Photoactivation Toxicity

A number of studies over the last 20 years have demonstrated increased toxicity of PAHs when they are exposed to ultraviolet (UV) light. Some PAHs are known to absorb UV light, which alters the reactivity of the PAH and can render it more toxic. One of the main determinants of photoactivation is the HOMO-LUMO gap (highest occupied and lowest unoccupied molecular orbitals). PAHs that possess a gap in the range of 6.8-7.6 eV are known to be activated by UV light. Anthracene, ben-z[a]anthracene, fluoranthene, and benzo[£]fluoranthene are susceptible to UV activation, whereas this has not been observed for chrysene or dimethylphenanthrene. One critical feature of PAH phototoxicity is that these compounds must be bioaccumulated and retained in the tissue for photoactivation toxicity to occur. For many species, this does not occur, implying that photoactivation is only a minor concern. Few detailed studies have been conducted on those species that are known to bioaccu-mulate PAHs and are exposed to relatively high levels of UV radiation. The results from these and future studies become increasingly important as the protective ozone layer breaks down, allowing higher levels of UV radiation to reach the biosphere.

The environmental relevance of phototoxicity has been addressed recently. Some authors acknowledge the laboratory studies and mechanistic explanation for PAH phototoxicity; however, they conclude that several factors in the environment will protect species from the expected increase in tissue damage. They also point out that very few, if any, field studies have demonstrated adverse effects. Because UV light attenuates rapidly in water and soil, the most logical place to look for adverse effects would be in species that live aboveground or in shallow pools.

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