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PFOA, PFOS, PFBA, PFBS, ADONA and GenX: Toxicological Profile for Freshwater Ecosystems

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24 June 2025

Posted:

24 June 2025

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Abstract
Per- and polyfluoroalkyl substances (PFAS) represent a diverse group of chemicals widely used in industrial and consumer products due to their unique physicochemical properties. This review critically examines the ecotoxicological profiles of six key PFAS—PFOA, PFOS, PFBA, PFBS, GenX, and ADONA—focusing on their effects on standard aquatic model organisms (Daphnia magna, Raphidocelis subcapitata, and Aliivibrio fischeri). The data highlight that legacy compounds such as PFOA and PFOS generally show greater toxicity, particularly with reproductive and growth endpoints in D. magna and growth inhibition in R. subcapitata, at lower concentrations compared to their short-chain analogues (PFBA, PFBS). GenX and ADONA, introduced as replacements for long-chain PFAS, have been the subject of far fewer studies. Available data, mainly from regulatory sources, suggest lower acute and chronic toxicity for these alternatives under standard test conditions. However, the lack of comprehensive data—especially regarding sub-lethal, chronic, and mixture effects—precludes firm conclusions about their environmental safety. The findings underscore the need for further ecotoxicological research on emerging PFAS and call for integrating bioassays with chemical analyses to better assess risks associated with PFAS mixtures in aquatic ecosystems.
Keywords: 
ecotoxicity
;  
PFAS
;  
water
Subject: 
Environmental and Earth Sciences  -   Water Science and Technology

1. Introduction

Per- and polyfluoroalkyl substances (PFASs) are a wide class of anthropogenic compounds that have been manufactured since the late 1940s . The universe of PFAS was depicted by the new OECD definition, drafted in 2021 and based on the OECD 2018 PFAS List [1]in addition to the recent non target screening studies, which renewed the previous definition [2] addressing some gaps and ambiguous descriptions. The revision's goal is not to broaden the PFAS world, but to accurately outline it and provide a reference point for all users. As a result, PFASs are defined as fluorinated substances that contain at least one fully fluorinated methyl or methylene carbon atom (without any H/Cl/Br/I atom attached to it), i.e., with a few noted exceptions, any chemicals with at least a perfluorinated methyl group (-CF2-) [1], [3]
High electronegativity, low polarizability and small size of the fluorine atoms which result in a strong C-F bond, weak intermolecular interaction, low surface energy and the formation of a sheath around the backbone structure guarantee the thermal and chemical stability, electrical inertness in addition to hydrophobic and lipophobic surfactant properties [4]. These different physicochemical features have led to PFAS being used in a wide range of industrial applications as well as consumer items. In the chemical industry, PFAS are used as processing aids in the polymerization of fluoropolymers (such as PTFE and PVDF), as wetting agents in metal plating, and as film formers in aqueous foam producing foams in fire-fighting foam (AFFFs). Significant amounts of PFAS have been used as surface protectors in textile items (raincoats, snowsuits, umbrellas, tents, and awnings), food contact material (plates, popcorn bags, pizza boxes, food containers, and non-stick cookware), upholstery, and leather products due to their water repellency and stain resistance [2], [5,6,7]
Due to their persistence and tendency to bioaccumulate, these compounds have become widespread throughout various environmental compartments, including rivers, lakes, groundwater, sediments, soils, air, and living organisms [8,9,10]. Concerns over their potential toxicity and related health risks have driven several researchers to undertake ecotoxicological studies using a range of biological models. Intergenerational research using two waterflea species (D. magna and Moina macrocopa) found that chronic exposure to both PFOA and PFOS in the parent generation resulted in substantial reductions in reproductive and population growth rates in their offspring [11]. Acute, developmental ad transgenerational toxicity on zebrafish was observed, testing single toxicity and mixtures of different compounds [12,13,14]. A 21-day reproduction test in D. magna at sub-lethal GenX concentrations resulted in substantial reductions in the number of offspring with exposure doses of 8.13 mg/L or higher [15]; similar findings were also found with sub-lethal exposure to legacy PFAS contaminants (PFOS and PFOA[16,17]
However, there is little known regarding their combined toxicity to aquatic organisms. In the present study, a single exposure of PFOA, PFOS, PFBA, PFBS to Daphnia magna, Raphidocelis subcapitata and Aliivibrio fischeri were investigated. Subsequently, the collected data were refined in order to determine the theoretically combined toxicity using the concentration addition model, as demonstrated by [18]. This calculation simulates the toxicity-shift in the replacement legacy PFAS phase by observing the toxicity pattern of a PFAS mixture in which the various components are present in variable proportions.
Historically, nearly all manufacturers utilized ammonium or sodium perfluorooctanoate (APFO and NaPFO) as processing aids in the emulsion polymerization of polytetrafluoroethylene (PTFE), perfluorinated ethylene-propylene copolymer (FEP), perfluoroalkoxy polymer (PFA), and specific fluoroelastomers; and employed ammonium perfluorononanoate (APFN) in the emulsion polymerization of polyvinylidene fluoride (PVDF) [19] . However, during the recent transition, most of the producers have developed their own alternatives: GenX from DuPont and ADONA from 3M/Dyneon [6]
GenX chemicals act as substitutes for the longer-chain PFOA, which had been phased out in the United States by 2015 after an agreement between manufacturers and the U.S. Environmental Protection Agency (EPA) under the PFOA Stewardship Program initiated in 2006. GenX chemicals are used in the production of fluoropolymers, which have several industrial uses throughout the medical, automotive, electronics, aerospace, energy, and semiconductor sectors [20]

