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MTBE (methyl--butyl-ether) is the most important fuel additive to have been used in the USA and Germany within the last 20 years. In the last 3 years, California and some other American states have substituted MTBE by ethanol. In Germany MTBE was replaced by ETBE (ethyl--butyl-ether). Due to widespread MTBE use, spills from underground fuel tanks locally has caused intensive groundwater contamination, which is favoured by the tracer-like behaviour of the compound. In cases of remediation needs, MTBE is difficult to clean due to its physical-chemical-biological characteristics. The possible remediation technologies are classified and described. These technologies can be differentiated into “pump-and-treat measures” and “alternative technologies”. For groundwater cleaning applying pump-and-treat, several procedures can be chosen. However, in most cases stripping is used, which results in high costs for cleaning of the stripped air. Regarding alternative technologies, a lot of lessons have been learnt in optimizing the biological technologies over the last 5 years. Since MTBE-degrading bacteria at most sites have developed some years after the spill event, biostimulation by biobarrier techniques have a good chance of cleaning MTBE-contaminated groundwater by an in-situ method. In the case of successful remediation, large amounts of costs can be saved compared to pump-and-treat applications.

MTBE and other fuel oxygenates threaten the water sources for drinking water production. Due to their persistence in the environment, these substances pass through the subsoil unchanged and thus are not reliably retained by riverbank filtration. Conventional drinking water treatment technology—i.e., aeration and adsorption on activated carbon—are not able to remove them in a feasible manner. New adsorption materials show better performance but high costs and low availability prevent their use in drinking water production. Chemical oxidation by advanced oxidation technology (i.e., ozone/H2O2 or UV-induced advanced oxidation processes) is most likely able to eliminate MTBE and other ethers, however, only with high expenses. Nanofiltration might be an option since the retention by nanofiltration membranes is quite high. However, for the production of drinking water, the resulting water has to be further conditioned in order to meet drinking water standards. In this book chapter the treatment technologies currently available for water treatment are illuminated in detail on their potential for removing MTBE and other fuel oxygenates from water.

Metabolism and kinetic studies have shown that the overall elimination of ETBE and MTBE from blood in volunteers was multiphasic, (two or four phases in the case of ETBE and two or three phases for MTBE). The half-lives varied in different experiments and ranged from a few minutes for early phases up to a terminal half-life of 33 h in one experiment each with ETBE and MTBE. The kinetic data obtained from experiments with rats exposed to ETBE are restricted to a statement that the apparent half-life of elimination of ETBE from blood is about 0.8 h, but it is not clear if this only refers to an initial half-life. Some guidance may be possible from the known behaviour of MTBE. Its elimination from rat blood appears to be biphasic, with an initial half-life of less than 1 h and second half-lives ranging from 37 h to 92 h (reviewed in McGregor 2006). Elimination occurs in exhaled air (mainly unchanged ethers) and urine (metabolites). The main circulating metabolite is TBA formed by oxidation of ethers by cytochrome isoenzymes, while the main urinary metabolites are 2-hydroxyisobutyrate and 2-methyl-1,2-propanediol. The half-life of TBA in the blood of volunteers exposed to the ethers is about 8 to 12 h. Comparable measurements have not been made in rodents. Exposure of volunteers to the ethers at concentrations of up to 25 or 50 ppm (106 or 212 mg/m) for 2h produced a slight impairment (3.2 to 4.4%) in pulmonary function, but other measures and subjective reports show little effect of exposure. Non-human experimental studies have not revealed significant general toxicity, neurotoxicity, toxicity to reproduction or genotoxicity. Neither MTBE nor ETBE is acutely toxic following oral, dermal or inhalation administration or an eye irritant, while MTBE, but not ETBE is considered to be a skin irritant. Sensitisation has not been demonstrated with either compound in guinea-pig maximisation tests.

Other studies of systemic toxicity of MTBE and ETBE were largely restricted to a nephropathy in male rats that was associated with the accumulation of hyaline droplets that immunohistochemically stained for α-globulin. Apparently, the same type of nephropathy occurs in TBA-treated rats. In addition, MTBE exposure during a two-year study in rats led to exacerbation in males of the spontaneously occurring chronic progressive nephropathy (CPN), even to the most severe or “end-stage” in some cases. The effects of MTBE, ETBE and TBA on renal tubule cells are weak, specific to male rats, and not observed in mice of either sex. They are not necessarily due to metabolically generated TBA alone, although this metabolite, which is common to both ethers, does persist in the blood of rats at higher concentrations and for a longer time than the parent ethers. In vitro studies with MTBE demonstrated its specific binding to kidney proteins from male rats and that it interacts with α-globulin. Under the conditions of these experiments, metabolism of MTBE to TBA was not likely to be significant. It is reasonable to predict that similar experiments with ETBE would produce similar results. The available data on ETBE are not extensive, but they support the hypothesis that the mode of action is dependent on α-globulin nephropathy, which is widely considered to be of no human relevance. In CD-1 mice of both sexes there was a minimal renal nephropathy, but this occurred in all groups, including controls, at frequencies that varied between 27% and 64% with little indication of a dose-response relationship. It is unlikely to have been caused by ETBE treatment. The only other effect of note was treatment-associated bone marrow congestion in female rats exposed to 1750 ppm (7420 mg/m) ETBE for 3 months. There was no accompanying effect on the haematopoietic cell population, and an increase in mean corpuscular volume was not considered clinically relevant. No similar effect was reported for male rats or for mice of either sex.

With regard to carcinogenicity, low incidences of renal tubule cell adenomas were found in male rats treated with MTBE. This effect appears to be associated with exacerbation of CPN to end-stage as well as α2u-globulin nephropathy induction. Both conditions are male rat specific. TBA also induces adenomas of the renal tubule cells and this response is also associated with α2u-globulin nephropathy. Neither of the conditions predisposing to renal tubule cell neoplasia has human relevance. ETBE has not been tested for carcinogenicity, but results from short-term studies suggest that it would also induce kidney tumours by the same modes of action as MTBE.

Thyroid follicular cell adenomas were increased in female mice treated with TBA, but this result lacks any independent supporting evidence from a number of studies in mice and rats. There was no evidence for a hepatic effect of TBA within this mouse carcinogenicity study; therefore, no internal evidence exists for a hormonal mechanism of thyroid follicular cell induction. No thyroid neoplasms were increased in the carcinogenicity studies of MTBE.

The World Health Organization (WHO) Guidelines for drinking water quality are one of the most important sources of advice on the safety and acceptability of drinking water around the world. They are used as the basis for standards in a substantial part of the world and are respected for their independence and transparency. WHO bases its evaluations on international peer-reviewed evaluations where possible, but will also use peer-reviewed documents prepared by member states. In the case of methyl -butyl ether (MTBE), several such documents exist that provide the basis for an international consensus on the science surrounding water contamination by MTBE. The toxicology of MTBE indicates that while it induces tumours in rodents, there is doubt as to the significance to humans and the mechanism appears to be a high-dose, non-genotoxic phenomenon. MTBE can be detected in water by taste and odour at low concentrations. WHO considered that it was unnecessary to set a health-based guideline value, since any such value would be substantially above the concentration at which MTBE could be detected by taste and odour.