natgillin/translations-raw huggingface dataset:
Omdannelsen i rotteleverceller katalyseres af cytochrom P-450 enzymsystemer (Martin et al., 2005). 
The transformation in rat hepatocytes is catalyzed by cytochrom P-450 (Martin et al. 2005).
Omkring 20% af en oraldosis på100 ppm EtFOSE omdannes i hanrotter til PFOS (Thomford et al., 2002). 
About 20% of an oral dose of 100 ppm EtFOSE is in male rat metabolised to PFOS (Thomford et al. 2002).
Rottelevers microsomale fraktion nedbryder også EtFOSE via de-alkylering til PFOSE og videre til PFOSA og sluttelig til PFOS (Xu et al., 2004). 
Rat liver microsomal fractions also degrade EtFOSE by de-alkylation to FOSE and further to FOSA and finally to PFOS (Xu et al. 2004).
PFOA og PFOS binder til proteiner og akkumulerer - mere eller mindre afhængig af dyrearter og køn - i forskellige kropsvæv, hovedsagelig i blod, lever og nyrer i udsatte dyr (i alt 88% i hanrotter), men også i lunger, hjerte, hud, testikler (3% i hanrotter) og hjerne (Vanden Heuvel et al., 1992; Austin et al., 2003; Hundley et al., 2006). 
PFOA and PFOS bind to proteins and accumulate - more or less depending on animal species and sex - in various body tissues, mainly in blood, liver, and kidneys of exposed organisms (in total 88% in male rats) but also in lungs, heart, skin, testes (3% in male rats) and brain (Vanden Heuvel et al 1992; Austin et al. 2003; Hundley et al. 2006).
Akkumuleringen i fedtvæv og muskler er minimal. 
The accumulation in fat tissues and muscles is, however, minimal.
Kudo og medarbejdere (2001) undersøgte PFCA'er med forskellig kædelængde (C7 - C10) i hanrottelever. 
Kudo and co-workers (2001) studied PFCAs with different chain length (C7 - C10) in male liver.
Resultatet viste, at jo længere en kæde, desto mere af forbindelsen blev akkumuleret i leveren. 
The result showed that the longer the chain the more of the compound was accumulated in the liver.
Er PFOA en gang absorberet i kroppen, elimineres PFOA som den frie carboxylsyre hovedsageligt med urinen og i mindre omfang i fæces. 
Once absorbed in the body PFOA is eliminated as the free carboxylic acid mainly with urine and to a less extent in faeces.
Derfor er eliminering via nyrerne kritisk for detoksificering af disse stoffer (Vanden Heuvel et al., 1991). 
Thus the renal elimination is critical for detoxification (Vanden Heuvel et al. 1991).
Forskellen skyldes hovedsageligt forskellen i nyreudskillelsen, som blev markant reduceret af probenezid, hvad der tyder på, at PFOA udskilles af organiske anionbærere. 
The difference was mainly due to the difference in renal clearance, which was significantly reduced by probenezid, suggesting that PFOA is excreted by organic anion transporters.
Kastrering af hanrotter forårsagede en stigning på 14 gange i nyreudskillelsen, så den blev sammenlignelig med hunrotter. 
Castration of male rats caused a 14-fold increase in renal clearance, comparable with female rats.
Stigningen blev reduceret igen ved behandling med testosteron. 
The increase was reduced again by treatment with testosterone.
Behandling med estradiol øgede også nyreudskillelsen, og i hunrotter fik fjernelse af æggestokke nyreklaringen til at stige (Kudo et al., 2002). 
Treatment with estradiol also increased the renal clearance, and in female rats ovariectomy increased the renal clearance (Kudo et al. 2002).
Elimineringen af PFOA øges med alderen i hunrotter, men ikke i hanrotter (Hinderliter et al., 2006). 
Elimination of PFOA increases with age in female rats but not in male rats (Hinderliter et al. 2006).
Kønsforskelle i udskillelsen var mest markant for PFOA. 
The sex differences were most marked for PFOA.
Den kønsrelaterede eliminering af PFOA varierer mellem dyrearter (Hundley et al., 2006). 
The sex-related clearance of PFOA differs between animal species (Hundley et al. 2006).
I hamstre er det modsat, hvad det er i rotter. 
In hamsters it is opposite of in rats.
Han- og hunhamstre udskiller henholdsvis 99% og 58% af en dosis på 5 dage. 
Male and female hamsters excrete respectively 99% and 58% of a dose in 5 days.
