This Event is licensed under the Creative Commons BY-SA license. This license allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use. If you remix, adapt, or build upon the material, you must license the modified material under identical terms.
Event: 360
Key Event Title
Decrease, Population growth rate
Short name
Biological Context
Level of Biological Organization |
---|
Population |
Key Event Components
Process | Object | Action |
---|---|---|
population growth rate | population of organisms | decreased |
Key Event Overview
AOPs Including This Key Event
AOP Name | Role of event in AOP | Point of Contact | Author Status | OECD Status |
---|---|---|---|---|
Androgen receptor agonism leading to reproductive dysfunction | AdverseOutcome | Evgeniia Kazymova (send email) | Open for citation & comment | WPHA/WNT Endorsed |
Aromatase inhibition leading to reproductive dysfunction | AdverseOutcome | Cataia Ives (send email) | Open for citation & comment | WPHA/WNT Endorsed |
Estrogen receptor agonism leading to reproductive dysfunction | AdverseOutcome | Allie Always (send email) | Under Development: Contributions and Comments Welcome | |
Estrogen receptor antagonism leading to reproductive dysfunction | AdverseOutcome | Evgeniia Kazymova (send email) | Open for citation & comment | Under Review |
Cyclooxygenase inhibition 2 | AdverseOutcome | Cataia Ives (send email) | Under Development: Contributions and Comments Welcome | |
Prolyl hydroxylase inhibition | AdverseOutcome | Allie Always (send email) | Under Development: Contributions and Comments Welcome | |
Unknown MIE leading to reprodl | AdverseOutcome | Evgeniia Kazymova (send email) | Under Development: Contributions and Comments Welcome | |
DIO2i posterior swim bladder | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Under Development: Contributions and Comments Welcome | WPHA/WNT Endorsed |
DIO2i anterior swim bladder | AdverseOutcome | Arthur Author (send email) | Under Development: Contributions and Comments Welcome | WPHA/WNT Endorsed |
DIO1i posterior swim bladder | AdverseOutcome | Agnes Aggy (send email) | Under Development: Contributions and Comments Welcome | WPHA/WNT Endorsed |
DIO1i anterior swim bladder | AdverseOutcome | Allie Always (send email) | Under Development: Contributions and Comments Welcome | WPHA/WNT Endorsed |
TPOi anterior swim bladder | AdverseOutcome | Evgeniia Kazymova (send email) | Under Development: Contributions and Comments Welcome | WPHA/WNT Endorsed |
Cyclooxygenase inhibition 3 | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Under Development: Contributions and Comments Welcome | |
Cyclooxygenase inhibition 4 | AdverseOutcome | Arthur Author (send email) | Under Development: Contributions and Comments Welcome | |
Cyclooxygenase inhibition 1 | AdverseOutcome | Agnes Aggy (send email) | Under Development: Contributions and Comments Welcome | |
Cyclooxygenase inhibition 5 | AdverseOutcome | Agnes Aggy (send email) | Under Development: Contributions and Comments Welcome | |
tyrosinase, fish | AdverseOutcome | Agnes Aggy (send email) | Open for citation & comment | Under Development |
AHR mediated epigenetic reproductive failure | AdverseOutcome | Arthur Author (send email) | Under development: Not open for comment. Do not cite | |
AChE inhibition - acute mortality | AdverseOutcome | Cataia Ives (send email) | Under Development: Contributions and Comments Welcome | Under Development |
AChE inhibition - acute mortality via predation | AdverseOutcome | Allie Always (send email) | Under development: Not open for comment. Do not cite | |
GR Agonism Leading to Impaired Fin Regeneration | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Open for citation & comment | |
DNMT inhibtion leading to population decline (1) | AdverseOutcome | Agnes Aggy (send email) | Under Development: Contributions and Comments Welcome | |
DNMT inhibtion leading to population decline (2) | AdverseOutcome | Allie Always (send email) | Under Development: Contributions and Comments Welcome | |
DNMT inhibtion leading to population decline (3) | AdverseOutcome | Evgeniia Kazymova (send email) | Under Development: Contributions and Comments Welcome | |
