42461-84-7MGCCHNLNRBULBU-QGLAHWQJSA-NMGCCHNLNRBULBU-QGLAHWQJSA-N
Flunixin meglumineDTXSID104558422071-15-4DKYWVDODHFEZIM-UHFFFAOYNA-NDKYWVDODHFEZIM-UHFFFAOYSA-N
KetoprofenBenzeneacetic acid, 3-benzoyl-α-methyl-
(.+-.)-2-(3-Benzoylphenyl)propionic acid
(.+-.)-3-Benzoyl-α-methylbenzeneacetic acid
(.+-.)-Ketoprofen
(.+-.)-m-Benzoylhydratropic acid
(RS)-Ketoprofen
2-(3-Benzoylphenyl)propanoic acid
2-(3-Benzoylphenyl)propionic acid
2-(m-Benzoylphenyl)propionic acid
3-Benzoylhydratropic acid
3-Benzoyl-α-methylbenzeneacetic acid
Alrheumat
Alrheumun
Bi-profenid
Capisten
Hydratropic acid, m-benzoyl-
Kefenid
Ketonal
Ketoprofene
ketoprofeno
Ketopron
Ketoprophen
Ketorin
m-Benzoylhydratropic acid
Menamin
Meprofen
Orugesic
Oruvail
Oscorel
Profenid
PROPIONIC ACID, 2-(3-BENZOYLPHENYL)-
Racemic ketoprofen
Rhofenid
α-(3-Benzoylphenyl)propionic acid
DTXSID602077115307-79-6KPHWPUGNDIVLNH-UHFFFAOYSA-MKPHWPUGNDIVLNH-UHFFFAOYSA-M
Diclofenac sodiumBenzeneacetic acid, 2-[(2,6-dichlorophenyl)amino]-, monosodium salt
[2-[(2,6-dichlorophenyl)amino]phenyl]acetate de sodium
[2-[(2,6-diclorofenil)amino]fenil]acetato de sodio
[o-(2,6-Dichloroanilino)phenyl]acetic acid sodium salt
{2-[(2,6-Dichlorophenyl)amino]phenyl}acetate de sodium
2-(2,6-Dichloroanilino)phenylacetic acid sodium salt
2-[(2,6-Dichlorophenyl)amino]benzene acetic acid monosodium salt
Acetic acid, [o-(2,6-dichloroanilino)phenyl]-, monosodium salt
Allvoran
Assaren
Benfofen
Benzeneacetic acid, 2-[(2,6-dichlorophenyl)amino]-, sodium salt (1:1)
Cataflam
Delphimix
Diacron
Dichronic
Diclobene
Diclobenin
Diclodyn
Diclofen SR 100
Diclofenac sodium salt
Diclofenac-Na Emulgel
Diclofenacsodium Emulgel
Diclokalium
Diclophenac sodium
Diclo-Phlogont
Diclo-Puren
Diclord
Diclorep
Dicloreum
Diklovit
Dolobasan
Duravolten
Dyloject
Effekton
Evofenac
Feloran
Fortfen
Hyanalgese D
Inflaban
Kriplex
N-(2,6-Dichlorophenyl)-o-aminophenylacetic acid sodium salt
Natrium-[2-[(2,6-dichlorphenyl)amino]phenyl]acetat
Neriodin
Novapirina
Orthofen
Orthophen
Primofenac
Profenac
Prophenatin
Rhumalgan
sodium [2-[(2,6-dichlorophenyl)amino]phenyl]acetate
Sodium [o-(2,6-dichloroanilino)phenyl]acetate
Sodium 2-(2,6-dichloroanilino)-phenyl-acetate
Sodium diclofenac
Sorelmon
Tsudohmin
Valetan
Voltaren
Voltaren Ophtha
Voltaren Ophtha CD
Voltarol
Voveran
DTXSID3037208637-07-0KNHUKKLJHYUCFP-UHFFFAOYSA-NKNHUKKLJHYUCFP-UHFFFAOYSA-N
Clofibrateethyl-p-chlorophenoxyisobutyrate
Propanoic acid, 2-(4-chlorophenoxy)-2-methyl-, ethyl ester
2-(p-Chlorophenoxy)-2-methylpropionic acid ethyl ester
Abitrate
Amotril
Anparton
Arteriosan
Artevil
Ateculon
Ateriosan
Atheropront
Atromid S
Atromidin
Azionyl
Bioscleran
Cartagyl
Claripex
Claripex CPIB
Clobren SF
Clofibrat
clofibrato
Clofinit
Ethyl (p-chlorophenoxy) isobutyrate
Ethyl 2-(4-chlorophenoxy)-2-methylpropionate
Ethyl 2-(4-chlorophenoxy)isobutyrate
Ethyl 2-(p-chlorophenoxy)-2-methylpropionate
Ethyl 2-(p-chlorophenoxy)isobutyrate
Ethyl clofibrate
Ethyl p-chlorophenoxyisobutyrate
Ethyl α-(4-chlorophenoxy)isobutyrate
Ethyl α-(4-chlorophenoxy)-α-methylpropionate
Ethyl α-(p-chlorophenoxy)isobutyrate
Ethyl α-(p-chlorophenoxy)-α-methylpropionate
Hyclorate
Lipavil
Lipavlon
Lipomid
Liprinal
Miscleron
Misclerone
Neo-Atromid
Normolipol
NSC 79389
p-Chlorophenoxyisobutyric acid ethyl ester
Propionic acid, 2-(p-chlorophenoxy)-2-methyl-, ethyl ester
Recolip
Regelan
Serotinex
Sklerepmexe
Sklerolip
Skleromexe
Sklero-Tablinene
Ticlobran
Xyduril
DTXSID302033653-86-1CGIGDMFJXJATDK-UHFFFAOYSA-NCGIGDMFJXJATDK-UHFFFAOYSA-N