I mus og kaniner var der ingen forskel for kønnene, og mus havde en langsom udskillelse som hanrotter, og kaniner havde en hurtig udskillelse som hunrotter. 
In mice and rabbits there was no sex difference, and mice had a slow excretion as male rats, and rabbits had a fast excretion as female rats.
I hunde var plasmahalveringstiden af PFOA ca. 20 dage i hanhunde og det halve i hunhunde. 
In dogs the plasma half-life of PFOA was about 20 days in males and the half in females.
The elimination halveringstider i han- og hun Cynomolgus aber for PFOA var henholdsvis 33 dage og 21 dage, og urinen var den vigtigste udskilningsrute (Butenhoff et al., 2004a). 
The elimination half-lives in male and female Cynomolgus monkeys for PFOA were 33 days and 21 days, respectively, and the urine was the major excretion route (Butenhoff et al. 2004a).
PFOS har en langsommere udskillelseshastighed, og halveringstiden af PFOS i Cynomolgus aben var ca. 200 dage (Seacat et al., 2002a; Andersen et al., 2006). 
PFOS has a slower elimination rate, and the half-life of PFOS in the Cynomolgus monkey was about 200 days (Seacat et al. 2002a; Andersen et al. 2006).
Efter en oraldosering af 8:2 FTOH blev hovedparten af det 14C-mærkede stof udskilt med fæces, og 37-55% forekom som 8:2 FTOH. 
After an oral dosing of 8:2 FTOH, the majority of the 14C-labelled substance was excreted with feces and 37-55% occurred there as 8:2 FTOH.
En mindre del (1%) blev udskilt som PFOA i urinen (Fasano et al., 2006). 
A small part (1%) was excreted as PFOA in urine (Fasano et al. 2006).
Generelt stiger toksiciteten af de testede perfluorkemikalier med længden af alkylkæden. 
Generally, the toxicity of perfluorinated chemicals tested increases with the length of the alkyl chain.
10.2.2 Påvirkninger på leveren 
10.2.2 Effects on the liver
Toksikologiske undersøgelser har vist, at leveren er det primære målorgan for POFS og PFOA, og kropsvægttab, forøget levervægt, levercellehypertrofi og ændret fedtstofskifte med reduktion i serum-cholesterol er tidlige udtryk i forsøgsdyr (Kennedy et al. 2004; Seacat et al. 2003). 
Toxicological studies have demonstrated that the liver is the primary target organ for PFOS and PFOA, and body weight loss, increased liver weight, liver cell hypertrophy and changed lipid metabolism with reduction in serum cholesterol are early responses in experimental animals (Kennedy et al. 2004; Seacat et al. 2003).
Det ikke-observerede uønskede bivirkningsniveau (NOAEL) for leverpåvirkninger i hanrotter, der blev eksponeret for PFOS i føden i 14 uger, var 5 mg/kg/dag (Seacat et al., 2003). 
The no-observed-adverse effect level (NOAEL) for liver effects in male rats exposed for PFOS during 14 weeks feeding was 5 mg/kg/d (Seacat et al. 2003).
NOAEL og LOAEL for leverpåvirkninger af PFOA i hanrotter, der blev udsat via foderet i 13 uger, var henholdsvis 0,06 og 0,64 mg/kg/d (Perkins et al., 2004). 
NOAEL and LOEAL for liver effects by PFOA in male rats exposed by feeding in 13 weeks were 0.06 and 0.64 mg/kg/d, respectively (Perkins et al. 2004).
PFDA, der har en længere kæde end PFOA, var mere toksisk i rotter, hamster, mus og marsvin (van Rafelgheim et al., 1987; Kawashima et al., 1995). 
PFDA having a longer chain than PFOA was more toxic in rat, hamster, mouse and Guinea pig (van Rafelgheim et al. 1987; Kawashima et al. 1995).
Rotter ser ud til at tolerere noget højere leverkoncentrationer af PFOS end aber, fordi NOAEL i en 6 måneder lang abeundersøgelse var 0,15 mg/kg/d (Seacat et al., 2002a). 
Rats seem to tolerate somewhat higher liver concentrations of PFOS than monkeys, because the NOAEL in a 6-month monkey study was 0.15 mg/kg/d (Seacat et al. 2002a).
PFOA med en LOAEL på 3 til 10 mg/kg/d er markant mindre levertoksisk i aber end PFOS, og angrebspunktet er forskelligt (Butenhoff, 2002a). 
