Microbial oxidation, PAHs

Microbial oxidation of sediment-associated PAHs can be minimal. Herbes and Schwall (1978) found that for PAHs in contaminated freshwater sediments the turnover times (1/rate constant) increased while the rate constants and transformation rates (jig g hr" ) decreased with increasing number of aromatic rings (increasing hydrophobicity). For example, they determined the turnover times for naphthalene, benz[a]anthracene, and benzo[a]pyrene to be 7 hr, 400 d, and 3.3 yr, respectively. Furthermore, they reported that HPAHs in sediments that had been contaminated for years were resistant to microbial transformation, even with an assumed bacterial population that was capable of transforming LPAH compounds. In their study, benz[a]anthracene and benzo[a]pyrene were almost totally refractory to microbial oxidation. This pattern, in conjunction with higher solubility for LPAHs, may explain why many sediments are enriched with HPAHs. 

The mechanism of action for diesel fuels is not well characterized due to the complexity of its petroleum hydrocarbon mixture. The presence of additives that improve fuel combustion or prevent microbial growth may contribute to toxicity. Based on research conducted with individual components of diesel fuels, the primary mechanism of action for central nervous system (CNS) depression from diesel fuel is the reversible, physical interaction of the aromatic and aliphatic hydrocarbons with cell membranes. Renal toxicity is possibly attributed to oxidative metabolites of some of the aromatic constituents. Eye and skin injury are attributable to direct irritant action and the high lipid solubility that may dissolve protective skin oils and allow penetration into the skin tissue. The dermal carcinogenesis observed in rodents subjected to chronic dermal exposure to diesel may be attributed to the genotoxic activity of PAHs and the promoting activity of repeated dermal injury. 

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