1-(p-Chlorobenzoyl)-5-methoxy-2-methyl-Indole-3-acetic acid1H-Indole-3-acetic acid, 1-(4-chlorobenzoyl)-5-methoxy-2-methyl-
[1-(4-Chlorobenzoyl)-5-methoxy-2-methyl-1H-indol-3-yl]acetic acid
1-(4-Chlorobenzoyl)-2-methyl-5-methoxyindole-3-acetic acid
1-(4-Chlorobenzoyl)-5-methoxy-2-methyl-1H-indole-3-acetic acid
1-(4-Chlorobenzoyl)-5-methoxy-2-methylindole-3-acetic acid
1-(p-Chlorobenzoyl)-2-methyl-5-methoxy-3-indolylacetic acid
1-(p-Chlorobenzoyl)-2-methyl-5-methoxyindole-3-acetic acid
1-(p-Chlorobenzoyl)-5-methoxy-2-methyl-3-indolylacetic acid
1-(p-Chlorobenzoyl)-5-methoxy-2-methylindole-3-acetic acid
Artracin
Artrinovo
Artrivia
Bonidin
Bonidon Gel
Chibro-Amuno
Chrono-Indicid
Chrono-Indocid 75
Confortid
Dolcidium
Dolcidium PL
Dolovin
Durametacin
Elmetacin
Idomethine
Imbrilon
Indacin
Indocid
Indocin
Indocollyre
Indole-3-acetic acid, 1-(p-chlorobenzoyl)-5-methoxy-2-methyl-
Indomecol
Indomed
Indomee
indometacin
indometacina
Indometacine
Indomethacine
Indomethine
Indomod
Indonol
Indo-Phlogont
Indoptic
Indoptol
Indo-Rectolmin
Indorektal
IndoRich
Indo-Tablinen
Indoxen
Inflazon
Infrocin
Innamit
Inteban
Inteban SP
Metacen
Metartril
Methazine
Metindol
Mezolin
Mikametan
Mobilan
N-(p-Chlorobenzoyl)-2-methyl-5-methoxy-3-indolylacetic acid
NSC 77541
Reumacide
Rheumacin LA
Sadoreum
Vital Vitacid
α-[1-(p-Chlorobenzoyl)-2-methyl-5-methoxy-3-indolyl]acetic acid
DTXSID902074015687-27-1HEFNNWSXXWATRW-UHFFFAOYNA-NHEFNNWSXXWATRW-UHFFFAOYSA-N
IbuprofenBenzeneacetic acid, α-methyl-4-(2-methylpropyl)-
(.+-.)-2-(p-Isobutylphenyl)propionic acid
(.+-.)-Ibuprofen
(.+-.)-Ibuprophen
(.+-.)-α-Methyl-4-(2-methylpropyl)benzeneacetic acid
(4-Isobutylphenyl)-α-methylacetic acid
(RS)-Ibuprofen
2-(4-Isobutylphenyl)propanoic acid
2-(4'-Isobutylphenyl)propionic acid
2-(4-Isobutylphenyl)propionic acid
2-(p-Isobutylphenyl)propionic acid
4-Isobutylhydratropic acid
4-Isobutyl-α-methylphenylacetic acid
Actiprofen
Algi-Flanderil
Algiflex
Algofen
Amibufen
Anflagen
Antarene
Antiflam
Apo-Ibuprofen
Apsifen
Artofen
Balkaprofen
Betaprofen
Brufanic
Brufen Retard
Bruflam
Brufort
Buburone
Buluofen
Butacortelone
Butylenin
Codral Period Pain
Combiflam
Dansida
Dentigoa
Dibufen
dl-Ibuprofen
Dolgirid
Dolmaral
Dolocyl
Dolo-Dolgit
Dolofen
Dolofen F
Dolomax
Donjust B
Doretrim
Dorival
Easifon
Epobron
Femadon
Fenspan
Gynofug
Haltran
Hydratropic acid, p-isobutyl-
Ibosure
Ibu-Attritin
Ibuflamar
Ibugesic
Ibuleve
Ibulgan
Ibumetin
Ibupirac
Ibupril
Ibuprocin
Ibuprofene
ibuprofeno
Ibuprohm
Ibu-slow
Ibu-Tab
Inabrin
Iprogel
Lamidon
Librofem
Lidifen
Mensoton
Motrin IB
Mynosedin
Nagifen-D
Napacetin
Nobafon
Nobfelon
Noritis
Novogent
Novoprofen
NSC 256857
Nurofen
Optifen
Opturem
Ostarin
Ostofen
p-(2-Methylpropyl)-α-methylphenylacetic acid
Paduden
Panafen
Pantrop
Paxofen
Pediaprofen
Perofen
PHENYLACETIC ACID, 2-METHYL-4-(2-METHYLPROPYL)-
p-Isobutyl-2-phenylpropionic acid
p-Isobutylhydratropic acid
Proartinal
Proflex
Prontalgin
Quadrax
Ranofen
Recidol
Relcofen
Roidenin
Seclodin
Suspren
Syntofene
Tabalon
Tabalon 400
Tatanal
Trendar
Unipron
Uprofen
α-(4-Isobutylphenyl)propionic acid
α-Methyl-4-(2-methylpropyl)benzeneacetic acid
DTXSID502073271125-38-7ZRVUJXDFFKFLMG-UHFFFAOYSA-NZRVUJXDFFKFLMG-UHFFFAOYSA-N
Meloxicam2H-1,2-Benzothiazine-3-carboxamide, 4-hydroxy-2-methyl-N-(5-methyl-2-thiazolyl)-, 1,1-dioxide
Coxflam
Melonex
Metacam
Mobicox
Movalis
Revmoksikam
DTXSID1020803169590-42-5RZEKVGVHFLEQIL-UHFFFAOYSA-NRZEKVGVHFLEQIL-UHFFFAOYSA-N
CelecoxibBenzenesulfonamide, 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-