DNMT inhibtion leading to population decline (4) | AdverseOutcome | Cataia Ives (send email) | Under Development: Contributions and Comments Welcome | |
DNMT inhibtion leading to transgenerational effects (1) | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Under Development: Contributions and Comments Welcome | |
DNMT inhibtion leading to transgenerational effects (2) | AdverseOutcome | Arthur Author (send email) | Under Development: Contributions and Comments Welcome | |
5α-reductase,female fish | AdverseOutcome | Cataia Ives (send email) | Open for citation & comment | Under Development |
retinaldehyde dehydrogenase inhibition,population decline | AdverseOutcome | Arthur Author (send email) | Under Development: Contributions and Comments Welcome | Under Development |
Aromatase inhibition leads to male-biased sex ratio via impacts on gonad differentiation | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Under Development: Contributions and Comments Welcome | WPHA/WNT Endorsed |
Thermal stress leading to population decline (3) | AdverseOutcome | Evgeniia Kazymova (send email) | Under development: Not open for comment. Do not cite | |
Thermal stress leading to population decline (2) | AdverseOutcome | Allie Always (send email) | Under development: Not open for comment. Do not cite | |
Thermal stress leading to population decline (1) | AdverseOutcome | Agnes Aggy (send email) | Under development: Not open for comment. Do not cite | |
TPOi retinal layer structure | AdverseOutcome | Allie Always (send email) | Open for citation & comment | Under Review |
11β-hydroxylase inhibition, infertility in fish | AdverseOutcome | Allie Always (send email) | Under development: Not open for comment. Do not cite | Under Development |
11βHSD inhibition, decreased population trajectory | AdverseOutcome | Agnes Aggy (send email) | Under development: Not open for comment. Do not cite | Under Development |
AR agonism leading to male-biased sex ratio | AdverseOutcome | Evgeniia Kazymova (send email) | Open for citation & comment | WPHA/WNT Endorsed |
ROS production leading to population decline via photosynthesis inhibition | AdverseOutcome | Arthur Author (send email) | Under development: Not open for comment. Do not cite | |
ROS production leading to population decline via mitochondrial dysfunction | AdverseOutcome | Agnes Aggy (send email) | Under development: Not open for comment. Do not cite | |
DNA damage leading to population decline via programmed cell death | AdverseOutcome | Allie Always (send email) | Under development: Not open for comment. Do not cite | |
OEC damage leading to population decline via photosynthesis inhibition | AdverseOutcome | Evgeniia Kazymova (send email) | Under development: Not open for comment. Do not cite | |
TPOi eye size | AdverseOutcome | Evgeniia Kazymova (send email) | Under development: Not open for comment. Do not cite | Under Development |
TPOi photoreceptor patterning | AdverseOutcome | Cataia Ives (send email) | Under development: Not open for comment. Do not cite | Under Development |
Inhibition of Fyna leading to increased mortality | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Open for citation & comment | |
GSK3beta inactivation leads to increased mortality | AdverseOutcome | Cataia Ives (send email) | Open for citation & comment | |
Deposition of energy leading to population decline via DSB and follicular atresia | AdverseOutcome | Evgeniia Kazymova (send email) | Under development: Not open for comment. Do not cite | |
Deposition of energy leading to population decline via DSB and apoptosis | AdverseOutcome | Agnes Aggy (send email) | Under development: Not open for comment. Do not cite | |
Energy deposition leading to population decline via DNA oxidation and follicular atresia | AdverseOutcome | Allie Always (send email) | Under development: Not open for comment. Do not cite | |
Energy deposition leading to population decline via DNA oxidation and oocyte apoptosis | AdverseOutcome | Agnes Aggy (send email) | Under development: Not open for comment. Do not cite | |
