Diffusion of TCE Through Soil-Bentonite Slurry Walls

Diffusion experiments performed using both a dissolved solution of trichloroethylene (TCE) and a pool of free phase TCE adjacent to a simulated soil-bentonite (SB) wall are described. These tests examine a multi-layer system that includes both contaminated sand and a SB barrier. Results obtained from experiments with dissolved TCE as the primary source are shown to be consistent with those obtained with free-phase TCE as the source of contaminant. Diffusion and sorption coefficients of a soil-bentonite slurry wall are reported to be 3.5 × 10^?10 m ² /s and 0 cm ³ /g, respectively. These diffusion and sorption coefficients were used to evaluate the effectiveness of a hypothetical SB slurry wall located adjacent to a TCE spill.     

Recovery of trichloroethylene removal efficiency through short-term toluene feeding in a biofilter enriched withPseudomonas putida F1

Trichloroethylene (TCE) is an environmental contaminant provoking genetic mutation and damages to liver and central nerve system even at low concentrations. A practical scheme is reported using toluene as a primary substrate to revitalize the biofilter column for an extended period of TCE degradation. The rate of trichloroethylene (TCE) degradation byPseudomonas putida F1 at 25°C decreased exponentially with time, without toluene feeding to a biofilter column (11 cm I.D.×95 cm height). The rate of decrease was 2.5 times faster at a TCE concentration of 970 μg/L compared to a TCE concentration of 110 μg/L. The TCE itself was not toxic to the cells, but the metabolic intermediates of the TCE degradation were apparently responsible for the decrease in the TCE degradation rate. A short-term (2 h) supply of toluene (2,200 μg/L) at an empty bed residence time (EBRT) of 6.4 min recovered the relative column activity by 43% when the TCE removal efficiency at the time of toluene feeding was 58%. The recovery of the TCE removal efficiency increased at higher incoming toluene concentrations and longer toluene supply durations according to the Monod type of kinetic expression. A longer duration (1.4∼2.4 times) of toluene supply increased the recovery of the TCE removal efficieny by 20% for the same toluene load.     

A Review of the Epidemiology of Trichloroethylene and Kidney Cancer

The occupational epidemiological studies of trichloroethylene (TCE) exposure and kidney cancer are reviewed. Seven occupational cohort studies, conducted in the U.S., Finland, and Sweden involving over 130,000 workers, do not report statistically increased risks of kidney cancer among TCE-exposed workers. These studies were based on well-defined cohorts and exposure assessments involving urine biomonitoring or some type of job exposure matrix. In contrast, two German studies reported eight- to eleven-fold increased risks for renal cancer among TCE-exposed workers. However, numerous methodological and analytical shortcomings severely limit any interpretation of the German studies. We conclude that the more reliable epidemiologic data do not support a causal relationship between kidney cancer and TCE exposure.     

Trichloroethylene: Using New Information To Improve the Cancer Characterization

The views expressed in this paper are those of the authors and do not necessarily reflect the views or policies of the U.S. Environmental Protection Agency. Assessments of TCE's potential to cause cancer in humans have had to address issues concerning the strength of the human evidence and the relevance of the animal tumors to humans. The epidemiological database now includes analyses of multiple studies and molecular information. A recent analysis strongly suggests that TCE may induce cancer in humans at multiple sites, including kidney, liver, and lympho-hematopoietic cancer. Molecular analyses have found mutations of the von Hippel-Lindau tumor suppressor gene in renal tumors of TCE-exposed individuals. The animal bioassays have been followed up with mechanistic studies that provide insight into TCE's possible modes of action at each tumor site. This information suggests that TCE may act through mechanisms that can be relevant to human cancers. The mechanistic information can also be used to identify risk factors that may make some people more susceptible to TCE's adverse effects, allowing a fuller characterization of TCE's cancer potential in different groups of people.