2. Target Molecules and Model Organisms: Selection Criteria

The subject of this review is six compounds, highly significant in terms of production volumes, environmental contamination (both diffuse and point-source pollution), and toxicological concerns, supported by substantial available data. In particular, perfluorooctanoic acid (PFOA) and its sulfonic analogue perfluorooctane sulfonic acid (PFOS) were selected. PFOA began to be produced in the 1940s, initially as a by-product and later as a commercial product for various industrial applications, including non-stick coatings and fire-fighting foams. PFOS production started in the 1950s, mainly for use in fire-fighting foams, water-repellent treatments, and paper and textile coatings. Additionally, the review includes perfluorobutanoic acid (PFBA) and perfluorobutane sulfonic acid (PFBS), both of which have seen increased use since the early 2000s as replacements for long-chain PFAS compounds, following the phase-out of PFOA and PFOS due to environmental and health concerns. PFBA and PFBS, thanks to their shorter chains, have been marketed as alternatives considered to have a lower bioaccumulation potential, although their environmental persistence remains a critical issue. Finally, two other substances were considered, namely, two substitutes for long-chain PFASs (with similar industrial performance and desired lower potential for bioaccumulation and toxicity): GenX and ADONA. GenX, or hexafluoropropylene oxide dimer acid (HFPO-DA), has been produced since around 2009 as a replacement for PFOA in fluoropolymer manufacturing. ADONA, or ammonium 4,8-dioxa-3H-perfluorononanoate, has been manufactured since the early 2000s. However, recent studies have raised concerns about their environmental persistence, mobility, and possible health effects, indicating that these substitutes also warrant careful monitoring and risk assessment.
This literature review focused on gathering data on the model organisms most widely used to assess potential risks to aquatic ecosystems. The use of these organisms has been prescribed or recommended by international regulations since the 1990s. Their adoption has been facilitated by the relative simplicity of the test procedures, as well as the availability of reagents, test kits, and equipment compliant with established standards and guidelines. Specifically, the study focused on decomposers (belonging to the detritus-based food web), primary producers (at the first trophic level), and primary consumers, with the aim of defining a minimum battery of tests that could represent the aquatic ecosystem. Among decomposers, the bioluminescent bacterium A. fischeri was selected; for primary producers, the unicellular alga R. subcapitata was chosen; and for primary consumers, the cladoceran crustacean D. magna was considered. Table 1 lists the compounds considered in this review and details their acronym, CAS number, molecular formula, average molar mass and structural formula.

3. Results

The results of the critical literature review were summarized in tables, each providing information for a specific compound and a selected model organism.

3.1. Toxicity Quantified with the Crustacean Daphnia Magna

3.1.1. PFOA

Table 2 reports the main toxicological findings for PFOA; the unit of measurement was standardized and all original values expressed in mg/L.

3.1.2. PFOS

Table 3 reports the main toxicological findings for PFOS, the analogue sulfonated of PFOA; the unit of measurement was standardized and all original values expressed in mg/L.

3.1.3. PFBA

Table 4 reports the main toxicological findings for PFBA, the perfluorinated carboxylic acid with 4 carbon atoms; the unit of measurement was standardized and all original values expressed in mg/L.

3.1.4. PFBS

Table 5 reports the main toxicological findings for PFBS, the perfluorinated sulfonic acid with 4 carbon atoms; the unit of measurement was standardized and all original values expressed in mg/L.

3.1.5. Gen-X

Table 6 reports the main toxicological findings for the compound Gen-X, perfluoroether carboxylic acid derivative; the unit of measurement was standardized and all original values expressed in mg/L.

3.2. Toxicity Quantified with the Unicellular Green Alga Raphidocelis Subcapitata

3.2.1. PFOA

Table 7 reports the main toxicological findings for PFOA; the unit of measurement was standardized and all original values expressed in mg/L.

3.2.2. PFOS

Table 8 reports the main toxicological findings for PFOS; the unit of measurement was standardized and all original values expressed in mg/L.

3.2.3. PFBA

Table 9 reports the main toxicological findings for PFBA; the unit of measurement was standardized and all original values expressed in mg/L.

3.2.4. PFBS

Table 10 reports the main toxicological findings for PFBS; the unit of measurement was standardized and all original values expressed in mg/L.

3.2.5. Gen-X

Table 11 reports the main toxicological findings for Gen-X; the unit of measurement was standardized and all original values expressed in mg/L.

3.3. Toxicity Quantified with the Luminescent Bacteria Aliivibrio fischeri

3.3.1. Different Compounds

Table 12 reports the main toxicological findings for the considered molecules; the unit of measurement was standardized and all original values expressed in mg/L.
Regarding ADONA, the lack of bibliographic references led us to consult the ECHA database, specifically the substance registration dossier. Regarding acute short-term toxicity on aquatic invertebrates, exposure of D. magna for 48 hours resulted in an EC50 greater than 100 mg/L. A 21-day exposure produced an EC50 of 100 mg/L. For the alga R. subcapitata, after 96 hours of exposure, the EC50 was 100 mg/L. A 72-hour exposure led to both an EC10 and an EC50 greater than 1,000 mg/L.