Deposition of energy leads to reduced cocoon hatchability | AdverseOutcome | Allie Always (send email) | Under development: Not open for comment. Do not cite | |
OAT1 inhibition | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Under Development: Contributions and Comments Welcome | |
Cox1 inhibition renal failure | AdverseOutcome | Agnes Aggy (send email) | Under Development: Contributions and Comments Welcome | |
5-HTT block to population decline | AdverseOutcome | Agnes Aggy (send email) | Under Development: Contributions and Comments Welcome | |
5-HTT leading to population decline | AdverseOutcome | Allie Always (send email) | Under Development: Contributions and Comments Welcome | |
Inhibition of CYP7B leads to decreased locomotor activity | AdverseOutcome | Brendan Ferreri-Hanberry (send email) | Not under active development | |
Inhibition of CYP7B activity leads to decreased sexual behavior | AdverseOutcome | Arthur Author (send email) | Not under active development | |
PPARa Agonism Impairs Fish Reproduction | AdverseOutcome | Arthur Author (send email) | Open for citation & comment |
Taxonomic Applicability
Term | Scientific Term | Evidence | Link |
---|---|---|---|
all species | all species | High | NCBI |
Life Stages
Life stage | Evidence |
---|---|
All life stages | Not Specified |
Sex Applicability
Term | Evidence |
---|---|
Unspecific | Not Specified |
Key Event Description
A population can be defined as a group of interbreeding organisms, all of the same species, occupying a specific space during a specific time (Vandermeer and Goldberg 2003, Gotelli 2008). As the population is the biological level of organization that is often the focus of ecological risk assessments, population growth rate (and hence population size over time) is important to consider within the context of applied conservation practices.
If N is the size of the population and t is time, then the population growth rate (dN/dt) is proportional to the instantaneous rate of increase, r, which measures the per capita rate of population increase over a short time interval. Therefore, r, is a difference between the instantaneous birth rate (number of births per individual per unit of time; b) and the instantaneous death rate (number of deaths per individual per unit of time; d) [Equation 1]. Because r is an instantaneous rate, its units can be changed via division. For example, as there are 24 hours in a day, an r of 24 individuals/(individual x day) is equal to an r of 1 individual/(individual/hour) (Caswell 2001, Vandermeer and Goldberg 2003, Gotelli 2008, Murray and Sandercock 2020).
Equation 1: r = b - d
This key event refers to scenarios where r < 0 (instantaneous death rate exceeds instantaneous birth rate).
Examining r in the context of population growth rate:
● A population will decrease to extinction when the instantaneous death rate exceeds the instantaneous birth rate (r < 0).
● The smaller the value of r below 1, the faster the population will decrease to zero.
● A population will increase when resources are available and the instantaneous birth rate exceeds the instantaneous death rate (r > 0)
● The larger the value that r exceeds 1, the faster the population can increase over time
● A population will neither increase or decrease when the population growth rate equals 0 (either due to N = 0, or if the per capita birth and death rates are exactly balanced). For example, the per capita birth and death rates could become exactly balanced due to density dependence and/or to the effect of a stressor that reduces survival and/or reproduction (Caswell 2001, Vandermeer and Goldberg 2003, Gotelli 2008, Murray and Sandercock 2020).
Effects incurred on a population from a chemical or non-chemical stressor could have an impact directly upon birth rate (reproduction) and/or death rate (survival), thereby causing a decline in population growth rate.
● Example of direct effect on r: Exposure to 17b-trenbolone reduced reproduction (i.e., reduced b) in the fathead minnow over 21 days at water concentrations ranging from 0.0015 to about 41 mg/L (Ankley et al. 2001; Miller and Ankley 2004).
Alternatively, a stressor could indirectly impact survival and/or reproduction.
