# It's about time: integrating micro- and macro-evolutionary perspectives into ecotoxicology for improved predictions and long-term assessment of ecosystem health

Thomas Sol Dourdin, Cassandre Aimon, Scott Mccairns, Marie-Agnès Coutellec

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## To cite this version:

Thomas Sol Dourdin, Cassandre Aimon, Scott Mccairns, Marie-Agnès Coutellec. It's about time: integrating micro- and macro-evolutionary perspectives into ecotoxicology for improved predictions and long-term assessment of ecosystem health. Current Opinion in Environmental Science & Health, 2025, pp.100688. 10.1016/j.coesh.2025.100688. hal-05342018

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It's about time: integrating micro- and macro-evolutionary perspectives into
ecotoxicology for improved predictions and long-term assessment of ecosystem
health

Thomas Sol Dourdin, Cassandre Aimon, Scott McCairns, Marie-Agnès Coutellec

PII: S2468-5844(25)00097-2

DOI: https://doi.org/10.1016/j.coesh.2025.100688

Reference: COESH 100688

To appear in: *Current Opinion in Environmental Science & Health*

Received Date: 15 May 2025

Revised Date: 1 September 2025

Accepted Date: 27 October 2025

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Please cite this article as: Dourdin TS, Aimon C, McCairns S, Coutellec M-A, It's about time: integrating micro- and macro-evolutionary perspectives into ecotoxicology for improved predictions and long-term assessment of ecosystem health, *Current Opinion in Environmental Science & Health*, https://doi.org/10.1016/j.coesh.2025.100688.

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© 2025 The Author(s). Published by Elsevier B.V.
1 **Article title**

2 It's about time: integrating micro- and macro-evolutionary perspectives into ecotoxicology for

3 improved predictions and long-term assessment of ecosystem health

4

5 **Authors**

6 Thomas Sol Dourdin¹ (thomas.sol_dourdin@univ-lr.fr). Co-first author

7 Cassandre Aimon² (cassandre.aimon@inrae.fr). Co-first author

8 Scott McCairns² (scott.mccairns@inrae.fr)

9 Marie-Agnès Coutellec² (corresponding author: marie-agnes.coutellec@inrae.fr)

10

11

12 **Affiliations**

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14 ¹ Littoral Environnement et Sociétés (LIENSs), UMR 7266 CNRS – La Rochelle Université, 2 rue

15 Olympe de Gouges, 17000, La Rochelle, France.

16

17 ² DECOD (Ecosystem Dynamics and Sustainability), INRAE, L'Institut Agro, Ifremer

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19

20 **Acknowledgements:**

21

22 The authors are grateful to Dr Paolo Pastorino for inviting to us to contribute to this special

23 issue.

24

25 **Author contributions: CrediT**

26

27 • Conceptualization : TSD, CA, SMC, MAC

28 • Investigation TSD, CA, SMC, MAC

29 • Supervision MAC

30 • Visualization TSD

31 • Writing – original draft : TSD, CA

32 • Writing – review and editing TSD, CA, SMC, MAC

33

34
35 **Abstract**

36 Whilst ecology has served as a foundational inspiration for risk assessment in ecotoxicology, far less 37 attention has been given to evolution, despite its importance. As the need for a new paradigm in 38 ecotoxicology is becoming increasingly evident in the face of Global change, the consideration of 39 evolutionary processes and patterns should provide a way to progress towards this objective. This 40 review draws on the recent literature to feed this idea, with a particular attention to the interplay 41 between evolutionary paces. Doing so, we recast ecotoxicology as an innovative, exciting discipline, 42 conceptually equipped to meet the challenges of the Anthropocene era. 43

44 **Keywords:** evolutionary ecotoxicology; plasticity; transgenerational effects; epigenetics; multi-stress 45