4-[5-(4-Methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide
Celebra
Celebrex
Celecox
Celocoxib
DTXSID002277751803-78-2HYWYRSMBCFDLJT-UHFFFAOYSA-NHYWYRSMBCFDLJT-UHFFFAOYSA-N
NimesulideMethanesulfonamide, N-(4-nitro-2-phenoxyphenyl)-
2-Phenoxy-4-nitromethanesulfonanilide
4'-Nitro-2'-phenoxymethanesulfonanilide
4-Nitro-2-phenoxymethanesulfonanilide
Mesulid
N-(4-Nitro-2-phenoxyphenyl)methanesulfonamide
Nimepast
Nimesulid
nimesulida
Nimulid
Nise*Gel
Nisulid
Orthobid
Sulidene
DTXSID303725050-33-9VYMDGNCVAMGZFE-UHFFFAOYSA-NVYMDGNCVAMGZFE-UHFFFAOYSA-N
4-Butyl-1,2-diphenyl-3,5-Pyrazolidinedione3,5-Pyrazolidinedione, 4-butyl-1,2-diphenyl-
1,2-Diphenyl-3,5-dioxo-4-butylpyrazolidine
1,2-Diphenyl-3,5-dioxo-4-n-butylpyrazolidine
1,2-Diphenyl-4-butyl-3,5-pyrazolidinedione
3,5-Dioxo-1,2-diphenyl-4-n-butylpyrazolidine
4-Butyl-1,2-diphenyl-3,5-dioxopyrazolidine
4-Butyl-1,2-diphenyl-3,5-pyrazolidinedione
4-Butyl-1,2-diphenylpyrazolidine-3,5-dione
4-n-Butyl-1,2-diphenyl-3,5-pyrazolidinedione
Alindor
Alkazone
Antadol
Anuspiramin
Arthrizon
Artrizin
Artropan
Benzone
Betazed
Bizolin 200
Bunetzone
Butacote
Butadion
Butadione
Butalidon
Butapirazol
Butapirazole
Butartrina
Butatron
Butazina
Butazolidin
Butazolidine
Butidiona
Diphebuzol
Diphenylbutazone
Ecobutazone
Equipalazone
Fenibutal
Fenibutazona
fenilbutazona
Fenilbutina
Fenotone
Fenylbutazon
Flexazone
Mephabutazon
NSC 25134
Phebuzine
Phen-Buta
Phenylbutazon
Pirarreumol B
Pyrabutol
Reumazin
Reumuzol
Robizone
Shigrodin
Tencodyne
Tevcodyne
Ticinil
Todalgil
Zolaphen
Alkabutazona
Alqoverin
Anerval
Anpuzone
Artrizone
Azobutyl
Bizolin
BRN 0290080
Buta phen
Butacompren
Butadiona
Butadionum
Butagesic
Butalgina
Butaluy
Butapyrazole
Butarecbon
Butartril
Butazona
Butiwas-simple
Butylpyrin
Buvetzone
Chembutazone
Digibutina
Diossidone
3,5-Dioxe-4 buty-1, diphenyl-pyrazolidine
3,5-Dioxo-1,2-diphenyl-4-n-butyl-pyrazolidin
1,2-Diphenyl-4-butyl-3,5-dioxopyrazolidine
EINECS 200-029-0
Elmedal
Equi bute
Eributazone
Exrheudon N
Febuzina
Fenartil
Fenibutasan
Fenibutol
Fenilbutine
Fenilidina
Intalbut
Intrabutazone
Intrazone
Ipsoflame
Malgesic
Mephabutazone
Merizone
Nadazone
Nadozone
NCI-C56531
Neo-zoline
Novophenyl
Phebuzin
Phen-Buta-Vet
Phenbutazol
Phenopyrine
Phenylbutaz
Phenyl-mobuzon
Phenyzone
Praecirheumin
Pyrazolidin
Rectofasa
Reumasyl
Reumazol
Reumune
Reupolar
Robizon-V
Robizone-V
Rubatone
Scanbutazone
Schemergen
Fenilbutazone
Phenylbutazonum
UNII-GN5P7K3T8S
Fenilbutazon
DTXSID902113653716-49-7PUXBGTOOZJQSKH-UHFFFAOYNA-NPUXBGTOOZJQSKH-UHFFFAOYSA-N
Carprofen9H-Carbazole-2-acetic acid, 6-chloro-α-methyl-
(dl)-6-Chloro-α-methylcarbazole-2-acetic acid
2-(6-Chlorocarbazol-2-yl)propionic acid
6-Chloro-α-methyl-9H-carbazole-2-acetic acid
6-Chloro-α-methylcarbazole-2-acetic acid
9H-Carbazole-2-acetic acid, 6-chloro-α-methyl-, (.+-.)-
Carprodyl
carprofene
carprofeno
NSC 297935
Rimadyl
Ro 20-5720/000
DTXSID1045871CHEBI:15553prostaglandin F2alphaUBERON:0002113kidneyCHEBI:26216potassium atomPR:000013427prostaglandin G/H synthase 1D001145Arrhythmias, CardiacCHEBI:27226uric acidPCO:0000001population of organismsD007511ischemiaMP:0004154renal tubular necrosisD009026mortalityGO:0004666prostaglandin-endoperoxide synthase activityMP:0003674oxidative stressPCO:0000008population growth rate2decreased3occurrence1increasedflunixin meglumine2016-11-29T18:42:272016-11-29T18:42:27Ketoprofen2016-11-29T18:42:272016-11-29T18:42:27Diclofenac