● Example of indirect effect on r: Exposure of non-sexually differentiated early life stage fathead minnow to the fungicide prochloraz has been shown to produce male-biased sex ratios based on gonad differentiation, and resulted in projected change in population growth rate (decrease in reproduction due to a decrease in females and thus recruitment) using a population model. (Holbech et al., 2012; Miller et al. 2022)
Density dependence can be an important consideration:
● The effect of density dependence depends upon the quantity of resources present within a landscape. A change in available resources could increase or decrease the effect of density dependence and therefore cause a change in population growth rate via indirectly impacting survival and/or reproduction.
● This concept could be thought of in terms of community level interactions whereby one species is not impacted but a competitor species is impacted by a chemical stressor resulting in a greater availability of resources for the unimpacted species. In this scenario, the impacted species would experience a decline in population growth rate. The unimpacted species would experience an increase in population growth rate (due to a smaller density dependent effect upon population growth rate for that species).
Closed versus open systems:
● The above discussion relates to closed systems (there is no movement of individuals between population sites) and thus a declining population growth rate cannot be augmented by immigration.
● When individuals depart (emigrate out of a population) the loss will diminish population growth rate.
Population growth rate applies to all organisms, both sexes, and all life stages.
How It Is Measured or Detected
Population growth rate (instantaneous growth rate) can be measured by sampling a population over an interval of time (i.e. from time t = 0 to time t = 1). The interval of time should be selected to correspond to the life history of the species of interest (i.e. will be different for rapidly growing versus slow growing populations). The population growth rate, r, can be determined by taking the difference (subtracting) between the initial population size, Nt=0 (population size at time t=0), and the population size at the end of the interval, Nt=1 (population size at time t = 1), and then subsequently dividing by the initial population size.
Equation 2: r = (Nt=1 - Nt=0) / Nt=0
The diversity of forms, sizes, and life histories among species has led to the development of a vast number of field techniques for estimation of population size and thus population growth over time (Bookhout 1994, McComb et al. 2021).
● For stationary species an observational strategy may involve dividing a habitat into units. After setting up the units, samples are performed throughout the habitat at a select number of units (determined using a statistical sampling design) over a time interval (at time t = 0 and again at time t = 1), and the total number of organisms within each unit are counted. The numbers recorded are assumed to be representative for the habitat overall, and can be used to estimate the population growth rate within the entire habitat over the time interval.
● For species that are mobile throughout a large range, a strategy such as using a mark-recapture method may be employed (i.e. tags, bands, transmitters) to determine a count over a time interval (at time = 0 and again at time =1).
Population growth rate can also be estimated using mathematical model constructs (for example, ranging from simple differential equations to complex age or stage structured matrix projection models and individual based modeling approaches), and may assume a linear or nonlinear population increase over time (Caswell 2001, Vandermeer and Goldberg 2003, Gotelli 2008, Murray and Sandercock 2020). The AOP framework can be used to support the translation of pathway-specific mechanistic data into responses relevant to population models and output from the population models, such as changing (declining) population growth rate, can be used to assess and manage risks of chemicals (Kramer et al. 2011). As such, this translational capability can increase the capacity and efficiency of safety assessments both for single chemicals and chemical mixtures (Kramer et al. 2011).
Some examples of modeling constructs used to investigate population growth rate:
● A modeling construct could be based upon laboratory toxicity tests to determine effect(s) that are then linked to the population model and used to estimate decline in population growth rate. Miller et al. (2007) used concentration–response data from short term reproductive assays with fathead minnow (Pimephales promelas) exposed to endocrine disrupting chemicals in combination with a population model to examine projected alterations in population growth rate.
● A model construct could be based upon a combination of effects-based monitoring at field sites (informed by an AOP) and a population model. Miller et al. (2015) applied a population model informed by an AOP to project declines in population growth rate for white suckers (Catostomus commersoni) using observed changes in sex steroid synthesis in fish exposed to a complex pulp and paper mill effluent in Jackfish Bay, Ontario, Canada. Furthermore, a model construct could be comprised of a series of quantitative models using KERs that culminates in the estimation of change (decline) in population growth rate.