46
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49 **Introduction**

Since the industrial revolution, one emblematic phase of the Anthropocene era (1), much of human economic activity has relied upon the extraction of a constantly growing amount of resources and the release of myriad toxic chemicals into the environment. These unprecedented anthropogenic forces have triggered rapid, large-scale modifications to most of the Earth's equilibria, referred to as "Global change". Given this context, biodiversity is of major concern since organisms will have to adapt to combined environmental changes. These phenomena are also likely to interact, triggering negative feedback on human health via the concomitant degradation of ecosystem services and expansion of zoonoses to name but a few. The complexity of these interdependencies has been conceptualized under the One Health paradigm (2). We expect One Health to play a pivotal role in advancing predictive ecotoxicology beyond observational approaches towards more mechanistic understanding (3). One promising avenue is the development of comparative approaches that combine knowledge of evolutionary conservation of pathways involved in diseases and toxicological responses with adverse outcome pathways (4).

Yet global changes are also likely to have evolutionary impacts on organisms. In this regard, ecotoxicologists have long been aware of the potential effects of pollutants up to micro-evolutionary scales, and it is now been more than 30 years since evolutionary concepts have spread into the discipline (e.g., (5)). Several studies have documented evolutionary impacts of pollutants in natural populations, as well as using experimental assays (e.g. special issues in Ecotoxicology 2011 and 2013, and Evol. Appl. 2017), thereby providing convincing arguments for the need to consider such effects in ecological risk assessment of chemicals. However, to date, evolutionary (eco-)toxicology has largely embraced concepts from the modern evolutionary synthesis (e.g. genetic diversity, selection, fitness, gene flow) to focus mostly on genetic-based adaptation and micro-evolution triggered by xenobiotics (6,7). Doing so, macro-evolutionary aspects and non-genetic mechanisms have generally been overlooked. Regarding the latter, this has probably led to biased interpretations in favour of genetic adaptation, under experimental multigeneration designs in which parental effects were neglected or not considered at all (e.g., lack of monitoring of post-exposed generations). In our opinion, one remaining challenge is to properly consider the different evolutionary timescales, as well as their interplay. This is needed to improve the capacity of ecotoxicology to (i) predict the current effects of xenobiotics on a diversity of organisms (macro-evolutionary legacy), and (ii) to understand the influence of environmental contamination on the capacity of organisms to cope with impending environmental changes (adaptation and micro-evolutionary processes) (7). Although the trend is well established, we believe that a more explicit consideration of all the evolutionary dynamics is necessary to reach a true milestone in this endeavour. Therefore, our aim is to identify, from the most recent
83 literature, some innovative concepts to better anchor ecotoxicology in a comprehensive eco-
84 evolutionary framework bridging past evolutionary histories and on-going evolutionary principles,
85 thereby going beyond the conventional conception (Fig. 1).

<figure><img src="image_5.png" /><figcaption>Figure 1: Conceptual diagramm illustrating the updated view of what evolutionary ecotoxicology should encompass to reach a comprehensive eco-evolutionary framework able to improve its predictive and descriptive efficacy. The arrows illustrate the influence of the boxes on each other.</figcaption></figure>

A. Plasticity and long-term individual responses to xenobiotics

Phenotypic plasticity (the ability of a genotype to produce different phenotypes depending on the environment (8)) can facilitate adaptation by either reducing extinction and prolonging the time for adaptive evolution to occur, or through canalization via the genetic assimilation of a phenotype with optimal fitness (9). In the face of toxicant exposures, an organism's response via homeostatic regulation can be viewed as a form of phenotypic plasticity (9). The persistence of a given phenotype through life, or even in its progeny (i.e. transgenerational plasticity), is likely to depend upon the nature of the environmental trigger (e.g. predictable vs unpredictable), the timing of its occurrence during the life cycle (e.g. during development vs adult stages), as well as the trait itself (e.g. behaviour vs morphology). As major regulatory factors of gene expression, epigenetic mechanisms (see box 1) play a key role in plasticity, potentially compensating for genetic constraints, hence enabling rapid, reversible acclimation to environmental stressors. Recent studies have also highlighted the role of epigenetics in shaping resilience at individual, population, and ecosystem levels (10–12).

