Objective: Unreclaimed mine tailings sites are a worldwide problem, with thousands of unvegetated, exposed tailings piles presenting a source of contamination for nearby communities. Tailings disposal sites in arid and semiarid environments are especially subject to eolian dispersion and water erosion. Phytostabilization, the use of plants for in situ stabilization of tailings and metal contaminants, is a feasible alternative to costly remediation practices. In this review we emphasize considerations for phytostabilization of mine tailings in arid and semiarid environments, as well as issues impeding its long-term success. Data sources: We reviewed literature addressing mine closures and revegetation of mine tailings, along with publications evaluating plant ecology, microbial ecology, and soil properties of mine tailings. Data extraction: Data were extracted from peer-reviewed articles and books identified in Web of Science and Agricola databases, and publications available through the U.S. Department of Agriculture, U.S. Environmental Protection Agency, and the United Nations Environment Programme. Data synthesis: Harsh climatic conditions in arid and semiarid environments along with the innate properties of mine tailings require specific considerations. Plants suitable for phytostabilization must be native, be drought-, salt-, and metal-tolerant, and should limit shoot metal accumulation. Factors for evaluating metal accumulation and toxicity issues are presented. Also reviewed are aspects of implementing phytostabilization, including plant growth stage, amendments, irrigation, and evaluation. Conclusions: Phytostabilization of mine tailings is a promising remedial technology but requires further research to identify factors affecting its long-term success by expanding knowledge of suitable plant species and mine tailings chemistry in ongoing field trials.

The Amish and Hutterites are U.S. agricultural populations whose lifestyles are remarkably similar in many respects but whose farming practices, in particular, are distinct; the former follow traditional farming practices whereas the latter use industrialized farming practices. The populations also show striking disparities in the prevalence of asthma, and little is known about the immune responses underlying these disparities. We studied environmental exposures, genetic ancestry, and immune profiles among 60 Amish and Hutterite children, measuring levels of allergens and endotoxins and assessing the microbiome composition of indoor dust samples. Whole blood was collected to measure serum IgE levels, cytokine responses, and gene expression, and peripheral-blood leukocytes were phenotyped with flow cytometry. The effects of dust extracts obtained from Amish and Hutterite homes on immune and airway responses were assessed in a murine model of experimental allergic asthma. Despite the similar genetic ancestries and lifestyles of Amish and Hutterite children, the prevalence of asthma and allergic sensitization was 4 and 6 times as low in the Amish, whereas median endotoxin levels in Amish house dust was 6.8 times as high. Differences in microbial composition were also observed in dust samples from Amish and Hutterite homes. Profound differences in the proportions, phenotypes, and functions of innate immune cells were also found between the two groups of children. In a mouse model of experimental allergic asthma, the intranasal instillation of dust extracts from Amish but not Hutterite homes significantly inhibited airway hyperreactivity and eosinophilia. These protective effects were abrogated in mice that were deficient in MyD88 and Trif, molecules that are critical in innate immune signaling. The results of our studies in humans and mice indicate that the Amish environment provides protection against asthma by engaging and shaping the innate immune response. (Funded by the National Institutes of Health and others.)

Little is known about the interaction of biosurfactants with bacterial cells. Recent work in the area of biodegradation suggests that there are two mechanisms by which biosurfactants enhance the biodegradation of slightly soluble organic compounds. First, biosurfactants can solubilize hydrophobic compounds within micelle structures, effectively increasing the apparent aqueous solubility of the organic compound and its availability for uptake by a cell. Second, biosurfactants can cause the cell surface to become more hydrophobic, thereby increasing the association of the cell with the slightly soluble substrate. Since the second mechanism requires very low levels of added biosurfactant, it is the more intriguing of the two mechanisms from the perspective of enhancing the biodegradation process. This is because, in practical terms, addition of low levels of biosurfactants will be more cost-effective for bioremediation. To successfully optimize the use of biosurfactants in the bioremediation process, their effect on cell surfaces must be understood. We report here that rhamnolipid biosurfactant causes the cell surface of Pseudomonas spp. to become hydrophobic through release of lipopolysaccharide (LPS). In this study, two Pseudomonas aeruginosa strains were grown on glucose and hexadecane to investigate the chemical and structural changes that occur in the presence of a rhamnolipid biosurfactant. Results showed that rhamnolipids caused an overall loss in cellular fatty acid content. Loss of fatty acids was due to release of LPS from the outer membrane, as demonstrated by 2-keto-3-deoxyoctonic acid and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis and further confirmed by scanning electron microscopy. The amount of LPS loss was found to be dependent on rhamnolipid concentration, but significant loss occurred even at concentrations less than the critical micelle concentration. We conclude that rhamnolipid-induced LPS release is the probable mechanism of enhanced cell surface hydrophobicity.