A circular economy approach to drinking water treatment residue management in a catchment impacted by historic metal mines.

Drinking water treatment residues (DWTR) from mining areas which remove and contain potentially toxic elements (PTE) could still potentially be used as a soil amendment to restore contaminated sites in the same catchment, thus eliminating waste and reducing the chemical and physical mobility of the pollutants. To assess this restorative and regenerative approach to DWTR management, field and pot trials were established with soils from a historic Pb-Zn mine site in the North East of England, amended with either local DWTR or the nearest available municipal green waste compost (GWC). Soils from the mine site were found to have very low levels of nutrients and very high levels of PTE (Pb and Zn > 13, 000 mg/kg). The perennial grass species Phalaris arundinacea, known for many ecosystem service benefits including soil stabilization, was used throughout this study. The application of the BCR sequential extraction to soils amended with the DWTR in the pot trials found a significant decrease in the bioavailability of Pb and Cu (p < 0.05) after plant growth when compared with an unamended control. The field trial involved 648 pre-grown grass plants planted-out into mine soils amended with either DWTR, GWC or a mixture (MIX) of the two, all at rates of 25-30% w/w. Both amendments and the MIX had significant positive effects on biomass production compared to the unamended control in the following order GWC > MIX > DWTR (p < 0.05). Results of the elemental analysis of biomass from the field trial were generally ambiguous and did not reflect the decreased bioavailability noted in the pot trials using the BCR procedure. Pot trials, however, showed increases in plant growth and decreases in concentrations of Cr, Cu, Pb and Zn in above ground biomass following the application of both amendments. Further work should involve the testing of a mixture of DWTR and other soil amendments to enhance plant growth. The success of these trials should provide confidence for those working in drinking water treatment and catchment management to reuse the waste residues in a circular economy and a sustainable way that could improve water quality over time.

Clinical applications of urinary organic acids. Part I: Detoxification markers.

Modern instrumentation allows the measurement of organic acids in urine in their physiological concentration ranges. Eight of the compounds that are reported can serve as markers for specific toxicant exposure or detoxification challenges. Xylene exposure causes elevation of 2-methylhippurate, and orotic acid elevation reveals ammonia challenge that exceeds the capacity of the urea cycle. General hepatic detoxification stimulation by natural compounds, drugs, or xenobiotic compounds causes elevated levels of glucaric acid. Abnormalities of alpha-hydroxybutyrate, pyroglutamate, and sulfate can indicate up-regulated glutathione biosynthesis, impaired reformation of glutathione in the gamma-glutamyl cycle, and depleted total body glutathione status, respectively. Patterns of these compounds measured in a simple overnight urine specimen help to identify focal areas of clinical concern and monitor patient responses to detoxification interventions.

Clinical applications of urinary organic acids. Part 2. Dysbiosis markers.

Part 1 of this series focused on urinary organic acids as markers of detoxification; part 2 focuses on dysbiosis markers. Intestinal microbial growth is accompanied by the release of products of their metabolism that may be absorbed and excreted in urine. Several organic acids are known to be specific products of bacterial metabolic action on dietary polyphenols or unassimilated amino acids or carbohydrates. Associated gastrointestinal or neurological symptoms may result from irritation of the intestinal mucosa or systemic distribution of absorbed neurotoxic products. Detection of abnormally elevated levels of these products is a useful diagnostic tool for patients with gastrointestinal or toxicological symptoms. Test profiles of urinary organic acids associated with microbial overgrowth can include benzoate, hippurate, phenylacetate, phenylpropionate, cresol, hydroxybenzoate, hydroxyphenylacetate, hydroxyphenylpropionate and 3,4-dihydroxyphenylpropionate, indican, tricarballylate, D-lactate, and D-arabinitol. Effective treatments for the associated microbial overgrowths may be directed at reducing microbial populations, introducing favorable microbes, and restoring intestinal mucosal integrity.

Estrogen metabolism and the diet-cancer connection: rationale for assessing the ratio of urinary hydroxylated estrogen metabolites.

Estrogens are known for their proliferative effects on estrogen-sensitive tissues resulting in tumorigenesis. Results of experiments in multiple laboratories over the last 20 years have shown that a large part of the cancer-inducing effect of estrogen involves the formation of agonistic metabolites of estrogen, especially 16-alpha-hydroxyestrone. Other metabolites, such as 2-hydroxyestrone and 2-hydroxyestradiol, offer protection against the estrogen-agonist effects of 16-alpha-hydroxyestrone. An ELISA method for measuring 2- and 16-alpha-hydroxylated estrogen (OHE) metabolites in urine is available and the ratio of urinary 2-OHE/16-alpha-OHE (2/16-alpha ratio) is a useful biomarker for estrogen-related cancer risk. The CYP1A1 enzyme that catalyzes 2-hydroxyestrone (2-OHE1) formation is inducible by dietary modification and supplementation with the active components of cruciferous vegetables, indole-3-carbinol (I-3-C), or diindolylmethane (DIM). Other dietary components, especially omega-3 polyunsaturated fatty acids and lignans in foods like flax seed, also exert favorable effects on estrogen metabolism. Thus, there appear to be effective dietary means for reducing cancer risk by improving estrogen metabolism. This review presents the accumulated evidence to help clinicians evaluate the merit of using tests that measure estrogen metabolites and using interventions to modify estrogen metabolism.