Trichloroethene and cis-1,2-dichloroethene concentration-dependent toxicity model simulates anaerobic dechlorination at high concentrations: I. batch-fed reactors

Authors

  • Andrew R. Sabalowsky,

    Corresponding author
    1. Center for Biofilm Engineering, 366 EPS Building, P.O. Box 173980, Montana State University, Bozeman, Montana 59717-3980; telephone: 406-994-2674; fax: 406-994-6098
    • Center for Biofilm Engineering, 366 EPS Building, P.O. Box 173980, Montana State University, Bozeman, Montana 59717-3980; telephone: 406-994-2674; fax: 406-994-6098.
    Search for more papers by this author
  • Lewis Semprini

    1. School of Chemical, Biological and Environmental Engineering, Oregon State University, Corvallis, Oregon
    Search for more papers by this author

Abstract

A model was developed to describe toxicity from high concentrations of chlorinated aliphatic hydrocarbons (CAHs) on reductively dechlorinating cultures under batch-growth conditions. A reductively dechlorinating anaerobic Evanite subculture (EV-cDCE) was fed trichloroethene (TCE) and excess electron donor to accumulate cis-1,2-dichloroethene (cDCE) in batch-fed reactors. A second Point Mugu (PM) culture was also studied in the cDCE accumulating batch-fed experiment, as well as in a time- and concentration-dependent cDCE exposure experiment. Both cultures accumulated cDCE to concentrations ranging from 9,000 to 12,000 µM before cDCE production from TCE ceased. Exposure to approximately 3,000 and 6,000 µM cDCE concentrations for 5 days during continuous TCE dechlorination exhibited greater loss in activity proportional to both time and concentration of exposure than simple endogenous decay. Various inhibition models were analyzed for the two cultures, including the previously proposed Haldane inhibition model and a maximum threshold inhibition model, but neither adequately fit all experimental observations. A concentration-dependent toxicity model is proposed, which simulated all the experimental observations well. The toxicity model incorporates CAH toxicity terms that directly increase the cell decay coefficient in proportion with CAH concentrations. We also consider previously proposed models relating toxicity to partitioning in the cell wall (KM/B), proportional to octanol–water partitioning (KOW) coefficients. A reanalysis of previously reported modeling of batch tests using the Haldane model of Yu and Semprini, could be fit equally well using the toxicity model presented here, combined with toxicity proportioned to cell wall partitioning. A companion paper extends the experimental analysis and our modeling approach to a completely mixed reactor and a fixed film reactor. Biotechnol. Bioeng. 2010;107: 529–539. © 2010 Wiley Periodicals, Inc.

Ancillary