The aerobic bacterial catabolism of aromatic compounds involves a wide variety of peripheral pathways that activate structurally diverse substrates into a limited number of common intermediates that are further cleaved and processed by a few central pathways to the central metabolism of the cell [55]. Metabolic pathways and encoding genes responsible for the degradation of specific members of a highly diverse range of aromatic compounds have been characterized for many isolated bacterial strains, predominantly from the Proteobacteria and Actinobacteria phyla [56]. Degradation by such isolates is typically initiated by members of one of the three superfamilies: the Rieske non-heme iron oxygenases (RNHO), the flavoprotein monooxygenases (FPM) and the soluble diiron multicomponent monooxygenases (SDM). Further metabolism is achieved through di- or trihydroxylated aromatic intermediates. Alternatively, activation is mediated by CoA ligases where the formed CoA derivates are subjected to selective hydroxylation [58, 53]. In the case of hydrophobic pollutants, such as benzene, toluene, naphthalene, biphenyl or polycyclic aromatics, aerobic degradation is usually initiated by activation of the aromatic ring through oxygenation reactions catalyzed by RNHO enzymes or, as intensively described for toluene degradation, through members of SDM enzymes [56].