1) Xenobiotic-induced epigenetic modifications

One of the most dynamic fields in evolutionary ecotoxicology is the study of xenobiotic-
induced epigenetic modifications, a task facilitated by developments in "-omics" technologies (13).
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Epigenetic modifications can be induced by environmental stressors, including chemical toxicants (e.g. reviewed in Chatterjee et al., 2018 (14)). To date, the most studied epigenetic mark is DNA methylation, known to be influenced by a large variety of toxicants, from pesticides (15,16) to metals (17) and PFAs (18). However, it remains difficult to accurately link specific epigenetic changes to gene expression modifications (19), highlighting the need for further research in this area.

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2) Transgenerational plasticity mediated by epigenetic mechanisms

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Beyond direct exposure effect, transgenerational plasticity (which may be contributed by the transmission of epigenetic, cytoplasmic, and microbiotic elements, as well as behaviors through learning (20)) is thought to play an important role at the population level (21). Furthermore, non-genetic inheritance may still have evolutionary consequences, by exposing specific phenotypes to natural selection (22). However, transgenerational plasticity may not always be adaptive, as for example in case of a mismatch between the frequency of environmental change and the generation time of a given organism. Also, stressful conditions imposed on parents may have persistent consequences in subsequent generations. Regarding epigenetics, the stability of toxicant-induced DNA methylation changes remains questionable. Some effects are reversible, ceasing by the second generation (23), while others have lasting impacts on fitness and selection (e.g., beyond the F3 generation (24)). Also, contrary to the initial thought that parental effects are mainly transmitted via mothers, sex-specific patterns are important to consider. Studies on *Caenorhabditis elegans* demonstrate that paternal, but not maternal, exposure to ionizing radiation leads to transgenerational embryonic lethality (25). Similar sex-dependent effects have been observed in fish and mammalian models, where paternal exposure to endocrine disruptors alters sperm epigenetic marks, leading to metabolic and developmental changes in offspring (26).

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It is perhaps noteworthy that evolutionary ecologists tend to be more interested in the adaptive potential of transgenerational plasticity, whereas ecotoxicologists typically track the persistence of adverse impacts across generations. An effort to integrate these divergent perspectives may yield a more synthetic appreciation for the evolutionary consequences of transgenerational plasticity.

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## B. Micro-evolution and adaptation to xenobiotics in natural populations

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1) Population diversity and structure
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In the last decade, contamination-mediated micro-evolutionary dynamics in natural populations have been increasingly documented. Examples of increased genetic diversity induced by toxicant mutagenicity, as exemplified by the effects of ionizing radiation on tree frog mitochondrial DNA following the Chernobyl disaster (27), are rare. The most reported effect is that of reduced diversity, mainly interpreted as the result of directional selection induced by toxicants acting on population standing genetic variation. Several studies revealed this pattern in exposed populations at (i) targeted genes/genomic regions (e.g. *Gambusia affinis* exposed to arsenic (28)), or at (ii) neutral markers (e.g. *Crassostrea honkongensis* and metal contamination (29); *Gammarus pulex* and pesticides (30)). Moreover, local adaptation to environmental contamination may lead to population genetic structuring. For instance, the genomic signature of metal exposure in *Salmo trutta* populations was found to be associated with population divergence in gene expression (31), and gene sequence divergence in several stress-related markers (Cytb, CUP1A1, p53) was identified in *Crocidura russula* populations after heavy metal pollution (32). Likewise, evidence of selective pressures exerted by pyrethroid pesticides on targeted genetic variation (specifically voltage-gated sodium channel) were found repeatedly and independently in various populations of *Hyalella azteca* (33). A striking case of rapid parallel adaptation after independent colonization of metal-contaminated sites has also been described in *Silena uniflora* (34). Together, these examples suggest that environmental contamination should be considered as a selective pressure in its own right, capable of triggering adaptive dynamics, and thus raising the question of the consequences of such adaptive processes in the context of Global change.