3. Discussion

The results of bioassays on the aquatic model organisms: D. magna, R. subcapitata, and A. fischeri reported in the tables above provide a clear overview of the toxicological profiles of PFOA, PFOS, PFBA, PFBS, GenX, and ADONA.
For D. magna, legacy compounds (PFOA and PFOS) showed lower effect concentration values compared to the analogue short-chain molecules (PFBA, PFBS) and the newer substitutes (GenX, ADONA). In particular, after a chronic exposure, reproductive endpoints (e.g., fecundity, time to first progeny) appeared to be especially sensitive, with LOEC and NOEC values for PFOS and PFOA often in the low mg/L or even sub-mg/L range. These findings highlight the potential for significant biological effects at concentrations below normal acute thresholds. On the contrary, short-chain PFAS like PFBA and PFBS generally required higher concentrations to produce comparable responses, supporting the perception of lower bioaccumulation potential but not excluding environmental persistence concerns.
In R. subcapitata, growth inhibition data confirmed the greater toxicity of PFOS and PFOA with respect to the alternatives. PFOS, for example, exhibited EC10 values near or below 20 mg/L, while PFBA, PFBS, and GenX displayed EC50 values typically above several hundreds of mg/L. This pattern suggests a lower inherent hazard for these shorter-chain or substitute compounds in primary producers, although high variability in sensitivity across studies emphasizes the need for standardized testing protocols.
The A. fischeri assays confirmed the lower sensitivity of this assay (although it should represent the decomposers: marine luminescent bacteria are increasingly considered a controversial model), with EC50 values exceeding 500 mg/L for both PFOA and PFOS, and significantly higher for PFBS. While this may suggest a reduced acute hazard at lower concentrations, the potential for sub-lethal effects or mixture toxicity is still an open issue.
Comparing PFOA and PFOS, which belong to the class of long-chain per- and polyfluoroalkyl substances (PFAS) but differ in their functional group, this structural difference play we can a different environmental behavior and toxicological profile can be highlighted.
Based on the results of bioassays on the model organisms, PFOS generally showed greater toxicity compared to PFOA. For D. magna, chronic and reproductive endpoints showed that PFOS caused effects at lower concentrations (lower NOEC and LOEC values), suggesting a higher potential to interfere with sensitive biological processes such as reproduction. This is consistent with PFOS greater tendency for bioaccumulation and stronger binding to proteins.
In R. subcapitata, PFOS also exhibited lower EC10 and EC50 values than PFOA, indicating a stronger inhibitory effect on algal growth. This phenomenon can be correlated with the higher hydrophobicity and stronger membrane affinity of sulfonic PFASs, which can disrupt cellular processes in primary producers more effectively than carboxylate ones.
For A. fischeri, although both compounds required relatively high concentrations to produce acute luminescence inhibition, PFOS typically presented slightly lower EC50 values compared to PFOA. This pattern, while less pronounced in bacteria, suggests the generally higher toxicity potential of sulfonic PFAS.
From a mechanistic perspective, the stronger acidic character and lower pKa of PFOS contribute to its higher persistence and bioaccumulation potential. This, combined with its stronger adsorption to sediments and biota, explains its enhanced ecotoxicological profile relative to PFOA [52] [53]
Overall, the comparison highlights that PFOS poses a higher ecological hazard than PFOA across trophic levels, supporting the recent policy actions that have prioritized the phase-out of sulfonic PFASs due to their elevated risk to aquatic ecosystems.
PFBA and PFBS represent the short-chain analogues of PFOA and PFOS, respectively, sharing a C4 perfluorinated backbone but differing in their functional groups—carboxylic for PFBA and sulfonic for PFBS. This structural variation, although subtle, influences their environmental fate and ecotoxicological profiles.
In D. magna, PFBS generally showed slightly higher toxicity than PFBA, although both compounds exhibited relatively low toxicity compared to their analogue long-chain molecules. Chronic endpoints (e.g., reproduction, growth) showed higher NOEC and LOEC values for PFBA, consistent with its greater water solubility and lower bioaccumulation potential. Although PFBS can be considered less bioaccumulable than PFOS, it showed greater capacity to cause adverse effects at comparable concentrations, likely due to the stronger acidic nature of its sulfonic group.
In R. subcapitata, both compounds required relatively high concentrations to affect algal growth, but PFBS tended to inhibit growth at lower concentrations compared to PFBA. This suggests that, as observed in long-chain PFAS, the sulfonic acid group confers greater potential for cellular interaction and disruption, even in short-chain variants.
For A. fischeri, acute toxicity tests demonstrated minimal differences between PFBA and PFBS, with both compounds showing low toxicity in terms of luminescence inhibition. This reflects the general trend that short-chain PFAS are less disrupting to bacterial processes at environmentally relevant concentrations.
Considering a mechanistic approach, the difference in functional groups explains the slightly higher ecotoxicity of PFBS: sulfonic acids tend to bind more effectively to biological surfaces and proteins compared to carboxylic acids, enhancing their interaction with aquatic organisms despite their small molecular size.
While both PFBA and PFBS are considered lower risk compared to long-chain PFAS, PFBS shows a slightly higher ecotoxicological concern. This confirms the growing attention to short-chain sulfonic PFAS in environmental monitoring and regulatory frameworks.
In contrast to the relatively well-documented toxicity profiles of traditional PFAS such as PFOA, PFOS, and their short-chain analogues, data on GenX (hexafluoropropylene oxide dimer acid, HFPO-DA) and ADONA (3H-perfluoro-3-[(3-methoxy-propoxy)propanoic acid]) are extremely scarce, particularly regarding their ecotoxicological effects on standard aquatic organisms such as D. magna, R. subcapitata, and A. fischeri. The toxicological studies presented in the scientific literature refer mainly on mammals or to marine ecosystems.
The few studies available suggest that GenX, despite being introduced as a safer alternative to long-chain PFAS, may still present a measurable toxicity. Chronic tests with D. magna and algal growth inhibition tests indicate that GenX can exert sub-lethal effects at concentrations in the low mg/L range, although its acute toxicity appears lower than that of PFOA. Likewise, effects on A. fischeri luminescence are reported only at relatively high concentrations, reinforcing the idea that acute microbial toxicity is limited.
For ADONA, the situation is even more critical: literature data are almost absent (for this reason, the ECHA registration dossiers [54]were considered in this review) providing basic toxicity information. These data show high NOEC and EC50 values (typically >100 mg/L) for D magna and R. subcapitata, suggesting low acute and chronic toxicity. However, the absence of peer-reviewed studies prevents drawing reliable assessments, and significant gaps remain regarding potential long-term effects, bioaccumulation potential, or sub-lethal impacts.
In conclusion, the lack of comprehensive ecotoxicological data for GenX and ADONA highlights a key challenge in evaluating the safety of emerging PFAS substitutes. Further studies are required to fill knowledge gaps and ensure that the adoption of these alternatives does not pose new environmental risks.