PFOA with a LOAEL of 3 to 10 mg/kg/d is considerably less liver toxic in monkeys than PFOS, and the target is different (Butenhoff, 2002a).
Den eneste effekt i aben ved de anførte doser var leverforstørrelse. 
The only site of change in the monkey was liver enlargement at the doses cited.
PFOA og PFOS fremkalder hepatomegaly, som er karakteriseret ved en subcellulær proliferation af cellebestanddele som fx ”smooth endoplasmic reticulum”, mitochondrier, men mest udpræget peroxisomer. 
PFOA and PFOS induce hepatomegaly characterized by the subcellular proliferation of organelles such as smooth endoplasmic reticulum, mitochondria, but most notably peroxisomes.
De observerede ændringer i leveren kunne være resultatet af processen: ”peroxisom proliferation”, en velkendt toksikologisk mekanisme i gnavere. 
The changes observed in the liver could be the result of peroxisome proliferation, a well-known toxicological mechanism in rodents.
Den kan forårsage fedtlever, blokering af energiproduktionen (oxidative phosphorylation) i mitochondrier, og reduktion af cirkulerende skjoldbruskkirtlens hormoner. 
It may cause lipid accumulation in the liver, uncoupling of the mitochondrial oxidative phosphorylation, and reduction of thyroid hormone in circulation.
Induktion af ”peroxisom proliferation” og forekomst af godartede levertumorer er forbundet med aktivering af hormon receptoren: Peroxisome proliferator-activated receptor-a (PPARa). 
Induction of peroxisome proliferation and benign liver tumors are associated with activation of the nuclear hormone receptor - peroxisome proliferator-activated receptor-a (PPARa).
Dette er en af de tre isoformer af PPAR, som koder med separate gener og udtrykkes forskelligt i forskellige væv, og findes i alle pattedyrsarter, der er undersøgt til dags dato. 
This is one of the three isoforms of PPAR encoded by separate genes and differentially expressed in various tissues, and are found in all mammalian species examined to date.
Ligander for PPAR er i stor udstrækning blevet udviklet til behandling af forskellige sygdomme, deriblandt forstyrrelser af fedstofskiftet og sukkersyge. 
Ligands for PPARs have been widely developed for the treatment of various diseases including dyslipidemias and diabetes.
Nogle cholesterol-dæmpende præparater, opløsningsmidler og miljømæssige kemikalier er ligander for PPARa og kan forårsage ”peroxisom proliferation”, for eksempel clofibrate, ftalater, chloroform, perchlorethylen, trichlorethylen, HFC-123 og MTBE. 
Some hypolipidemic drugs, solvents and environmental chemicals are ligands for PPARa and can induce peroxisome proliferation, for example, clofibrate, phthalates, chloroform, perchloroethylene, trichloroethylene, HFC-123, and MTBE.
Mennesker udviser ikke samme tegn på leverforgiftninger af disse kemikalier, som er fundet i gnavermodeller (Peraza et al., 2006). 
Humans do not exhibit the liver toxicities by these chemicals found in rodent models (Peraza et al. 2006).
Denne PPAR-receptor er højst sandsynligt endemålet for PFOA og PFOS i både gnavere og mennesker (Vanden Heuvel et al., 2006). 
This PPAR receptor is the most likely target of PFOA and PFOS both in rodents and humans (Vanden Heuvel et al. 2006).
Polyfluorsyrer er analoge ligander til naturlige langkædede fedtsyrer og kan fortrænge dem i biokemiske processer og i receptorer som f.eks. PPARa. 
Polyfluorinated acids are analogue ligands to natural long-chain fatty acids and may displace them in biochemical processes and at receptors such as PPARa.
Aktiveringen via PFOA og PFOS er mere selektiv men mindre kraftig. 
The activation by PFOA and PFOS is more selective but less potent.
PFOA er mere egnet end PFOS ved aktiveringen af PPARa, og mus er mere modtagelige end mennesker (Takacs og Abbott, 2007). 
PFOA is more capable than PFOS in activating PPARa, and mouse is more responsive than human in test systems (Takacs and Abbott 2007).
PFOA nedsætter immunsystemets effektivitet gennem tilførsel af PPAR og forstærker den IgE-formidlede overfølsomhedsreaktion på ovalbumin, og på denne måde kan det provokere astma (Fairley et al., 2007). 