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Epigenetic mechanisms can also be analysed at the population-level in natural populations, paving the way for a new research field: population epigenetics. Pioneering studies have already documented a complex relation between epigenetic and genetic variation in natural populations from various taxa, showing the relevance of the epigenetic structure of populations in micro-evolutionary dynamics (reviewed in Chapelle and Silvestre, 2022 (35)). Moreover, epigenetic structuring is likely to precede genetic structuring, as demonstrated in natural oyster populations differing in their susceptibility to Oyster Mortality Syndrome (36). Similar population-level effects apply equally to ecotoxicology contexts as well, as demonstrated by epigenomic variants identified in mayfly populations exposed to pesticides (37). Although in its infancy, population epigenetics appears to be an exciting research area for ecotoxicologists to address rapid population-level responses to pollutants, and to bridge the gap between xenobiotic-induced plasticity and micro-evolution.

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2) Population adaptive potential in the context of global change
General-Stress capacity, the ability of organisms to respond to myriad environmental stressors, may be reduced by toxicants. For instance, a recent study demonstrated that *Gammarus pulex* populations adapted to agricultural streams showed increased tolerance to a particular pesticide (clothianidin), yet increased vulnerability to combined stress (pesticide + warming) (38). Similar conclusions were drawn from independent studies on *Daphnia*, whose historical exposure to chemical stress led to a greater sensitivity to phenanthrene (39) or to sequential stresses (chlorpyrifos then heat spike) (40), thereby reducing their General-stress capacity. The putative synergistic interactions between climate change-related stressors and chemical contamination are already of major concern in ecotoxicology (i.e. warming vs chemicals (41)). Yet, these results add a new layer of complexity by pointing out the critical role of xenobiotics acting upstream as selective pressures, potentially reducing the ability of organisms to adapt to impending combined stressors. Likewise, the reduction in adaptive potential resulting from such adaptive dynamics has been poorly addressed in an ecotoxicological context. It is imperative to do so across a wide variety of taxa to broaden the phylogenetic range of our understanding, as well as improve its ecological relevance.

Conversely, adaptation to one stressor can sometimes confer cross-protection (i.e. enhanced tolerance) against another. This phenomenon plays a key role in organismal persistence within multi-stressor environments. Observed across diverse taxa and habitats, cross-protection has been documented in response to both natural and anthropogenic stressors, underscoring its relevance to Global change-related threats (42,43). However, it is a complex phenomenon which does not necessarily hold when the order of exposure is reversed (see Pallarés et al., 2017 (44) for the example of salinity vs desiccation). Moreover, cross-protection potentially comes with fitness-related trade-offs affecting life-histories such as reduced fecundity and lower activity levels in *B. glabrata* and *T. castaneum* (45,46). Understanding the mechanisms and costs underlying both trade-offs and cross-protection is therefore essential for predicting species resilience in a Global change context (see Box 2 for proposals based on Life History Theory). Future research should integrate field and laboratory studies (including multiple sequence exposure) to enhance ecological realism and refine predictions of adaptive responses to global change.

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## C. The legacy of evolutionary histories to enlighten todays ecotoxicology

Since the effects of all chemical combinations cannot be screened on all members of a community or biocenose, evaluating chemical risk for highly diversified communities of terrestrial and aquatic organisms remains one of the primary challenges of ecological risk assessment, especially in
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## 1) Phylogenetic signal in trait distribution

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the growing context of 3R rules (47). The task is indeed difficult because ecological interactions are complex, and because chemical contaminants may impair communities in multiple direct and indirect ways (48). Therefore, it is critical to employ methods to extrapolate toxicity and predict species sensitivity. Among these, two types of phylogeny-based approaches are currently gaining attention. The first relies on species phylogenies (possibly from taxonomy, or DNA sequence markers) and a partial knowledge of species sensitivities (e.g. phylogenetic signal (49,50)). The second category directly uses orthology and the evolutionary conservation of chemical targets [as based on their amino-acid sequence (SeqAPASS (51))], and now also on their predicted structure (ITASSER (52))], or of key genes and gene pathways implicated in the metabolism of xenobiotics (53).