sodium2016-11-29T18:42:092016-11-29T18:42:09Clofibrate2016-11-29T18:42:272016-11-29T18:42:27Indomethacin2016-11-29T18:42:172016-11-29T18:42:17Ibuprofen2016-11-29T18:42:262016-11-29T18:42:26Meloxicam2016-11-29T18:42:272016-11-29T18:42:27Celecoxib2016-11-29T18:42:262016-11-29T18:42:26nimesulide2016-11-29T18:42:272016-11-29T18:42:27Phenylbutazone2016-11-29T18:42:272016-11-29T18:42:27Carprofen2016-11-29T18:42:272016-11-29T18:42:27WikiUser_22all species8966Gyps coprotheres8967Gyps rueppelli36247Gyps fulvus36248Gyps himalayensis43491Gyps bengalensis43490Gyps africanus341451Gyps indicusWCS_9031Gallus gallusWCS_8959Aegypius monachusDecreased, Prostaglandin F2alpha concentration, plasma Decreased, Prostaglandin F2alpha concentration, plasma TissueUBERON:0001969blood plasma2016-11-29T18:41:292017-09-16T10:17:18Occurrence, renal ischemiaOccurrence, renal ischemiaTissue2016-11-29T18:41:292016-12-03T16:37:53Occurrence, renal proximal tubular necrosisOccurrence, renal proximal tubular necrosisTissueUBERON:0004134proximal tubule2016-11-29T18:41:292017-09-16T10:16:38Increased, blood potassium concentrationIncreased, blood potassium concentrationTissueUBERON:0000178blood2016-11-29T18:41:292017-09-16T10:16:39Increased MortalityIncreased MortalityPopulation<p><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Increased mortality refers to an increase in the number of individuals dying in an experimental replicate group or in a population over a specific period of time.</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="font-size:11pt"><span style="color:#212529"><span style="background-color:white">Mortality of animals is generally observed as cessation of the heart beat, breathing (gill or lung movement) and locomotory movements. Mortality is typically measured by observation. Depending on the size of the organism, instruments such as microscopes may be used. The reported metric is mostly the mortality rate: the number of deaths in a given area or period, or from a particular cause.</span></span></span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="font-size:11pt"><span style="color:#212529"><span style="background-color:white">Depending on the species and the study setup, mortality can be measured:</span></span></span></span></span></span></p>
<ul>
<li><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:11pt"><span style="color:#212529"><span style="background-color:white">in the lab by recording mortality during exposure experiments</span></span></span></span></span></li>
<li><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:11pt"><span style="color:#212529"><span style="background-color:white">in dedicated setups simulating a realistic situation such as mesocosms or drainable ponds for aquatic species</span></span></span></span></span></li>
<li><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:11pt"><span style="color:#212529"><span style="background-color:white">in the field, for example by determining age structure after one capture, or by capture-mark-recapture efforts. The latter is a method commonly used in ecology to estimate an animal population's size where it is impractical to count every individual.</span></span></span></span></span></li>
</ul>
<p>All living things are susceptible to mortality.</p>