5. Conclusions

This review highlights a significant variability in the ecotoxicological profiles of the considered PFASs, including both legacy compounds and their modern substitutes. The comparison between PFOA and PFOS confirms a generally higher toxicity of the sulfonic compound at the various trophic levels (based on the tests carried out on the model organisms D. magna, R. subcapitata, and A. fischeri ) at relatively low concentrations. Likewise, among short-chain analogues, PFBS appears more toxic than PFBA, although both exhibit a reduced toxicity with respect to their analogue long-chain molecules.
Interestingly, despite having been produced (as alternatives) since the early 2000s, GenX and ADONA, which have been introduced as alternatives, are characterized by a lack of ecotoxicological data. The few studies available, mainly deriving from regulatory dossiers rather than from scientific literature, show lower levels of acute and chronic toxicity under standard testing conditions. Nevertheless, this evidence remains too scarce to support definitive conclusions about their safety for aquatic ecosystems, especially concerning sub-lethal, long-term, or multigenerational effects.
The results of this review highlight the need for comprehensive and standardized ecotoxicological investigations on emerging PFAS, including GenX and ADONA. The integration of effect-based bioassays beside chemical analyses (aimed at their quantification in the different environmental matrices) could yield to a more realistic assessment of the ecological risks posed by complex PFAS mixtures, i.e., the actual situation in surface water, soil, groundwater.

Author Contributions

Conceptualization, R.P., Mi.Me.; software, Mi.Me., S.V.; writing—original draft preparation, R.P., Mi.Me, Ma.Ma.; writing—review and editing, R.P., G.B. All authors have read and agreed to the published version of the manuscript.”

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
ADONA Ammonium 4,8-Dioxa-3H-Perfluorononanoate1
AFFF Aqueous Film-Forming Foam
APFO Ammonium Perfluorooctanoate
CAS Chemical Abstracts Service
EC Effect Concentration
FEP Fluorinated Ethylene Propylene
HFPO-DA Hexafluoropropylene Oxide Dimer Acid (Or GenX)
LC Lethal Concentration
LOEC Lowest Observed Effect Concentration
MATC Maximum Acceptable Toxicant Concentration
NaPFO Sodium Perfluorooctanoate
NOEC No Observed Effect Concentration
PFAS Per- And Polyfluoroalkyl Substances
PFBA Perfluorobutanoic Acid
PFBS Perfluorobutane Sulfonate
PFOA Perfluorooctanoic Acid
PFOS Perfluorooctane Sulfonate
PTFE Polytetrafluoroethylene
PVDF Polyvinylidene Fluoride

