among plant species and cultivars of the same species. Studies like this on physical or physiological reasons for differences in tolerance to UV-B radiation among species need further attention.


The impact of elevated UV-B radiation on plant species is well understood, but knowledge of the effects of UV-B on insect pests and disease-causing pathogens (fungi and bacteria) is limited. Research conducted thus far has shown both a decrease and an increase in disease and pest damage in response to increased UV-B radiation. Effects of UV-B on diseases and insects could be attributed to direct effects on their growth and indirect effects through changes in tissue characteristics and/or composition. Caldwell et al. (2003) summarized the literature and concluded that higher levels of UV-B radiation generally led to less herbivore and/or reduced insect growth compared with lower levels of UV-B. The magnitude of the effects was sizable, with potential ecosystem-level consequences for species composition, organic matter decomposition, and nutrient cycling. Solar UV-B can affect insect herbivores through reduced growth, survivorship, and fecundity (Lindroth et al., 2000) through changes in leaf characteristics (appearance and composition). Insects can perceive UV-B (Mazza et al., 2002), modify their behavior to avoid UV-B radiation, and protect themselves by regulating their cuticular pigmentation to screen damaging wavelengths (Gunn, 1998). Studies demonstrated that thrips consumed less leaf tissue and Lepidopeteran larvae had lower survivorship in laboratory assay when fed on leaves grown under near-ambient solar UV-B compared with leaves from UV-B excluded plots (Mazza et al., 1999; Zavala et al., 2001). The lower larvae survival was attributed to higher levels of soluble phenolics and lower lignin content in the foliage exposed to UV-B radiation. Similarly, bioassay studies suggested that adult specimens of leaf beetles tend to preferentially feed on plants not exposed to UV-B if given the opportunity to choose between UV-B exposed and unexposed plant materials (Ballare et al., 1996). However, the impact of UV-B radiation on mechanisms of other behavior of adult insects, such as oviposition and breeding, that are more relevant under natural conditions are not well understood and need investigation.


Ultraviolet-B radiation changes the chemistry, morphology, and physiology of plants. This can directly influence pest and disease incidence. For example, UV-B can affect leaf nitrogen content, available carbohydrate, and fiber (Zavala et al., 2001) indirectly influencing insect growth and survival. Plants exposed to UV-B can also stimulate production of secondary metabolites, i.e., phenolics and jasmonic acid (Mazza et al., 2000; Izaguirre et al., 2003; Izaguirre et al., 2007) which can influence insect incidence or behavior by acting as either a deterrent or attractant (Harborne, 1988). Some insects protect themselves from UV-B radiation by feeding on the underside of the leaves where UV-B penetration is lower (Paul et al., 1997) and avoiding areas of plants where defensive chemicals accumulate (McCloud et al., 1992).




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