In the recent literature, studies merging species phylogeny and partial knowledge of species sensitivity revealed variation patterns of chemical sensitivity, transposing the phylogenetic signal concept (54) into the ecotoxicology framework (49). This method is potentially useful for patterns of sensitivity exhibiting a clear phylogenetic signal (55). However, to date only a few studies have investigated the correlation between species phylogenetic distance and sensitivity. Despite rare successful applications (e.g. diatoms and bioindication (56)), it remains poorly verified in more commonly studied taxa (e.g. fish (55,57); bivalves (58)) and needs to be further described. For instance, recent studies tested if phylogenetic signals of tolerance and sensitivity to more than 30 pesticides in Bilateria were stronger for synthetic versus natural compounds, for chemicals with a specific vs nonspecific MoA, and under chronic vs acute exposures (59). None of these hypotheses was verified, which would suggest a disqualification of the approach. Alternatively, the lack of signal may reflect limited statistical power or that the evolutionary lineages involved in the analyses were so remote that we should not expect to find toxicant targets or detoxification systems to be shared as inherited from a common ancestor. This is supported by studies highlighting strong signals when focusing on a more restricted taxonomic level. For instance, phylogeny seems to explain an important part of l-cyhalothrin sensitivity variation at the family and genera levels in 28 spider species (60). Similar examples can be found in Nematoda, for which the difference in copper sensitivity matches phylogenetic structure at the generic level (61).

Finally, another important component to consider is the process underlying the evolution of the trait of interest, which may alter the apparent phylogenetic signal across a set of taxa (e.g. trait canalization, stabilizing vs divergent selection, random genetic drift). We may expect different processes across categories of traits (e.g. morphological, physiological, behavioural traits), or depending on whether trait architecture is mono- vs poly-genic. Finally, correlational patterns of

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selection across traits may also blur phylogenetic signals, hence masking patterns of phylogenetic
relatedness.

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2) Evolutionary conservation of target sequences

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The issue of evolutionary remoteness, also points to the importance of the phylogenetic scale
for sequence-based comparative toxicology, which should be determined according to the expected
level of conservation of the potential targets and of their history (gene diversification and loss, loss of
function, etc.). For example, in the context of endocrine disrupters (EDs), nuclear receptors (NRs), as a
highly conserved protein family, should be appropriate for metazoan-level investigations, yet some
subfamilies are not present in invertebrates (adrenal and some sex steroid receptors), and some NRs
are ligand-activated in some lineages while constitutively active in others (62).

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Thus, whilst phylogeny-based methods have yet to prove their full effectiveness, they may
ultimately pave the way to improved predictability of ecotoxicology at a time where it is critical to
rapidly integrate a broader variety of taxa into the risk assessment framework.

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Conclusion

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Although far from an exhaustive list, the examples cited in this mini-review show that the
response to toxicants is both driven by and an influence on evolutionary processes, and that the two
are not mutually exclusive. This general observation implies that complex interactions between
environmental pressures and various processes occurring at different temporal paces and scales are
likely to underpin what can be observed as a response, both at individual and population levels. With
the aim of becoming more mechanistically based, predictive ecotoxicology is confronted with this
complexity. In this context, we argue that the extension of AOPs to pertinent evolutionary dimensions
may potentially provide a real improvement in our ability to relate ecotoxicological endpoints to their
suspected causes. It is also suggested that a deep knowledge of the evolutionary origin and
diversification of toxicant molecular targets is required to move forward in this direction. This aim
should be achievable in the foreseeable future thanks to recent advances in comparative genomics.
Likewise, improved knowledge of the diversity and evolution of epigenetic mechanisms, and on their
mode of transmission, appears a key step to progress on the front of micro-evolutionary ecotoxicology.
An effort to reconcile evolutionary toxicology (sensu Bickham 2011 (6)) and molecular comparative
toxicology (4) should motivate the new generation of ecotoxicologists to develop research projects
that will increase the scientific knowledge and the predictive ability of ecological risk assessment.
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**Box 1 - How universal are epigenetic marks and their functional significance?**