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Table 1. Acronym, preferred name, CAS, molecular formula and average molar mass of the molecules considered in this review (U.S. EPA ECOTOXicology Knowledgebase).
Table 1. Acronym, preferred name, CAS, molecular formula and average molar mass of the molecules considered in this review (U.S. EPA ECOTOXicology Knowledgebase).
Acronym Preferred name CAS number Molecular formula Average mass (g/mol) Structural formula
PFOA Perfluorooctanoic acid 335-67-1 C8HF15O2 414.07 Preprints 165017 i001
PFOS Perfluorooctanesulfonic acid 1763-23-1 C8HF17O3S 500.13 Preprints 165017 i002
PFBA Perfluorobutanoic acid 375-22-4 C4HF7O2 214.04 Preprints 165017 i003
PFBS Perfluorobutanesulfonic acid 375-73-5 C4HF9O3S 300.09 Preprints 165017 i004
HFPO-DA (Gen-X) Perfluoro-2-methyl-3-oxahexanoic acid
(also known as hexafluoropropylene oxide dimer acid)		 13252-13-6 C6HF11O3 330.05 Preprints 165017 i005
ADONA 4,8-Dioxa-3H-perfluorononanoic acid 919005-14-4 C7H2F12O4 378.07 Preprints 165017 i006
Table 2. Experimental findings obtained after the exposure (various time length) of D. magna to PFOA. The available endpoints were included (beside immobilization).
Table 2. Experimental findings obtained after the exposure (various time length) of D. magna to PFOA. The available endpoints were included (beside immobilization).
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
2 Intoxication Immobile EC05 182 mg/L NR - NR [21]
2 Intoxication Immobile EC10 195 mg/L NR - NR [21]
2 Intoxication Immobile EC50 67.2 mg/L 31.3 – 88.5 [22]
21 Mortality Lifespan EC10 11.12 mg/L NR - NR [23]
21 Reproduction Mean spawns per female EC10 7.02 mg/L NR - NR [23]
1 Intoxication Immobile EC50 219.87 mg/L 209.52 – 229.81 [24]
2 Intoxication Immobile EC50 211.59 mg/L 184.68 – 254.24 [24]
2 Intoxication Immobile EC50 239 mg/L 190 - 287 [21]
2 Intoxication Immobile EC50 109 mg/L NR - NR [25]
2 Intoxication Immobile EC50 476.52 mg/L 375.32 - 577.72 [11]
1 Intoxication Immobile EC50 675.05 mg/L 559.62 - 790.50 [11]
2 Intoxication Immobile EC50 223.60 mg/L 188.40 – 264.59 [22]
2 Intoxication Immobile EC50 110.7 mg/L NR - NR [26]
2 Mortality Mortality LC50 268.73 mg/L 225.67 – 313.04 [22]
2 Mortality Mortality LC50 139.0 mg/L NR - NR [26]
2 Mortality Mortality LC50 137 mg/L NR - NR [25]
2 Mortality Mortality LC50/ 120.91 mg/L NR - NR [27]
2 Mortality Mortality LC50 201.85 mg/L 134.68 - 302.50 [23]
2 Intoxication Immobile LOEC 500 mg/L NR - NR [11]
1 Intoxication Immobile LOEC 1000 mg/L NR - NR [11]
21 Growth Length LOEC 22.61 mg/L NR - NR [27]
21 Reproduction Time to first progeny LOEC 15.11 mg/L NR - NR [27]
21 Reproduction Progeny counts/numbers LOEC 10.10 mg/L NR - NR [27]
1 Intoxication Immobile LOEC 186.33 mg/L NR - NR [24]
2 Intoxication Immobile LOEC 227.74 mg/L NR - NR [24]
21 Reproduction Fecundity LOEC 0.16 mg/L NR - NR [26]
21 Reproduction Fecundity LOEC 4 mg/L NR - NR [26]
21 Reproduction Time to pregnancy/gravidity LOEC 4 mg/L NR - NR [26]
21 Reproduction Time to first progeny LOEC 4 mg/L NR - NR [26]
21 Growth Length LOEC 0.16 mg/L NR - NR [26]
21 Reproduction Time to first progeny LOEC 12.5 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers LOEC 25 mg/L NR - NR [11]
21 Growth Length LOEC 50 mg/L NR - NR [11]
21 Reproduction Fecundity LOEC 0.41 mg/L NR - NR [28]
21 Reproduction Time to first progeny LOEC 10.10 mg/L NR - NR [27]
1 Intoxication Immobile NOEC 165.63 mg/L NR - NR [24]
2 Intoxication Immobile NOEC 207.04 mg/L NR - NR [24]
21 Growth Length NOEC 0.032 mg/L NR - NR [26]
21 Reproduction Time to pregnancy/gravidity NOEC 0.8 mg/L NR - NR [26]
21 Reproduction Fecundity NOEC 0.032 mg/L NR - NR [26]
21 Reproduction Time to first progeny NOEC 0.8 mg/L NR - NR [26]
21 Reproduction Fecundity NOEC 37.97 mg/L NR - NR [23]
21 Reproduction Fecundity NOEC 0.8 mg/L NR - NR [26]
21 Reproduction Progeny counts/numbers NOEC 37.97 mg/L NR - NR [23]
21 Reproduction Time to first progeny NOEC 37.97 mg/L NR - NR [23]
21 Reproduction Progeny counts/numbers NOEC 12.5 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers NOEC 50 mg/L NR - NR [11]
21 Reproduction Time to first progeny NOEC 6.25 mg/L NR - NR [11]
21 Growth Length NOEC 25 mg/L NR - NR [11]
21 Mortality Survival NOEC 50 mg/L NR - NR [11]
1 Intoxication Immobile NOEC 500 mg/L NR - NR [11]
2 Intoxication Immobile NOEC 250 mg/L NR - NR [11]
21 Reproduction Time to first progeny NOEC 6.71 mg/L NR - NR [27]
21 Growth Length NOEC 15.11 mg/L NR - NR [27]
21 Reproduction Progeny counts/numbers NOEC 6.71 mg/L NR - NR [27]
21 Reproduction Time to first progeny NOEC 10.10 mg/L NR - NR [27]
21 Mortality Mortality NR-ZERO 6.25 mg/L NR - NR [11]
2 Intoxication Immobile EC50 181 mg/L 166 - 198 [29]*
21 Growth Length EC50 > 88.6/ mg/L NR/ - NR/ [30]
21 Reproduction Fecundity EC50 39.6/ mg/L 36.7/ - 42.5/ [30]
1 Intoxication Immobile EC50 298 mg/L 278 - 321 [29]*
2 Intoxication Immobile EC50 480 mg/L NR - NR [31]
21 Growth Length EC50 > 88.6 mg/L NR - NR [31]
21 Reproduction Time to first progeny EC50 39.6 mg/L NR - NR [31]
1 Intoxication Immobile EC50 599 mg/L NR - NR [31]
2 Intoxication Immobile EC50 156.9 mg/L NR - NR [32]*
21 Mortality Mortality LC50 > 100 mg/L NR - NR [33]*