PFOA is an immunosuppressant through induction of PPARs and enhance the IgE-mediated hypersensitivity response to ovalbumin, and in this way it may provoke asthma (Fairley et al. 2007).
Perfluorcarboxylsyrer (PFCA), især PFOA, PFNA og PFDA, er meget kraftige peroxisome proliferators i gnaverlevere og påvirker mitochondriale, microsomale og cytosoliske enzymer og proteiner, der er involverede i fedtmetabolismen (Ikeda et al., 1985; Vanden Heuvel, 1996; Upham et. al., 1998; Kudo et al., 2000). 
Perfluorocarboxylates (PFCA), particularly PFOA, PFNA and PFDA, are highly potent peroxisome proliferators in rodent livers and affect mitochondrial, microsomal, and cytosolic enzymes and proteins involved in lipid metabolism (Ikeda et al. 1985; Vanden Heuvel 1996; Upham et. al. 1998; Kudo et al. 2000).
PFOS er mindre reaktiv som peroxisome proliferator i gnavere, og EtFOSE har ingen indvirkning (Berthiaume og Wallace, 2002). 
PFOS is less reactive as peroxisome proliferator in rodents, and EtFOSE has no effect (Berthiaume and Wallace 2002).
PFBA har en mindre indvirkning på indikatorer af ”peroxisom proliferation” (Ikeda et al., 1985). 
PFBA has a slighter effect on indicators of peroxisome proliferation (Ikeda et al. 1985).
Forskellene mellem dyrearter er store for PFDA. 
The differences between animal species are large for PFDA.
”Peroxisom proliferation” var størst i mus og næsten fraværende i marsvin. 
Peroxisome proliferation was greatest in mice and almost absent in Guinea pigs.
Dog var akkumuleringen af små fedtdråber i leverceller mere udtalte i hamstere og marsvin end i rotter og mus, der blev eksponeret for PFDA (van Rafelgheim et al., 1987). 
However, accumulation of lipid droplets in liver cells was more pronounced in hamsters and guinea pigs than in rats and mice exposed to PFDA (van Rafelgheim et al. 1987).
Stigning i hepatisk fedtsyre b-oxideringsaktivitet (acyl-CoA oxidase) er en biokemisk målestok af ”peroxisom proliferation”. 
Increase in hepatic fatty acid b-oxidation activity (acyl-CoA oxidase) is a biochemical measure of peroxisome proliferation.
Kudo og medarbejdere (2001) undersøgte PFCAer med forskellig kædelængde (C7 - C10) i mænds lever. 
Kudo and co-workers (2001) studied PFCAs with different chain length (C7 - C10) in male liver.
Resultatet indikerede, at leverkoncentrationen og ikke kædelængden var afgørende, men jo længere kæde, desto mere af forbindelsen blev akkumuleret i leveren. 
The result indicated that the liver concentration and not the chain length was decisive, but the longer the chain the more of the compound was accumulated in the liver.
I en in vitro test blev forskellige perfluorkemikalier testet for interferens med det leverfedtsyrebindende protein (L-FABP). 
In an in vitro test various perfluorinated chemicals were tested for interference with the liver-fatty acid binding protein (L-FABP).
Det kraftigste kemikalie var PFOS, fulgt af EtFOSA, EtFOSE og PFOA (Luebker et al., 2002). 
The most potent chemical was PFOS followed by EtFOSA, EtFOSE, and PFOA (Luebker et al. 2002).
Denne interferens kan bidrage til toksiciteten af disse kemikalier. 
This interference may contribute to the toxicity of these chemicals.
Toxicogenomic analyse er i stand til at forudsige toksicitet og patologiske reaktioner, klassificere kemikalier, og belyse toksicitetsmekanismer. 
Toxicogenomic analysis is able to predict toxicity and pathological responses, categorize chemicals, and elucidate mechanism of toxicity.
En sådan analyse viste, at PFOA og PFOS havde ”peroxisome proliferator-activated receptor-a (PPARa)” agonist-lignende indvirkninger på gener der koder for enzymer involveret i fedtstofskiftet og fedtsyrebalancen (Shipley et al., 2004; Martin et al., 2007). 
Such analysis showed that PFOA and PFOS exhibited peroxisome proliferator-activated receptor a (PPARa) agonist-like effects on genes (enzymes etc.) associated with lipid metabolism and fatty acid homeostasis (Shipley et al. 2004; Martin et al. 2007).
Det resulterer f.eks. i 
It results e.g. in
Over 500 genudtryk blev ændret markant. 