● A quantitative adverse outcome pathway (qAOP) has been defined as a mathematical construct that models the dose–response or response–response relationships of all KERs described in an AOP (Conolly et al. 2017, Perkins et al. 2019). Conolly et al. (2017) developed a qAOP using data generated with the aromatase inhibitor fadrozole as a stressor and then used it to predict potential population‐level impacts (including decline in population growth rate). The qAOP modeled aromatase inhibition (the molecular initiating event) leading to reproductive dysfunction in fathead minnow (Pimephales promelas) using 3 computational models: a hypothalamus–pituitary–gonadal axis model (based on ordinary differential equations) of aromatase inhibition leading to decreased vitellogenin production (Cheng et al. 2016), a stochastic model of oocyte growth dynamics relating vitellogenin levels to clutch size and spawning intervals (Watanabe et al. 2016), and a population model (Miller et al. 2007).
● Dynamic energy budget (DEB) models offer a methodology that reverse engineers stressor effects on growth, reproduction, and/or survival into modular characterizations related to the acquisition and processing of energy resources (Nisbet et al. 2000, Nisbet et al. 2011). Murphy et al. (2018) developed a conceptual model to link DEB and AOP models by interpreting AOP key events as measures of damage-inducing processes affecting DEB variables and rates.
● Endogenous Lifecycle Models (ELMs), capture the endogenous lifecycle processes of growth, development, survival, and reproduction and integrate these to estimate and predict expected fitness (Etterson and Ankley, 2021). AOPs can be used to inform ELMs of effects of chemical stressors on the vital rates that determine fitness, and to decide what hierarchical models of endogenous systems should be included within an ELM (Etterson and Ankley, 2021).
Domain of Applicability
Consideration of population size and changes in population size over time is potentially relevant to all living organisms.
Regulatory Significance of the Adverse Outcome
Maintenance of sustainable fish and wildlife populations (i.e., adequate to ensure long-term delivery of valued ecosystem services) is a widely accepted regulatory goal upon which risk assessments and risk management decisions are based.
References
- Ankley GT, Jensen KM, Makynen EA, Kahl MD, Korte JJ, Hornung MW, Henry TR, Denny JS, Leino RL, Wilson VS, Cardon MD, Hartig PC, Gray LE. 2003. Effects of the androgenic growth promoter 17b-trenbolone on fecundity and reproductive endocrinology of the fathead minnow. Environ. Toxicol. Chem. 22: 1350–1360.
- Bookhout TA. 1994. Research and management techniques for wildlife and habitats. The Wildlife Society, Bethesda, Maryland. 740 pp.
- Caswell H. 2001. Matrix Population Models. Sinauer Associates, Inc., Sunderland, MA, USA
- Cheng WY, Zhang Q, Schroeder A, Villeneuve DL, Ankley GT, Conolly R. 2016. Computational modeling of plasma vitellogenin alterations in response to aromatase inhibition in fathead minnows. Toxicol Sci 154: 78–89.
- Conolly RB, Ankley GT, Cheng W-Y, Mayo ML, Miller DH, Perkins EJ, Villeneuve DL, Watanabe KH. 2017. Quantitative adverse outcome pathways and their application to predictive toxicology. Environ. Sci. Technol. 51: 4661-4672.
- Etterson MA, Ankley GT. 2021. Endogenous Lifecycle Models for Chemical Risk Assessment. Environ. Sci. Technol. 55: 15596-15608.
- Gotelli NJ, 2008. A Primer of Ecology. Sinauer Associates, Inc., Sunderland, MA, USA.
- Holbech H, Kinnberg KL, Brande-Lavridsen N, Bjerregaard P, Petersen GI, Norrgren L, Orn S, Braunbeck T, Baumann L, Bomke C, Dorgerloh M, Bruns E, Ruehl-Fehlert C, Green JW, Springer TA, Gourmelon A. 2012 Comparison of zebrafish (Danio rerio) and fathead minnow (Pimephales promelas) as test species in the Fish Sexual Development Test (FSDT). Comp. Biochem. Physiol. C Toxicol. Pharmacol. 155: 407–415.