ModerateUnspecificHighAll life stagesHigh2016-11-29T18:41:242022-07-08T07:32:26Inhibition, Cyclooxygenase 1 activityInhibition, Cyclooxygenase 1 activityMolecular2016-11-29T18:41:292016-12-03T16:37:53Occurrence, cardiac arrhythmiaOccurrence, cardiac arrhythmiaOrganUBERON:0000948heart2016-11-29T18:41:292017-09-16T10:17:22Increased, Oxidative StressIncreased, Oxidative StressMolecularCL:0000255eukaryotic cell2016-11-29T18:41:292022-02-03T14:20:13Increased, blood uric acid concentrationIncreased, blood uric acid concentrationTissueUBERON:0000178blood2016-11-29T18:41:292017-09-16T10:16:38Occurrence, tophi (urate) depositionOccurrence, tophi (urate) depositionTissue2016-11-29T18:41:292016-12-03T16:37:53Decrease, Population growth rateDecrease, Population growth ratePopulation<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">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</span> <span style="color:black">assessments, population growth rate (and hence population size over time) is important to consider within the context of applied conservation practices.</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">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). </span></span></span></span></p>
<p style="margin-left:144px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Equation 1: r = b - d</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">This key event refers to scenarios where r < 0 (instantaneous death rate exceeds instantaneous birth rate).</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Examining r in the context of population growth rate:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A population will decrease to extinction when the instantaneous death rate exceeds the instantaneous birth rate (r < 0). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black"> ● The smaller the value of r below 1, the faster the population will decrease to zero. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A population will increase when resources are available and the instantaneous birth rate exceeds the instantaneous death rate (r > 0)</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black"> ● The larger the value that r exceeds 1, the faster the population can increase over time </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">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. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Alternatively, a stressor could indirectly impact survival and/or reproduction. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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)</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Density dependence can be an important consideration:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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). </span> </span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Closed versus open systems:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● When individuals depart (emigrate out of a population) the loss will diminish population growth rate. </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Population growth rate applies to all organisms, both sexes, and all life stages.</span></span></span></span></p>
<p> </p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">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, N</span><sub><span style="font-size:9pt"><span style="color:black">t=0 </span></span></sub><span style="color:black">(population size at time t=0), and the population size at the end of the interval, N</span><sub><span style="font-size:9pt"><span style="color:black">t=1 </span></span></sub><span style="color:black">(population size at time t = 1), and then subsequently dividing by the initial population size. </span></span></span></span></p>
