Recommendations for the advancement of oil-in-water media and source oil characterization in aquatic toxicity test studies

During toxicity testing, chemical analyses of oil and exposure media samples are needed to allow comparison of results between different tests as well as to assist with identification of the drivers and mechanisms for the toxic effects observed. However, to maximize the ability to compare results between different laboratories and biota, it has long been recognized that guidelines for standard protocols were needed. In 2005, the Chemical Response to Oil Spills: Ecological Effects Research Forum (CROSERF) protocol was developed with existing common analytical methods that described a standard method for reproducible preparation of exposure media as well as recommended specific analytical methods and analyte lists for comparative toxicity testing. At the time, the primary purpose for the data collected was to inform oil spill response and contingency planning. Since then, with improvements in both analytical equipment and methods, the use of toxicity data has expanded to include their integration into fate and effect models that aim to extend the applicability of lab-based study results to make predictions for field system-level impacts. This paper focuses on providing a summary of current chemical analyses for characterization of oil and exposure media used during aquatic toxicity testing and makes recommendations for the minimum analyses needed to allow for interpretation and modeling purposes.publishedVersio

The accumulation of metals, PAHs and alkyl PAHs in the roots of Echinacea purpurea.

We examined the accumulation of polycyclic aromatic hydrocarbons (PAHs), alkyl PAHs, and toxic metals in soils by the roots of Echinacea purpurea (L.) Moench, in a 20-week greenhouse study and a 2-year field study. In the greenhouse study, inoculation by arbuscular mycorrhizal fungus (AMF), Rhizoglomus intraradices (N.C. Schenck & G.S. Sm.). increased the first order accumulation rates (k1) for PAHs by 10-fold, though had no effect on the bioaccumulation rates of toxic metals. In the greenhouse study, PAHs concentrations in soil increased over time with AMF inoculation, suggesting AMF promote 'solvent depletion' in soils by enhancing absorption of minerals and carbon by roots, concentrating the more hydrophobic PAHs in the residual soil. Under field conditions, contaminant concentrations in soils remained unchanged over the 2-year duration of the study. Despite this, all contaminants in E. purpurea roots increased significantly, as a result of a long term extraction of contaminants by plants from soil and a reduction in soil volume as a result of plant growth. First order accumulation rates by roots were inversely correlated to log Kow for the PAHs and alkyl PAHs, indicating that accumulation is inversely related to the compound's hydrophobicity. This study is the first to our knowledge to assess the accumulation of alkyl PAHs by roots, with implications for soil bioremediation by plants because alkyl PAHs are a major source of petrogenic contamination in soils

Pathogen dynamics in a crop canopy and their evolution under changing climate

Canopy-level interactions have been largely ignored in epidemiological models and their applications in defining disease risks under climate change, although these interactions are important for disease management. This paper uses anthracnose of Stylosanthes scabra as a case study and reviews research on dynamics of the pathogen (Colletotrichum gloeosporioides) at the canopy level and pathogen evolution under changing climate. It argues that linking of pathogen dynamics, crop growth and climate models is essential in predicting disease risks under climate change. A plant functional-structural model was used to couple S. scabra growth and architecture with disease under ambient and elevated CO(2). A level of induced resistance in plants with enlarged canopy determined anthracnose severity at elevated CO(2). Moisture-related microclimatic variables determined infection at ambient but not at elevated CO(2). At high CO(2) increased disease level from raised pathogen fecundity in enlarged canopy accelerated pathogen evolution after 25 sequential infection cycles. Modelling of pathogen dynamics under climate change currently suffers from a paucity of quantitative data, mismatch of scales in coupling climate and disease models, and model uncertainties. Further experimental research on interactions of biotic and abiotic factors on plant diseases under climate change and validation of models are essential prior to their use in climate-change prediction. Understanding and anticipating trends in host-pathogen evolution under climate change will improve the durability of resistance and lay the foundation for increased crop adaptation through pre-emptive plant breeding