Research Project Search
- Development and Use of Adverse Outcome Pathways that Predict Adverse Developmental Neurotoxicity - Open: September 13, 2012 - Closing: December 12, 2012
Closed Solicitations (for reference):
- Developing High-Throughput Assays for Predictive Modeling of Reproductive and Developmental Toxicity Modulated Through the Endocrine System or Pertinent Pathways in Humans and Species Relevant to Ecological Risk Assessment - Open: January 28, 2010 - Closed May 5, 2011
- Development and Characterization of Biological Systems for Studying Low Dose Effects of Endocrine Disrupting Chemicals
- Computational Toxicology and Endocrine Disruptors: Use of Systems Biology in Hazard Identification and Risk Assessment
- Development of High-Throughput Screening Approaches for Prioritizing Chemicals for the Endocrine Disruptors Screening Program
- Endocrine Disruptors: Epidemiologic Approaches (in partnership with NIOSH, EPA, NIEHS, and NCI)
- Endocrine Disruptors(in partnership with EPA, DOI, NIEHS, NOAA)
- Research on the environmental transport and fate of natural and synthetic steroid hormones that accompany discharges and the disposal of animal wastes from CAFOs;
- Research on ecological effects associated with steroid hormones in animal waste from CAFOs including impacts on individual fitness of aquatic and/or terrestrial organisms and/or changes in population structure in proximity to CAFOs;
- Evaluation of how various animal waste handling/management strategies impact the transport, fate, potential exposure, and associated effects of steroid hormones discharged from CAFOs.
- Development of analytical methods for measurement of mixtures of EDCs in environmental media at relevant concentrations.
- Development of rapid chemical or biological detection methods or technologies for environmental exposure monitoring.
- Development of activity-based biological indicators (androgen, estrogen, and/or thyroid) for assessing EDC exposure in environmental media.
- Identify the critical determinants that dictate the shape of the dose-response relationship. These could include, for example, pharmacokinetics, receptor pharmacology, homeostatic feedback loops and repair capabilities, and how they differ across target end points;
- Identify and evaluate sensitive and, if possible, easily measured molecular or biochemical markers as indicators of low-dose effects of (anti)estrogenic, (anti)androgenic, (anti)thyroid agents;
- Allow a systematic determination of mechanistic events associated with low-dose effects;
- Characterize any critical windows of sensitivity, strain- or sex-differences, and elucidate any qualitative differences in the responses to the various test substances; and
- Allow assessment of the complete time course for any observed effects and a determination of the long-term health consequences of the earlier detected molecular or biochemical markers; that is, studies should characterize whether or not these observations early in life are predictive of or associated with any specific adverse outcomes during later life stages.
- Development of integrative, quantitative models of the function of the hypothalamic-pituitary-gonadal or hypothalamic-pituitary-thyroid axes with emphasis on the descriptions of the normal physiological processes and mechanisms of perturbation following exposure to xenobiotics (e.g., endocrine disrupting chemicals), in rats or a commonly used small fish toxicology model (e.g., fathead minnow, medaka, zebrafish).
- Cross-species extrapolation of integrative, quantitative models of the perturbed hypothalamic-pituitary-gonadal or hypothalamic-pituitary-thyroid axes following exposure to xenobiotics from rats to humans or a commonly used small fish toxicology model (e.g., fathead minnow, medaka, zebrafish) to other vertebrates (i.e., within the same class or across classes). The cross-species extrapolation should be based on models as described in item (1). Proposals should demonstrate the existence of these models and their validity.
- New approaches that can lead to the development of high-throughput screening systems to assist in prioritization of chemicals for further screening and testing of their potential as endocrine disruptors.
2001: Endocrine Disruptors: Epidemiologic Approaches (in partnership with NIOSH, EPA, NIEHS, and NCI)
- This joint interagency program by NIOSH, EPA, NIEHS, and NCI supports research on the relationship between exposure to endocrine disruptors and adverse health effects in humans, particularly reproductive and developmental, with a focus on epidemiologic approaches.
1999: Endocrine Disruptors (in partnership with EPA, DOI, NIEHS, NOAA)
- Population-level effects of EDCs in wildlife
- Effects of exposure to EDCs during development on human health
1997: Endocrine Disruptors
- Studies that examine endocrine disruptor-related effects in wildlife populations, as well as studies which include significant attention to issues related to the types, levels, sources, and fates of endocrine-disrupting chemicals in the environment.
1996: Endocrine Disruptors
- Refinement of methods to monitor and characterize exposure of humans and/or wildlife to endocrine disruptors, including aspects such as exposure half-life, speciation, uptake, and phase equilibrium.
- Development and validation of models to estimate exposure to endocrine disruptors from different sources via multiple pathways.
- Development and validation of biomarkers of endocrine disruptor exposure and effect.
- Development and validation of in vitro and short-term in vivo test systems to screen for chemicals with specific mechanisms of action expressed via different endocrine pathways; test systems that are applicable across multiple phylogenetic levels are of particular interest.
- Development of Physiologically-Based Pharmacokinetic (PB-PK), Physiologically-Based Toxicokinetic (PB-TK), and Biologically-Based Dose-Response (BBDR) models that incorporate key species-specific parameters critical to the extrapolation of effects across phyla.
- Refinement and validation of methods and models that relate effects observed at subcellular levels to adverse impacts in individuals (both human and wildlife species) and in wildlife populations.