Reveal abiotic factors significantly influencing chemical toxicity.
Compare toxic effects in unicellular and multicellular organisms in different exposure scenarios and in simplified food-chain model.
Identify effects of exposure conditions on D. magna.

New information on chemical effects on bacteria, algae and crustaceans in different exposure scenarios and food-chains.
New potential biomarkers and toxicity endpoints to increase environmental relevance of laboratory data (with ESR3 and ESR5).

Villem Aruoja, NICPB
Kairi Koort, Tallinn University
Margit Heinlaan, NICPB
Knut Erik Tollefsen, NIVA
Anne Kahru, NICPB

Jaroslav Slobodnik, EI
Ludek Blaha, MU

To characterize MoAs and ecotoxicological effects of novel classes of flame retardants (FRs) in zebrafish.
To establish AOP network linking metabolic-endocrine-reproduction disruption caused by FRs.

MIEs, KEs and AOs related to toxicity of novel FRs including toxicogenomics responses.
In vitro assay(s) for high through-put screening (HTS) or ecotoxicant effects.
Characterization of a (network of) AOPs linking metabolic-endocrine-reproduction outcomes relevant for FRs.

To establish and evaluate the AOP “Chitin synthesis inhibitors leading to developmental disorders and death in freshwater crustaceans”.
To implement a suite of bioassays and effect tools characterize the AOP and establish quantitative effect relationships along the AOP continuum (qAOP) in Daphnia magna.
Establish computational solutions to support extrapolation of AOP and qAOP data to hazard and risk assessment.

Conceptual AOP developed and evaluated, submitted to the AOP-wiki and knowledge gaps identified to guide experimental studies.
Experimentally consolidate the AOP with molecular (with ESR2), functional, and adverse outcomes data (with ESR6) in D. magna to develop qAOPs, and 3) Demonstrate use of computational solutions (e.g. statistics, bioinformatics and machine learning) to support cross-species extrapolations and use of AOP/qAOP data to support environmental hazard and risk assessment (with ESR3).

To develop a combined in vivo and in vitro metabolomic approach to investigate molecular mechanisms and pathways of neonicotinoid toxicity.
Establish/evaluate AOP for neurodevelopmental and behavioural effects of neonicotinoids on Lymnaea stagnalis (aquatic) and Folsomia candida (soil) by linking involved metabolic pathways with phenotypic/developmental/behavioural changes.
To link tissue specific exposure information to molecular information at the anatomical level.

New insights into molecular mechanisms and pathways of neonicotinoid toxicity. In vitro and combined cross-omic strategy (metabolomics, proteomics and genomics; collaboration with ESR5) to confirm MoA and toxicity mechanism associated with the AOP.
Anchoring of metabolic profiles with pathways observed in other in vitro (ESR1, ESR2, ESR3, ESR4) and in vivo assays.
Anchoring of the chemical exposure, molecular tissue distribution and organism health profiles to MIE, KE and AO of selected AOPs.
Revised conceptual AOP for neurodevelopmental disorders and final version submitted to the OECD-EAMST for expert evaluation.

Marja Lamoree, VUA
Pim Leonards, VUA

University of Girona

Closed

Characterize the relation of endocrine disruption via interference with retinoid and thyroid hormone signaling with adverse effects of pollutants on early development of fish.
Explore the role of nuclear receptors RAR/RXR and TR signaling in the AOP of selected environmental toxicants and mixtures.
Link mechanistic changes in retinoid and thyroid hormone signaling with higher level adverse outcomes (developmental and embryonal toxicity, altered growth or behavior) by employing proteomics and targeted metabolomics and transcriptomics approaches.

Assessment of early developmental effects in aquatic vertebrates (fish) with key role of retinoid and thyroid hormone signaling; their increased occurrence leads to adverse outcomes to structure (ageing) and growth of populations.
AOP linking molecular modulations of retinoid and thyroid hormone signaling with biomarkers of key events and health outcomes in vivo at organismal - embryonal level.
Information on the predictability of adverse effects intensity from initiating events assessed by in vitro tools

Use energy-budget, population and food-web models to extrapolate chemical-induced changes in feeding rate to population and community-level responses that underpin key ecosystem functions and service.
Identify effect thresholds for each level of biological organization.
Apply modelling framework to case study chemicals.

Empirical evidence of individual-based threshold effect levels for study chemicals.
Application of energy-budget and population models to translate individual-level effects to changes in populations.
Relationships between individual-level effects and community processes and response to chemical exposure.
Understanding of how chemical-induced effects on the feeding rate translates into changes in population growth and community-level processes and the ecosystem functions and services they drive.
Elucidation of the association between individual-level physiological responses and changes in molecular markers (with ESR7).
Inter-specific comparison of the translation function linking individual-level effects and population-level responses (with ESR10).

Lorraine Maltby, USFD
Philip Warren, USFD

University of Sheffield

Closed

Investigating the effects of chemical stressors on ecosystem services (i.e. soil fertility) provided by soil micro-arthropods.
Linking gene expression and individual level responses by combining AOP and trait-based approaches.

Effects at different levels of biological organization, from gene expression to population and potential for recovery of Folsomia candida (Collembola).
Trait-based approach combined with functional endpoints to establish role of Collembola in soil fertility (i.e. N cycling).
Potential of AOP approach, extended with biochemical and physiological endpoints, dedicated microcosm data on Collembola communities, and combined with trait-based approaches for predicting ecosystem services effects.

Evaluate available tools for applying ecosystem services approach to chemical risk assessment. Identify key information gaps.
Use novel approaches from ecology, ecotoxicology and modelling to address information gaps identified in first objective.
Apply novel and existing approaches to evaluate the risk of chemical to ecosystem service of case study chemicals.

Systematic review of the applicability of current ecotoxicological methods for assessing the risk of chemicals and other stressors to ecosystem service delivery.
Tools for facilitating translation of conventional ecotoxicological endpoints to ecosystem service assessment endpoints.
The tools and approaches required to assess the effects of chemical on ecosystem service delivery.

Developing novel methods for socio-economic evaluation of chemical effects on provision of ecosystem services and natural capital.
Quantifying economic damage accounting for distribution of impacts across different stakeholders in time and space.
Testing impact of risk communication formats on public perception and valuation of chemicals and ecosystem services.

Improved economic cost/benefit analysis of chemical impacts on ecosystem services delivery and natural capital to support current and future decision-making related to implementation of REACH, affecting chemical industry and regulatory authorities.
Link with 2004 European Environmental Liability Directive aimed at the prevention and remedying of environmental damage based on the polluter pays principle.
Improved methodological approaches to provide empirical data and information about socio-economic impacts of selected chemicals on ecosystems across the EU to support European policy makers and regulatory agencies.

Pieter J.H. van Beukering, VUA
Radka Vokurková, Consulteco
Roy Brouwer, UWaterloo/VUA
Michiel Rutgers, RIVM

To translate ecotoxicological effects from chemical exposure via different AOPs into damages on ecosystems expressed in measures of genetic diversity.
To link ecosystem damages to ecosystem functions and ecosystem services related damages expressed in measures of functional diversity.

Set of consistent metrics relating distinct ecotoxicological effects to damage on genetic diversity (i.e. species loss) at the level of ecosystems.
Quantified comparative damage factors differentiated according to species groups and/or groups of MOAs and/or groups of AOPs.
Approach for systematically linking genetic species diversity to ecosystem functions and services.
Damage factors for functional diversity differentiated according to ecosystem functions and services groups and/or species groups fulfilling similar/same functions or ecosystem services.