Over 500 gene expressions were significantly altered.
De fleste kategorier af inducerede opregulerede gener var de, som var involveret i transport og metabolisme af fedtstoffer, især fedtsyrer. 
The largest categories of induced up-regulated genes were those involved in transport and metabolism of lipids, particularly fatty acids.
Andre inducerede gener var involverede i cellekommunikation, binding, vækst, apoptose, veje for hormonregulering, proteolyse og peptidolyse og signaltransduktion. 
Other induced genes were involved in cell communication, adhesion, growth, apoptosis, hormone regulatory pathways, proteolysis and peptidolysis and signal transduction.
De fleste ændringer var forbundet med PPARa receptoren. 
Most changes were associated with the PPARa receptor.
10.2.5 Påvirkninger på cellemembraner 
10.2.5 Effects on cell membranes
Til trods for dens lipofobiske karakter kan PFOS og i mindre grad PFOA fordele sig i model bi-lag og cellemembraner, hvor det forårsager ændringer i membranstruktur og funktion med øget fluiditet. 
Despite of its lipophobic character PFOS and to a lesser extend PFOA can partition into model bilayers and cell membranes, where it causes changes in membrane structure and function and increased fluidity.
Interaktion med lungeoverfladestoffer, som f.eks. dipalmitoylphoshatidylcholin (DPPF), kan være en mekanisme, ved hvilken PFOS forårsager perinatal dødelighed i dyrestudier (Xie et al., 2007). 
Interaction with pulmonary surfactants such as dipalmitoylphoshatidyl choline (DPPC) may be a mechanism by which PFOS causes perinatal mortality in animal studies (Xie et al. 2007).
Orienteringen af PFAS-molekylerne i membranerne er med den funktionelle gruppe bundet til membranproteiner og med fluorkulstof halen stikkende ud som hår (Roon et al. 2006). 
The orientation in the membrane of the PFAS molecules is with the functional group end combined to membrane proteins with the fluorocarbon tails sticking out like hairs (Roon et al. 2006).
Nogle af de observerede effekter af perfluorforbindelser kan skyldes forandringer i cellemembranens fluiditet, som er en målestok for den relative mobilitet af cellemembranens phospholipid bi-lag. 
Some of the observed effects of perfluorinated compounds may be due to alterations in cell membrane fluidity, which is a measure of the relative mobility of the phospholipid bilayer of the cell membrane.
Denne selektivt permeable cellemembran danner den første barriere, som beskytter cellen fra eksogene påvirkninger. 
This selectively permeable cell membrane forms the first barrier that separates the cell from exogenous exposures.
Påvirkninger på status af gennemtrængelighed af cellemembranenen kunne spille en vigtig rolle i formidlingen af de uønskede bivirkninger af nogle forureningsstoffer. 
Effects on the permeability status of the cell membrane could play an important role in mediating the adverse effects of a number of environmental contaminants.
I nogle in vitro analysesystemer øgede PFOS - men ikke den kortere kæde PFBS og PFHxS - på en doseringsafhængig måde markant membranfluiditeten fra fiskeleukocyter og reducerede mitochondriernes membranpotential bestemt af flowcytometri (Hu et al., 2003). 
In some in vitro assay systems PFOS - but not the shorter chain PFBS and PFHxS - significantly increased in a dose-dependent manner membrane fluidity of fish leukocytes, and decreased mitochondrial membrane potential determined by flow cytometry (Hu et al. 2003).
PFOA, PFOS og EtFOSE forårsagede en lille stigning i mitochondrenes indermembran, svarende til en ændring i membranfluiditeten af et overfladeaktivt stof (Starkov og Wallace, 2002). 
PFOA, PFOS and EtFOSE caused a slight increase in the intrinsic proton leak of the mitochondrial inner membrane, which resembled a surfactant-like change in membrane fluidity (Starkov and Wallace 2002).
10.2.6 Påvirkning af energiproduktionen i mitochondrier 
10.2.6 Effect on mitochondrial bioenergetics
PFOS, PFOA, PFOSA, PFOSAA, EtFOSA, EtFOSE og EtFOSAA havde alle evnen til at forstyrre mitochondrial respiration in vitro. 
PFOS, PFOA, FOSA, FOSAA, EtFOSA, EtFOSE and EtFOSAA had the capacity in vitro to interfere with mitochondrial respiration.
PFOSA var den kraftigste hæmmer af oxidative phosphorylering (Schnellmann og Manning, 1990; Starkov og Wallace, 2002). 