21 Mortality Mortality LC50/ > 88.6/ mg/L NR/ - NR/ [30]
2 Mortality Mortality LC50 226.70 mg/L NR - NR [32]
21 Reproduction Fecundity LOEC 44.2/ mg/L NR/ - NR/ [30]
21 Reproduction Time to first progeny LOEC 44.2 mg/L NR - NR [31]
2 Reproduction Progeny counts/numbers LOEC 100 mg/L NR - NR [33]
1 Reproduction Progeny counts/numbers LOEC 10 mg/L NR - NR [33]
21 Reproduction Time to first progeny LOEC 100 mg/L NR - NR [33]
21 Reproduction Progeny counts/numbers LOEC 32 mg/L NR - NR [33]
21 Growth Length LOEC 88.6/ mg/L NR/ - NR/ [30]
21 Mortality Mortality NOEC 88.6/ mg/L NR/ - NR/ [30]
21 Growth Length NOEC 44.2/ mg/L NR/ - NR/ [30]
21 Reproduction Time to first progeny NOEC 20 mg/L NR - NR [31]
21 Growth Length NOEC 44.2 mg/L NR - NR [31]
21 Mortality Survival NOEC 88.6 mg/L NR - NR [31]
21 Intoxication Immobile NOEC > 88.6 mg/L NR - NR [31]
21 Reproduction Progeny counts/numbers NOEC 20 mg/L NR - NR [31]
2 Reproduction Progeny counts/numbers NOEC 32 mg/L NR - NR [33]
1 Reproduction Progeny counts/numbers NOEC 3.2 mg/L NR - NR [33]
21 Reproduction Progeny counts/numbers NOEC 10 mg/L NR - NR [33]
21 Reproduction Time to first progeny NOEC 32 mg/L NR - NR [33]
21 Reproduction Fecundity NOEC 20.0/ mg/L NR/ - NR/ [30]
2 Intoxication Immobile NOEC 125 mg/L NR - NR [29]
1 Intoxication Immobile NOEC 125 mg/L NR - NR [29]
21 Mortality Survival NOEC > 100 mg/L NR - NR [33]
21 Mortality Survival NR NR/ mg/L 4.31/ - 88.6/ [30]
21 Reproduction Abort NR NR/ mg/L 4.31/ - 88.6/ [30]
21 Reproduction Progeny counts/numbers NR NR/ mg/L 4.31/ - 88.6/ [30]
21 Intoxication Immobile NR NR/ mg/L 4.31/ - 88.6/ [30]
(*) Values refer to CAS 3825-26-1, perfluorooctanoic acid ammonium salt.
Table 3. Experimental findings obtained after the exposure (various time length) of D. magna to PFOS. The available endpoints were included (beside immobilization).
Table 3. Experimental findings obtained after the exposure (various time length) of D. magna to PFOS. The available endpoints were included (beside immobilization).
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
1 Intoxication Immobile EC50 76.82 mg/L 62.09 - 91.56 [11]
2 Intoxication Immobile EC50 37.36 mg/L 30.72 - 43.99 [11]
2 Intoxication Immobile EC50 23.41 mg/L NR - NR [34]
2 Mortality Mortality LC50 49.27 mg/L NR - NR [34]
1 Mortality Mortality LC50 156.67 mg/L 132.21 - 179.03 [35]
2 Mortality Mortality LC50 116.52 mg/L 99.32 - 145.01 [35]
2 Intoxication Immobile LOEC 25 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers LOEC 2.5 mg/L NR - NR [11]
21 Reproduction Time to first progeny LOEC 2.5 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers LOEC 2.5 mg/L NR - NR [11]
21 Growth Length LOEC 0.008 mg/L NR - NR [34]
21 Reproduction Fecundity LOEC 0.04 mg/L NR - NR [34]
21 Reproduction Progeny counts/numbers LOEC 0.04 mg/L NR - NR [34]
21 Reproduction Fecundity LOEC 5.30 mg/L NR/ - NR/ [28]
21 Reproduction Time to pregnancy/gravidity LOEC 1 mg/L NR - NR [34]
21 Reproduction Time to first progeny LOEC 1 mg/L NR - NR [34]
1 Intoxication Immobile LOEC 50 mg/L NR - NR [11]
21 Mortality Survival NOEC 5 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers NOEC 1.25 mg/L NR - NR [11]
21 Growth Length NOEC 5 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers NOEC 1.25 mg/L NR - NR [11]
21 Reproduction Time to first progeny NOEC 1.25 mg/L NR - NR [11]
21 Reproduction Progeny counts/numbers NOEC 0.008 mg/L NR - NR [34]
21 Reproduction Time to pregnancy/gravidity NOEC 0.2 mg/L NR - NR [34]
21 Reproduction Fecundity NOEC 0.008 mg/L NR - NR [34]
2 Growth Growth rate NOEC 36/ mg/L NR/ - NR/ [36]
21 Reproduction Time to first progeny NOEC 0.2 mg/L NR - NR [34]
21 Reproduction Fecundity NOEC 0.53 mg/L NR/ - NR/ [28]
2 Intoxication Immobile NOEC 12.5 mg/L NR - NR [11]
1 Intoxication Immobile NOEC 25 mg/L NR - NR [11]
2 Mortality Mortality EC10 58.57 mg/L 12.16 – 100.56 [37]
21 Mortality Lifespan EC10 4.17 mg/L NR - NR [23]
21 Reproduction Mean spawns per female EC10 2.26 mg/L NR - NR [23]
1 Mortality Mortality EC10 90.62 mg/L 89.51 – 91.72 [37]
2 Intoxication Immobile EC50 67.2 mg/L 31.3 - 88.5 [22]
1 Intoxication Immobile EC50 193 mg/L 177 - 209 [29]
1 Mortality Mortality EC50 > 100.56 mg/L NR - NR [22]
2 Intoxication Immobile EC50 63 mg/L 58 - 69 [29]
2 Intoxication Immobile EC50 79.35 mg/L NR - NR [38]
2 Mortality Mortality EC50 67.41 mg/L 36.47 – 100.56 [37]
2 Mortality Mortality EC90 69.62 mg/L 12.15 – 100.56 [37]
1 Mortality Mortality EC90 > 100.56 mg/L NR - NR [37]
[22] N2 Mortality Mortality LC50/ 22.77 mg/L NR - NR [27]
2 Mortality Mortality LC50 78.09 mg/L 54.38 - 112.13 [23]
2 Mortality Survival LC50 130 mg/L 112 - 136 [22]
21 Mortality Mortality LC50 9.1 mg/L 7.3 - 11.5 [29]
21 Mortality Mortality LC50 42.9 mg/L 31.7 - 56.4 [22]
21 Reproduction Progeny counts/numbers LOEC 0.67 mg/L NR - NR [27]
2 Mortality Mortality LOEC 26.52 mg/L 24.86 – 27.63 [39]
21 Reproduction Time to first progeny LOEC 0.67 mg/L NR - NR [27]
21 Growth Length LOEC 1.01 mg/L NR - NR [27]
21 Reproduction Time to first progeny LOEC 0.67 mg/L NR - NR [27]
21 Mortality Mortality LOEC 26.52 mg/L 22.5 - 25.0 [39]
21 Reproduction Progeny counts/numbers LOEC 5 mg/L NR - NR [29]