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Epigenetics, defined as the study of changes in gene function that are mitotically and/or meiotically heritable without a change in DNA sequence (63), includes DNA methylation, histone modifications and non-coding RNAs, and plays a pivotal role in gene expression regulatory functions, development, phenotypic plasticity, and genome integrity (64). Deciphering the functional consequences of environmentally induced epigenetic modifications is an area of active research, especially in non-vertebrate organisms, as it is now clear that these molecular mechanisms and modifications are not homogeneous in the living world. For instance, despite an apparently conserved role of DNA methylation (m5Cytosine in CG dinucleotides associated with transcription repression), both the level and distribution of this epigenetic mark vary significantly in Eukaryotes. In Metazoans, invertebrates present a large range of DNA methylation profiles, including very low levels (e.g., *C. elegans*, *D. melanogaster*), and mosaic patterns with alternate methylated and unmethylated regions (various phyla). From a functional viewpoint, methylation of promoters is associated to the repression of gene expression whereas gene body methylation is more likely to reduce transcriptional noise (65). If the first was more studied in vertebrates and the latter in invertebrates, recent studies showed that they were common to both (66). Under unstable or fluctuating conditions, such as expected in anthropized environments, the weak level of DNA methylation which seems to characterize invertebrates could act as a positive factor on phenotypic plasticity (67). Finally, from an evolutionary perspective, highly methylated genes appear phylogenetically more conserved, and enriched for house-keeping functions, whereas methylation loss seems to be associated with genes involved in signalling and in reproductive processes (68). In addition, although epigenetic modifications are expected to mediate transgenerational consequences of environmental stress, the mechanisms by which epigenetic changes persist across generations remain a key research question. Their transmission can be "replicative" (i.e. directly passed to the next generation through meiosis), or "reconstructive" implying that the signal is first erased (reprogramming) and then reconstructed faithfully in the progeny (for a detailed review, see Fitz-James and Cavalli, 2022 (69)). Therefore, transgenerational epigenetic inheritance may rely on different mechanisms across species, depending on their reproductive system, and a replicative process may be more likely under apomictic parthenogenesis (e.g. daphnids) than under sexual reproduction which implies epigenetic reprogramming (70).
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**Box 2 – Ecotoxicological responses are adaptive yet costly: what can Life history theory teach us ?**

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As ecotoxicological responses entail an adaptive component, be it plastic or genetically selected, we suggest that they would be better understood under the integrative framework of a life history trade-off. The reason for this is two-fold. First, as for other traits, the phenotypic expression of a toxicological response is expected to be driven by various constraints (physical, phylogenetic, developmental) that may generate trade-offs at the organism level. Consistently, the response to toxicants often comes at a cost (e.g., reduced thermal tolerance in pyrethroid-adapted populations of *Hyalella azteca* (71); reduced life-history trait-values in cadmium-adapted populations of gammarids (72); see also Freeman et al. 2021 (73) for a meta-analysis of insecticide resistance). Second, contaminants can in turn modulate life-history trade-offs. The current literature on this issue is still sparse, but has some demonstrative value. For example, as an emergent contaminant, the pharmaceutical fluoxetin has been shown to disrupt trade-offs involving behaviour and life-history traits (pace-of-life syndrome (74)), and to affect trade-offs involved in host-pathogen relationships (75). The consideration of such relationships seems essential to make ecotoxicology truly predictive. To go further in this direction, we hereafter borrow the terminology and categorization defined by Garland et al. (2022) (76) in the frame of Life history theory, under which trade-offs occur because all fitness components cannot be maximised simultaneously.

