Workshop Report 28

Group 1C

group 1c

The following questions / concerns were discussed:

  1. Are all species of equal importance, or are there keystone species that are more important than others?

There was a clear consensus that not all species should be considered as equal to each other within an ecosystem. Species sensitivities to toxicants and other stressors clearly illustrate that there are sensitive taxa as well as tolerant taxa. A commonly held ideal is that in ecosystems there are keystone species. However, the concept of a keystone species is context dependent. For example: 1) a keystone species may refer to exquisite sensitivity to toxicants and/or other stressors; 2) a rare species, worth protecting via regulations (e.g. nature conservation); 3) a species that provides a valued service (e.g. salmon – human food); and 4) species that are so interdependent upon each other (e.g. snail kite and the apple snail, found in the Everglades, FL and in South America) that the larger ecosystem is dependent upon their continued survival. The role of a keystone species may be most impactful in simple food webs as compared to highly robust and redundant ecosystems. An example discussed within Syndicate 1C was that the elimination or reduced abundance of one taxa in an arctic ecosystem, where food webs are short, would be highly impactful to the entire system compared to highly complicated webs.

2. Is a generic PNEC derived from an SSD overly simplistic in terms of ecological representativeness or should we develop representative assemblages/communities (archetypes) to represent different typologies? Should protection goals account for local community composition?

There was a consensus that derivation of a PNEC should follow a tiered process as is commonly done in current risk assessments. Protection goals should be based upon what is to be protected and how it is related to environmental exposures. For some exposure scenarios, the generation species sensitivity distributions may not be necessary to generate species sensitivity distributions as the use of generic safety factors may be sufficient. For example, a chemical that is not toxic and used at low levels may not need a sophisticated assessment. However, with the availability of Interspecies Correlations Estimations (ICE) it is possible to estimate screening level HC5s based on data from a few laboratory tested species. The species present in the screening level SSDs provide a suite of traits worthy of protection. The development of traits-based SSDs and HC5s are considered as a generic manner of addressing different types of ecological sensitivities. However as SSDs are usually based on an array of single species toxicity test results, the ecological sensitivity will thus not include the variations due to indirect effects such as community effects (e.g. competition for resources, predation).

3. How does aquatic community sensitivity vary with species composition?

Detecting ecological sensitivity to chemical and/or physical stressors is dependent upon what are considered ‘reference conditions’. In general, reference conditions refer to ecological states which humans have not significantly altered. Detecting differences from the reference condition may be dependent upon how specious the ecological community is. For instance, highly diverse and specious ecological states may have traits and functions that are redundant among some taxa, hence – resiliency. Losing taxa in such situations may be more difficult to ascertain than say reference conditions in which there are few species (e.g. arctic systems or nutrient poor situations). In more simple systems the loss of taxa may have large ecological consequences.

There is a great need to provide a mechanistic argument for the use of traits. That is, there is a need to illustrate the links between biochemical responses to stressors and morphological, physiological and ecological consequences. If SSDs are to be accepted by the ecologically-scientifically minded community, links of species traits to community – level traits will be needed. A simple example includes r versus K (quantity versus quality of offspring) reproduction strategies of different species and how they lead to ecological community resilience to stress. Currently, SSDs do not provide such information, but should in the near future.

4. How can knowledge of chemical MoA help construct SSDs for HC5 estimation?

A chemical’s mode of action (MoA) and its potential effect in the construction of SSDs needs to take into account its intended as well as non-intended effects. MoAs are typically defined in terms of acute toxicity. As such, there are a limited number of MoAs. Further, they are often develop for and thus tied to specific taxa. For instance, insecticides are obviously more potent to arthropods than plants, however, fish may also be sensitive. The advent of adverse outcome pathways are an excellent tool to illustrate the probable causal relationships between the dose of a chemical at a subcellular level to the series of events leading to impairment of a population. However, chronic exposures may greatly change the potential for adverse ecological effects. Long-term exposures may affect more metabolic life stages of diverse taxa and thus provide a different array of species sensitivities. Traits such as those related to r or K reproductive strategies, body size, and accessibility to direct exposure to the chemical may be very different depending on taxa.

Tools, such as QSARs, ‘Omics, physiologically based pharmacokinetic (PBPK) and energy-based models are very useful in classifying the potential effects of a chemical’s MoA. Some caution needs to be exercised here, however, as for most taxa, such models do not exist. Indeed, reasonable data sets, that can tie a chemical’s MoA with biological effects exist for only a few taxa (e.g. zebrafish).

5. What are the research needs?

There are 2 key areas in which more research is needed regarding the use and generation of SSDs for environmental protection: 1) inclusion of adverse outcome pathways (AOPs) or mechanisms of toxicity and 2) linking mechanisms to species traits. Such research would provide knowledge on mechanistically-based outcome pathways and on determining taxa possessing these pathways. Establishing links between these aspects would eventually show a continuum between exposure and the propagation of effects. Based on such information, a SSD could then become more ecologically informative.