21 Mortality Survival LOEC 10 mg/L NR - NR [29]
2 Intoxication Immobile LOEC 100 mg/L NR - NR [38]
21 Reproduction Progeny counts/numbers LOEC 16 mg/L NR - NR [38]
21 Reproduction Fecundity LOEC 50 mg/L NR - NR [22]
21 Mortality Survival LOEC 50 mg/L NR - NR [22]
21 Reproduction Progeny counts/numbers LOEC 50 mg/L NR - NR [22]
21 Intoxication Immobile LOEC 50 mg/L NR - NR [40]
21 Mortality Mortality MATC 18.79 mg/L NR - NR [39]
21 Reproduction Fecundity NOEC 25 mg/L NR - NR [22]
21 Mortality Mortality NOEC 5.3 mg/L 2.5 - 9.2 [22]
21 Reproduction Progeny counts/numbers NOEC 25 mg/L NR - NR [22]
21 Mortality Survival NOEC 25 mg/L NR - NR [22]
21 Intoxication Immobile NOEC 25 mg/L NR - NR [40]
2 Reproduction Progeny counts/numbers NOEC 10 mg/L NR - NR [29]
21 Reproduction Fecundity NOEC 7.43 mg/L NR - NR [23]
21 Reproduction Time to first progeny NOEC 7.43 mg/L NR - NR [23]
21 Reproduction Progeny counts/numbers NOEC 7.43 mg/L NR - NR [23]
2 Intoxication Immobile NOEC 66 mg/L NR - NR [38]
21 Reproduction Progeny counts/numbers NOEC 8 mg/L NR - NR [38]
2 Mortality Mortality NOEC 12.71 mg/L 11.2 - 11.8 [39]
21 Growth Length NOEC 0.67 mg/L NR - NR [27]
2 Intoxication Immobile NOEC 20 mg/L NR - NR [29]
1 Intoxication Immobile NOEC 100 mg/L NR - NR [29]
21 Mortality Survival NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Reproduction Abort NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Mortality Mortality NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Reproduction Abort NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Growth Length NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Reproduction Fecundity NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Reproduction Time to first progeny NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Growth Weight NOEC 12.71 mg/L 12.38 – 13.04 [39]
21 Reproduction Progeny counts/numbers NOEC 1 mg/L NR - NR [29]
2 Intoxication Immobile NOEC 0.8 mg/L 0.6 - 1.3 [22]
21 Mortality Survival NOEC 5 mg/L NR - NR [29]
21 Reproduction Time to first progeny NOEC 10 mg/L NR - NR [29]
1 Reproduction Progeny counts/numbers NOEC 10 mg/L NR - NR [29]
21 Reproduction Progeny counts/numbers NOEC 10 mg/L NR - NR [29]
2 Mortality Survival NOEC 33.1 mg/L 32.8 - 34.1 [22]
(*) Values refer to CAS 2795-39-3, potassium perfluorooctanesulfonate.
Table 4. Experimental findings obtained after the exposure (various time length) of D. magna to PFBA. The available endpoints were included (beside immobilization).
Table 4. Experimental findings obtained after the exposure (various time length) of D. magna to PFBA. The available endpoints were included (beside immobilization).
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
2 Intoxication Immobile EC05 3014 mg/L NR - NR [17]
2 Intoxication Immobile EC10 3470 mg/L NR - NR [17]
2 Intoxication Immobile EC10 > 1006 mg/L NR - NR [41]
2 Intoxication Immobile EC50 5251 mg/L 3889 - 6614 [17]
2 Intoxication Immobile EC50 > 1006 mg/L NR - NR [41]
1 Intoxication Immobile EC50 > 4280.8 mg/L NR - NR [24]
2 Intoxication Immobile EC50 > 4280.8 mg/L NR - NR [24]
2 Intoxication Immobile EC50 181.51 mg/L 0.841 - 0.856 [24]
1 Intoxication Immobile EC50 185.14 mg/L 0.858 - 0.871 [24]
2 Mortality Mortality LC50 > 1006 mg/L NR - NR [41]
1 Intoxication Immobile LOEC 192.64 mg/L NR - NR [24]
2 Intoxication Immobile LOEC 181.93 mg/L NR - NR [24]
1 Intoxication Immobile NOEC 181.93 mg/L NR - NR [24]
2 Intoxication Immobile NOEC 177.65 mg/L NR - NR [24]
2 Mortality Mortality NR-ZERO 45 mg/L NR - NR [42]
Table 5. Experimental findings obtained after the exposure (various time length) of D. magna to PFBS. The available endpoints were included (beside immobilization).
Table 5. Experimental findings obtained after the exposure (various time length) of D. magna to PFBS. The available endpoints were included (beside immobilization).
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
1 Intoxication Immobile EC50 2598.36mg/L 1754.37 - 3871.53 [43]
2 Intoxication Immobile EC50 2236.68 mg/L 1754.37 - 3871.53 [43]
2 Intoxication Immobile LOEC 1748.98 mg/L NR - NR [43]
21 Mortality Mortality LOEC 1928.06 mg/L 1766.70 – 2135.66 [44]
21 Growth Length LOEC 1022.61 mg/L 972.25 – 1096.61 [44]
21 Reproduction Fecundity LOEC 1022.61 mg/L 972.25 – 1096.61 [44]
21 Reproduction Fecundity NOEC 515.93 mg/L 487.15 – 559.10 [44]
21 Mortality Mortality NOEC 1022.61 mg/L 972.25 – 1096.61 [44]
21 Growth Length NOEC 515.93 mg/L 487.15 – 559.10 [44]
2 Intoxication Immobile NOEC 907.79 mg/L NR - NR [43]
Table 6. Experimental findings obtained after the exposure (various time length) of D. magna to Gen-X. The available endpoints were included (beside immobilization).
Table 6. Experimental findings obtained after the exposure (various time length) of D. magna to Gen-X. The available endpoints were included (beside immobilization).
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
2 Mortality Mortality EC50 > 102 mg/L NR/ - NR/ [45]
2 Mortality Mortality LC50 183.14 mg/L NR - NR [46]
2 Mortality Mortality LC50 307.70 mg/L NR - NR [46]
2 Mortality Mortality LC50 156.24 mg/L NR - NR [46]
21 Mortality Survival LOEC 8.13 mg/L NR - NR [45]
21 Mortality Mortality LOEC 16.2 mg/L NR - NR [45]
