The influence of anaerobic conditions on aqueous-phase polycyclic aromatic hydrocarbon (PAH) bioavailability was investigated in laboratory microcosms. Highly aged (>70 years), PAH-contaminated soil was incubated under anaerobic conditions by using various anaerobic headspaces, anaerobic headspaces with an oxygen-scavenging complex (titanium(III) citrate) in the aqueous phase, or anaerobic headspaces with electron-acceptor amendments in the aqueous phase. Incubation of soil solely under anaerobic conditions resulted in increased aqueous concentrations of all PAHs tested (fluoranthene, pyrene, benz[a]anthracene, and benzo[a]pyrene). Benz[a]anthracene and benzo[a]pyrene extractable concentrations were above aqueous solubility, by as much as an order of magnitude for the latter. The degree of solubility increase observed was a function of molecular weight of the PAH regardless of initial soil concentration, suggesting formation of stable PAH-soluble organic matter associations. The soil samples incubated aerobically for 90 d before imposition of anaerobic conditions did not release PAHs to the aqueous phase. Methanogenic organisms and sulfate-reducing bacteria were seen to have the most significant effect on increases in aqueous-phase PAHs. Polycyclic aromatic hydrocarbons made more soluble under anaerobic conditions was available to be degraded or transformed under aerobic conditions.

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Human and B6C3F1 mouse liver tissue was exposed to trichloroethylene (TCE) to determine metabolic rate constants. Using a novel volatile exposure system based on precision-cut tissue explants, TCE biometabolism was measured by appearance of a major oxidative product trichloroacetic acid (TCA). TCE metabolic rate was linear in this system to 150 minutes, allowing calculation of Michaelis-Menten kinetic parameters, Km and Vmax. Both human and mouse liver explants tolerated exposure to TCE up to 750 microM without evidence of cytotoxicity. Km values for mouse and human tissue were 215 and 30.6 microM TCE, respectively, and Vmax estimates were 6.14 and 0.47 ng TCA produced per mg protein*min-1, mouse and human, respectively. These results are consistent with other reports in describing the greater capacity of mice to metabolize TCE. Metabolic differences such as these must be considered when interpreting the implications of TCE-induced toxicity in rodent models for human health assessment.

Trichloroethylene (TCE) was hypothesized to produce free radicals which could be detected using electron para magnetic resonance spectroscopy with the spin trap, PBN (α-phenyl tert-butyl nitrone). The free radicals detected following incubation of precision cut liver slices in media containing 10 mM PBN had hyperfine coupling constants aN=1.61 mT and aH=0.325 mT. There was a linear increase in free radicals detected in the bathing media when the headspace TCE concentration was increased from 2500- 10 000 p.p.m. The levels of conjugated dienes measured in the slices incubated in PBN supplemented media were less than slices exposed to TCE in incubation media without PBN. The PBN trap may act as a scavenger preventing the propagation of free radicals and inhibiting lipid peroxida tion. The experiments suggest that free radical formation by TCE leads to a concomitant increase in conjugated dienes in liver slices which may contribute to the pathological changes which occur in liver following TCE exposure.