- Kramer VJ, Etterson MA, Hecker M, Murphy CA, Roesijadi G, Spade DJ, Stromberg JA, Wang M, Ankley GT. 2011. Adverse outcome pathways and risk assessment: Bridging to population level effects. Environ. Toxicol. Chem. 30, 64-76.
- McComb B, Zuckerberg B, Vesely D, Jordan C. 2021. Monitoring Animal Populations and their Habitats: A Practitioner's Guide. Pressbooks, Oregon State University, Corvallis, OR Version 1.13, 296 pp.
- Miller DH, Villeneuve DL, Santana Rodriguez KJ, Ankley GT. 2022. A multidimensional matrix model for predicting the effect of male biased sex ratios on fish populations. Environmental Toxicology and Chemistry 41(4): 1066-1077.
- Miller DH, Tietge JE, McMaster ME, Munkittrick KR, Xia X, Griesmer DA, Ankley GT. 2015. Linking mechanistic toxicology to population models in forecasting recovery from chemical stress: A case study from Jackfish Bay, Ontario, Canada. Environmental Toxicology and Chemistry 34(7): 1623-1633.
- Miller DH, Jensen KM, Villeneuve DE, Kahl MD, Makynen EA, Durhan EJ, Ankley GT. 2007. Linkage of biochemical responses to population-level effects: A case study with vitellogenin in the fathead minnow (Pimephales promelas). Environ Toxicol Chem 26: 521–527.
- Miller DH, Ankley GT. 2004. Modeling impacts on populations: Fathead minnow (Pimephales promelas) exposure to the endocrine disruptor 17b-trenbolone as a case study. Ecotox Environ Saf 59: 1–9.
- Murphy CA, Nisbet RM, Antczak P, Garcia-Reyero N, Gergs A, Lika K, Mathews T, Muller EB, Nacci D, Peace A, Remien CH, Schultz IR, Stevenson LM, Watanabe KH. 2018. Incorporating suborganismal processes into dynamic energy budget models for ecological risk assessment. Integrated Environmental Assessment and Management 14(5): 615–624.
- Murray DL, Sandercock BK (editors). 2020. Population ecology in practice. Wiley-Blackwell, Oxford UK, 448 pp.
- Nisbet RM, Jusup M, Klanjscek T, Pecquerie L. 2011. Integrating dynamic energy budget (DEB) theory with traditional bioenergetic models. The Journal of Experimental Biology 215: 892-902.
- Nisbet RM, Muller EB, Lika K, Kooijman SALM. 2000. From molecules to ecosystems through dynamic energy budgets. J Anim Ecol 69: 913–926.
- Perkins EJ, Ashauer R, Burgoon L, Conolly R, Landesmann B,, Mackay C, Murphy CA, Pollesch N, Wheeler JR, Zupanic A, Scholzk S. 2019. Building and applying quantitative adverse outcome pathway models for chemical hazard and risk assessment. Environmental Toxicology and Chemistry 38(9): 1850–1865.
- Vandermeer JH, Goldberg DE. 2003. Population ecology: first principles. Princeton University Press, Princeton NJ, 304 pp.
- Villeneuve DL, Crump D, Garcia-Reyero N, Hecker M, Hutchinson TH, LaLone CA, Landesmann B, Lattieri T, Munn S, Nepelska M, Ottinger MA, Vergauwen L, Whelan M. Adverse outcome pathway (AOP) development 1: Strategies and principles. Toxicol Sci. 2014: 142:312–320
- Watanabe KH, Mayo M, Jensen KM, Villeneuve DL, Ankley GT, Perkins EJ. 2016. Predicting fecundity of fathead minnows (Pimephales promelas) exposed to endocrine‐disrupting chemicals using a MATLAB(R)‐based model of oocyte growth dynamics. PLoS One 11: e0146594.