21 Mortality Survival NOEC 4.17 mg/L NR - NR [45]
21 Growth Length NOEC > 33.0 mg/L NR - NR [45]
21 Reproduction Time to first progeny NOEC > 33.0 mg/L NR - NR [45]
21 Mortality Mortality NOEC 8.13 mg/L NR - NR [45]
21 Mortality Survival NOEC > 33.0 mg/L NR - NR [45]
Table 7. Experimental findings obtained after the exposure (various time length) of R. subcapitata to PFOA. The endpoints refer to the growth rate.
Table 7. Experimental findings obtained after the exposure (various time length) of R. subcapitata to PFOA. The endpoints refer to the growth rate.
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
NR Population Abundance EC10 19.72 mg/L NR - NR [47]
NR Population Abundance EC20 35.47 mg/L NR - NR [47]
3 Population Population growth rate EC50 96.2/ mg/L 88.6/ - 113.7/ [48]
NR Population Abundance EC50 96.75 mg/L NR - NR [47]
NR Population Abundance EC90 474.67 mg/L NR - NR [47]
2 Population Population growth rate EC10 > 500 mg/L NR - NR [49]
2 Population Population growth rate EC50 > 500 mg/L NR - NR [49]
4 Population Biomass EC50/ > 100 mg/L NR - NR [31]
3 Population Biomass EC50/ > 100 mg/L NR - NR [31]
3 Population Population growth rate EC50 > 100 mg/L NR - NR [31]
4 Population Population growth rate EC50 > 100 mg/L NR - NR [31]
3 Population Population growth rate LOEC 369.67 mg/L NR - NR [31]
4 Population Population growth rate LOEC 22.70 mg/L NR - NR [31]
3 Population Biomass LOEC 369.67 mg/L NR - NR [31]
4 Population Biomass LOEC 22.70 mg/L NR - NR [31]
3 Population Population growth rate NOEC 200 mg/L NR - NR [31]
4 Population Population growth rate NOEC 6.25 mg/L NR - NR [31]
3 Population Biomass NOEC 400 mg/L NR - NR [31]
3 Population Population growth rate NOEC 180.67 mg/L NR - NR [31]
4 Population Biomass NOEC 11.37 mg/L NR - NR [31]
4 Population Population growth rate NOEC 11.37 mg/L NR - NR [31]
3 Population Biomass NOEC 180.67 mg/L NR - NR [31]
4 Population Biomass NOEC 100 mg/L NR - NR [31]
(*) Values refer to CAS 3825-26-1, perfluorooctanoic acid ammonium salt.
Table 8. Experimental findings obtained after the exposure (various time length) of R. subcapitata to PFOS. The endpoints refer to the growth rate.
Table 8. Experimental findings obtained after the exposure (various time length) of R. subcapitata to PFOS. The endpoints refer to the growth rate.
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
2 Population Population growth rate EC10 17 mg/L 13 - 23 [49]
3 Population Population growth rate EC50 35.0 mg/L 34.2 - 35.5 [48]
2 Population Population growth rate EC50 109 mg/L 80 - 149 [49]
Table 9. Experimental findings obtained after 15 minutes exposure of A. fischeri to different molecules of PFAS. The endpoint is luminescence (linked to metabolism) inhibition.
Table 9. Experimental findings obtained after 15 minutes exposure of A. fischeri to different molecules of PFAS. The endpoint is luminescence (linked to metabolism) inhibition.
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
2 Population Population growth rate EC10 62 mg/L 42 - 92 [49]
2 Population Population growth rate EC50 1830 mg/L 1500 - 2230 [49]
Table 10. Experimental findings obtained after the exposure (various time length) of R. subcapitata to PFBS. The endpoints refer to the growth rate.
Table 10. Experimental findings obtained after the exposure (various time length) of R. subcapitata to PFBS. The endpoints refer to the growth rate.
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
3 Population Population growth rate EC50 > 20250 mg/L NR - NR [50]
2 Population Population growth rate EC10 299 mg/L 117 - 767 [49]*
2 Population Population growth rate EC50 > 1000 mg/L NR - NR [49]*
* Values refer to CAS number 29420493, potassium perfluorobutanesulfonate.
Table 11. Experimental findings obtained after the exposure (various time length) of R. subcapitata to Gen-X. The endpoints refer to the growth rate.
Table 11. Experimental findings obtained after the exposure (various time length) of R. subcapitata to Gen-X. The endpoints refer to the growth rate.
Exposure time (day) Response Response measurement Parameter Value Confidence interval Ref.
3 Population Population growth rate EC50 > 107/ mg/L NR/ - NR/ [45]
3 Population Abundance EC50 > 107/ mg/L NR/ - NR/ [45]
3 Population Biomass EC50 > 107/ mg/L NR/ - NR/ [45]
3 Population Biomass NOEC > 107/ mg/L NR/ - NR/ [45]
3 Population Population growth rate NOEC > 107/ mg/L NR/ - NR/ [45]
3 Population Abundance NOEC > 107/ mg/L NR/ - NR/ [45]
Table 12. Experimental findings obtained after the exposure (various time length) of R. subcapitata to Gen-X. The endpoints refer to the growth rate.
Table 12. Experimental findings obtained after the exposure (various time length) of R. subcapitata to Gen-X. The endpoints refer to the growth rate.
CAS number Exposure time (min) Response Response measurement Parameter Value Confidence interval Ref.
335671 15 Metabolism Luminescent inhibition EC50 524 mg/L NR - NR [48]
335671 30 Metabolism Luminescent inhibition EC50 570.19 mg/L 512.86 – 627.52 [51]
1763-23-1 15 Metabolism Luminescent inhibition EC50 >500 mg/L NR - NR [48]
375-73-5 15 Metabolism Luminescent inhibition EC50 17520 mg/L NR - NR [48]
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