FOSA was the most potent uncoupler of the oxidative phosphorylation (Schnellmann and Manning 1990; Starkov and Wallace 2002).
PFOA havde en lille påvirkning, mens PFOS og EtFOSE ingen påvirkning havde (O'Brien og Wallace, 2004). 
PFOA had a slight effect but PFOS and EtFOSE had no effect (O'Brien and Wallace 2004).
10.2.7 Påvirkning af intercellulær kommunikation 
10.2.7 Effect on intercellular communication
”Gap junction intercellular communication” (GJIC) er den vigtigste måde, som intracellulære signaler overføres på, og det er således vigtigt for normal cellevækst og cellefunktion. 
Gap junction intercellular communication (GJIC) is the major pathway of intracellular signal transduction, and it is thus important for normal cell growth and function.
Brist i denne kommunikation kan føre til fosterbeskadigelse, nervesygdom, barnløshed, sukkersyge, autoimmune forstyrrelser, cancer og andre sygdomme (Trosko et al., 1998). 
Defects in this communication may lead to teratogenesis, neuropathy, infertility, diabetes, autoimmune disorders, cancer, and other diseases (Trosko et al. 1998).
I forskellige testsystemer (in vitro og in vivo) hæmmer både PFOS, PFOSA, og PFHxS - men ikke PFBS - ”gap junction intercellular communication” dosis-afhængigt, og denne hæmning indtraf hurtigt og var reversibel (Hu et al., 2002). 
In various test systems (in vitro and in vivo) both PFOS, PFOSA, and PFHxS - but not PFBS - inhibit gap junction intercellular communication in a dose-dependent fashion, and this inhibition occurred rapidly and was reversible (Hu et al. 2002).
PFOA og PFOS kan påvirke fosterudviklingen i rotter og mus in vivo. 
PFOA and PFOS in rats and mice have showed developmental toxicity and other adverse effects in vivo.
Disse påvirkninger inkluder reduktion i fostervægt, ganespalte, anasarka, forsinket knogledannelse af skelettet og hjerteabnormiteter, så vel som dalende neonatal overlevelse efter in utero eksponering, gennemsnitligt efterfødselsvægt, ændret mælkekirteludvikling, forkortet svangerskabsperiode, ikke fuldt udviklet lunger med tung vejrtrækning og markant forsinkelse i kønslig modning. 
These effects included reduction of fetal weight, cleft palate, anasarca, delayed ossification of bones and cardiac abnormalities, as well as decreased neonatal survival following in utero exposure, reduction in mean post natal body weight, altered mammary gland development, decrease in gestation length, not fully matured lungs with laboured breathing, and significant delay in sexual maturation.
De strukturelle abnormiteter blev kun fundet i de højeste dosisgrupper (³ 30 mg/kg/d), hvor de gravide moderdyr havde markante reduktioner i vægtforøgelse og fødeindtagelse samt forøget dødelighed blandt ungerne (Case et al., 2001; Butenhoff et al., 2004b; Kennedy et al., 2004; Grasty et al., 2005; Luebker et al., 2005b; Lau et al., 2003, 2004, 2006; Thibodeaux et al., 2003; White at al., 2007). 
The structural abnormalities were only found in teratological studies at the highest dose groups (³ 30 mg/kg/d), where significant reductions of weight gain and food consumption and increase of mortality in the pups were also observed in the pregnant dams (Case et al. 2001; Butenhoff et al. 2004b; Kennedy et al. 2004; Grasty et al. 2005; Luebker et al. 2005b; Lau et al. 2003, 2004, 2006; Thibodeaux et al. 2003; White at al. 2007).
Samtidig eksponering til PFOS forstærker påvirkningerne (Fuentes et al., 2007). 
Concurrent exposure to PFOS and restraint stress enhance effects (Fuentes et al. 2007).
I et flergenerations undersøgelse af forplantningen i rotter var NOAEL-værdien for PFOS 0,1 mg/kg/d (Luebker et al., 2005a). 
In a two-generation reproduction study the NOAEL value in rats for PFOS was 0.1 mg/kg/d (Luebker et al. 2005a).
Ved dette lave moderdosisniveau reducerede the længere kædede forbindelse PFDA dog fødselsvægten markant i mus (Harris og Birnbaum, 1989). 
However, at this low maternal dose level the longer chain PFDA significantly reduced fetal body weight in mice (Harris and Birnbaum 1989).