Upstream eventReduction, Cumulative fecundity and spawning
Decrease, Population trajectory
Key Event Relationship Overview
AOPs Referencing Relationship
|AOP Name||Adjacency||Weight of Evidence||Quantitative Understanding|
|Aromatase inhibition leading to reproductive dysfunction||adjacent||Moderate||Moderate|
|Androgen receptor agonism leading to reproductive dysfunction (in repeat-spawning fish)||adjacent||Moderate||Moderate|
|Estrogen receptor antagonism leading to reproductive dysfunction||adjacent||Moderate||Moderate|
|Prolyl hydroxylase inhibition leading to reproductive dysfunction via increased HIF1 heterodimer formation||adjacent|
|Unknown MIE leading to reproductive dysfunction via increased HIF-1alpha transcription||adjacent|
|Embryonic Activation of the AHR leading to Reproductive failure, via epigenetic down-regulation of GnRHR||adjacent||Moderate||Moderate|
|fathead minnow||Pimephales promelas||Moderate||NCBI|
Life Stage Applicability
|All life stages||Not Specified|
Key Event Relationship Description
SEE BIOLOGICAL PLAUSIBILITY BELOW
Evidence Supporting this KER
Using a relatively simple density-dependent population model and assuming constant young of year survival with no immigration/emigration, reductions in cumulative fecundity have been predicted to yield declines in population size over time (Miller and Ankley 2004). Under real-world environmental conditions, outcomes may vary depending on how well conditions conform with model assumptions. Nonetheless, cumulative fecundity can be considered one vital rate that contributes to overall population trajectories (Kramer et al. 2011).
- Using a relatively simple density-dependent population model and assuming constant young of year survival with no immigration/emigration, reductions in cumulative fecundity have been predicted to yield declines in population size over time (Miller and Ankley 2004). However, it should be noted that the model was constructed in such a way that predicted population size is dependent on cumulative fecundity, therefore this is a fairly weak form of empirical support.
- In a study in which an entire lake was treated with 17alpha-ethynyl estradiol, Kidd et al. (2007) declines in fathead minnow population size were associated with signs of reduced fecundity.
Uncertainties and Inconsistencies
- Wester et al. (2003) and references cited therein suggest that although egg production is an endpoint of demographic significance, incomplete reductions of egg production may not translate in a simple manner to population reductions. Compensatory effects of reduced predation and reduced competition for limited food and/or habitat resources may offset the effects of incomplete reductions in egg production.
- Fish and other egg laying animals employ a diverse range of reproductive strategies and life histories. The nature of the relationship between reduced spawning frequency and cumulative fecundity and overall population trajectories will depend heavily on the life history and reproductive strategy of the species in question. Relationships developed for one species will not necessarily hold for other species, particularly those with differing life histories.
Quantitative Understanding of the Linkage
- Cumulative fecundity is one example of a vital rate that can influence population size over time. A variety of population model constructs can be adapted to utilize measurements or estimates of cumulative fecundity as a predictor of population trends over time (e.g., (Miller and Ankley 2004; Miller et al. 2013).
- The model of Miller et al. 20014 uses a relatively simple density-dependent population model and assuming constant young of year survival with no immigration/emigration, use measures of cumulative fecundity to predict relative change in in population size over time (Miller and Ankley 2004).
Known modulating factors
Known Feedforward/Feedback loops influencing this KER
Domain of Applicability
Spawning generally refers to the release of eggs and/or sperm into water, generally by aquatic or semi-aquatic organisms. Consequently, by definition, this KER is likely applicable only to organisms that spend a portion of their life-cycle in or near aquatic environments.
- Kidd KA, Blanchfield KH, Palace VP, Evans RE, Lazorchak JM, Flick RW. 2007. Collapse of a fish population after exposure to a synthetic estrogen. PNAS 104:8897-8901.
- Kramer VJ, Etterson MA, Hecker M, Murphy CA, Roesijadi G, Spade DJ, Spromberg JA, Wang M, Ankley GT. Adverse outcome pathways and ecological risk assessment: bridging to population-level effects. Environ Toxicol Chem. 2011 Jan;30(1):64-76. doi: 10.1002/etc.375. PubMed PMID: 20963853
- Miller DH, Ankley GT. 2004. Modeling impacts on populations: fathead minnow (Pimephales promelas) exposure to the endocrine disruptor 17b-trenbolone as a case study. Ecotoxicology and Environmental Safety 59: 1-9.
- Miller DH, Tietge JE, McMaster ME, Munkittrick KR, Xia X, Ankley GT. 2013. Assessment of Status of White Sucker (Catostomus Commersoni) Populations Exposed to Bleached Kraft Pulp Mill Effluent. Environmental toxicology and chemistry / SETAC (in press).
- Wester P, van den Brandhof E, Vos J, van der Ven L. 2003. Identification of endocrine disruptive effects in the aquatic environment - a partial life cycle assay with zebrafish. (RIVM Report). Bilthoven, the Netherlands: Joint Dutch Environment Ministry.