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**Proximate constraints on toxicological responses** – Occurring at the organism level, such constraints include *mechanistic functional conflicts* (often due to physical constraints), *allocation-based processes* (energy, resource use), and *the sharing of molecular pathways* by different functions (e.g. endocrine systems). We believe that at least the latter are directly transposable to the context of ecological risk assessment. Indeed, *energy allocation* (DEB theory) is the basis underlying some toxicokinetic-toxicodynamic models, which focus on toxicant effects on growth and reproduction through time (for a recent evaluation, see EFSA PPR Panel, 2018 (77)). Similarly, current research efforts devoted to *endocrine disruptors* provide a corpus of knowledge that would be highly valuable in an eco-evolutionary context.

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**Ultimate constraints on evolutionary toxicological responses** – Pivotal to the theory of Life history, ultimate constraints (*antagonistic pleiotropy*, *context-dependency*, *sexual vs natural selection*) also deserve close attention in evolutionary ecotoxicology. First, ecotoxicological responses are by definition *“context-dependant”*, triggered by external conditions (ecological and environmental), which may themselves act as selective forces. Next, the ecotoxicological context appears particularly appropriate to the focus on trade-offs mediated by *antagonistic pleiotropy*, as pleiotropic signalling factors represent potential toxicological targets (hormones, cytokines, transcription factors, neurotransmitters, oxidative stress). A nice example of such a pleiotropic integrator is AHR (Aryl
332 Hydrocarbon Receptor), first described as a xenobiotic receptor, but which also affects immune, 333 reproductive and cardiovascular functions (78). Transcription factors in general, due to their regulatory 334 function, are pleiotropic. Given their sensitivity to natural and xenobiotic stimulators (e.g. C-repeat 335 binding factors in mangrove plants, inducible by hormones, cold, salt, or heavy metals (79)), improved 336 knowledge into their evolutionary origin, or that of genes involved in their signalling pathways (e.g., 337 AHR pathway genes (80)), may prove essential in understanding the ultimate constraints limiting 338 responses to xenobiotic exposure.

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This article reports on conclusions and perspectives drawn from a workshop focusing on pharmaceuticals and personal care products and the lessons that can be gained from evolutionary conservation of the molecular targets of these substances across species and life stages in the context of potential adverse outcomes (AOPs) and effects. This timely overview of the main current ideas and concepts developed in this domain play as a plea for the development of precision ecotoxicology, as a new subdiscipline inspired from precision medicine, through improved omic approaches, quantitative AOPs, link between levels of biological organisation, etc.

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This article is a thorough review of factors that contribute to fish ecological resilience. In particular, the authors point to the critical role of genomic and epigenomic mechanisms underlying resilience expressed at higher levels of biological organisation, up to ecosystems. Collectively, the ideas developed in this analysis enrich current models developed to predict the response of biodiversity to environmental stress.

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This article provides empirical support for fitness cost associated with insecticide resistance in a non target species. In this study, daphnia clones experimentally selected for tolerance to the insecticide chlorpyrifos showed no fitness cost (they performed even better under chlorpyrifos than under control conditions) excepted when they were further exposed to heat. Conversely, no such synergistic interaction was observed in chlorpyrifos-sensitive clones. Results highlight the importance of considering different stressor combinations and their interaction with the genetic background when assessing chemicals’ ecological risk.

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This publication reports on an updated approach of cross species extrapolation of chemical toxicity, based on target sequence evolutionary conservation and structural molecular models. Currently, these comparative methods constitute the most advanced approach to deal with the diversity of modes of action and mechanisms of toxicity and appear most promising for the development of predictive toxicology.

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This study investigated the phylogenetic component of chemical sensitivity across a range of aquatic animal species and using data from a large set of contaminants. The method applied was based on the calculation of Pagel's index of phylogenetic signal for acute and chronic sensitivity data available in various invertebrate and vertebrate lineages. The general conclusion of this study is that strong phylogenetic signal (PS) for chemical sensitivity is a rare pattern. The article provides a thorough discussion on potential factors responsible for this result.
**Declaration of interests**

[x] The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

[ ] The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:

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