<p style="margin-left:96px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Equation 2: r = (N</span><sub><span style="font-size:9pt"><span style="color:black">t=1 </span></span></sub><span style="color:black">- N</span><sub><span style="font-size:9pt"><span style="color:black">t=0</span></span></sub><span style="color:black">) / N</span><sub><span style="font-size:9pt"><span style="color:black">t=0</span></span></sub></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">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). </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">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). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Some examples of modeling constructs used to investigate population growth rate:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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 (<em>Pimephales promelas</em>) exposed to endocrine disrupting chemicals in combination with a population model to examine projected alterations in population growth rate. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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).</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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.</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● 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).</span></span></span></span></p>
<p> </p>
<p>Consideration of population size and changes in population size over time is potentially relevant to all living organisms.</p>
Not SpecifiedUnspecificNot SpecifiedAll life stagesHigh<ul>
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2016-11-29T18:41:242023-01-03T09:09:06af66e2e1-3e36-436a-96aa-a26aac5ce033a2adc738-82b0-4bbf-972d-686b8dc43c6a2016-11-29T18:41:362016-12-03T16:38:042bcefe2b-e063-441d-acfa-b03076a9988bffc85e99-1f68-45a9-8f83-48ee30027cc52016-11-29T18:41:362016-12-03T16:38:04d26d1d45-f22b-41b4-bf82-77e2f5d3a7d4af66e2e1-3e36-436a-96aa-a26aac5ce0332016-11-29T18:41:362016-12-03T16:38:04ffc85e99-1f68-45a9-8f83-48ee30027cc5f0e1869c-120b-487f-8bc0-4cda6adcbc4c2016-11-29T18:41:362016-12-03T16:38:04f0e1869c-120b-487f-8bc0-4cda6adcbc4c901fa7fd-da68-466d-bb89-c46019a22e4f2016-11-29T18:41:362016-12-03T16:38:04a2adc738-82b0-4bbf-972d-686b8dc43c6aaca49fa5-9f10-4252-8907-ca1714235dbc2016-11-29T18:41:362016-12-03T16:38:04aca49fa5-9f10-4252-8907-ca1714235dbc2bcefe2b-e063-441d-acfa-b03076a9988b2016-11-29T18:41:362016-12-03T16:38:042bcefe2b-e063-441d-acfa-b03076a9988bfc3dd6e0-c2f4-4281-85af-17b36c16e6502016-11-29T18:41:362016-12-03T16:38:04fc3dd6e0-c2f4-4281-85af-17b36c16e6509a25c9d3-73b3-4cca-93d3-4e2cb096283f2016-11-29T18:41:362016-12-03T16:38:049a25c9d3-73b3-4cca-93d3-4e2cb096283f2bcefe2b-e063-441d-acfa-b03076a9988b2016-11-29T18:41:362016-12-03T16:38:04fc3dd6e0-c2f4-4281-85af-17b36c16e650aca49fa5-9f10-4252-8907-ca1714235dbc2016-11-29T18:41:362016-12-03T16:38:04Cyclooxygenase 1 (COX1) inhibition leading to renal failure and mortalityCox1 inhibition renal failure<p>Kellie Fay</p>
Under Development: Contributions and Comments WelcomeUnder Development1.29<p>Increased mortality is one of the most common regulatory assessment endpoints, along with reduced growth and reduced reproduction.</p>
<p>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.</p>
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