Toxicity of PFASs to Aquatic Invertebrates: History
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Contributor:
Tingting Ma
,
Chaoran Ye
,
Tiantian Wang
,
Xiuhua Li
,
Yongming Luo

Per- and polyfluoroalkyl substances (PFASs), recognized worldwide as emerging pollutants. Its accumulation in living organisms and foods has accentuated the importance of investigations into aquatic organisms at the bottom of the food chain, as the stability and integrity of the food web as well as the population quantity and structure of the aquatic ecosystem may be affected. In aquatic ecosystems, invertebrates, planktons, and microorganisms are essential for material circulation and energy flow. As such, the toxicity and bioaccumulation effects on aquatic organisms directly determine the survival of all other animals along this food chain, making them important study species.

  • toxicity
  • aquatic environment
  • benthic organisms

1. Introduction

Since their invention in the 1930s and proliferation through the 1940s and 1950s, per- and polyfluoroalkyl substances (PFASs) have been used in a variety of industries and products, including firefighting foam, aerospace technologies, furniture, cosmetics, food packaging, and paper products [1][2][3][4]. The exact number of unique PFAS compounds is unknown, with estimates ranging from four to five thousand [1]. Strong carbon–fluoride bonds render them incredibly resistant to both environmental and metabolic degradation, earning them the name of “forever chemicals” [5]. Their production peaked at 4650 t/a in 2000–2002, after which their use was discouraged due to concerns about toxic effects on humans that led to high cholesterol, thyroid disease, delayed child development and poor maternal health, ulcerative colitis, and kidney and testicular cancer [6].
Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are contaminants commonly studied not only due to their long-term persistence, long-distance transportability, and common occurrence in various environmental matrices, biotas, and human populations, but also for their possible disruptive effects on the immune, metabolic and endocrine systems of living organisms [7][8][9][10]. In 2009, PFOS and related compounds were listed in the Stockholm Convention on Persistent Organic Pollutants (POPs) (Annex B), an international environmental treaty, signed in 2001 and effective from May 2004, aimed at eliminating or restricting the production and use of POPs. In 2017, PFOA was listed in Annex A, subjecting it to global regulation [8][11]. In October 2019, the fifteenth meeting of the POPs review committee, in Italy, recommended the inclusion of perfluorohexyl sulfonate (PFHxS) on the list. PFOA has been classified as a potential human carcinogen by the International Agency for Research on Cancer [12]. In light of this, short-chain analogs, like F-53B [chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs)], OBS (sodium p-perfluorous nonenoxybenzenesulfonate), and GenX [2,3,3,3-tetrafluoro-2-(1,1,2,2,3,3,3-heptafluoropropoxy)-propanoic acid (HFPO-DA)] have attracted global attention and become widely used alternatives to PFOS and PFOA [13]. However, the prerequisite for the safe use of such substances is a thorough evaluation of the adverse ecotoxicity of commonly detected PFAS compounds and their substitutes.
In aquatic ecosystems, invertebrates, planktons, and microorganisms are essential for material circulation and energy flow. As such, the toxicity and bioaccumulation effects on aquatic organisms directly determine the survival of all other animals along this food chain, making them important study species. For example, benthic shellfish are important indicators of environmental pollution and are commonly used to study the bioavailability of various water pollutants owing to their wide distribution, large population numbers, easy capture and laboratory breeding, strong pollutant accumulation capacity, and low metabolic rate. Additionally, biological background data on these organisms are widely available [14]. Similarly, since the 1970s the zooplankton model species Daphnia magna has been widely used in toxicity studies due to its short life cycle, rapid reproduction rate (approximately 14 days until sexual maturity), sensitivity to toxins, and easy laboratory culturing. In addition, D. magna has a transparent body with visible organs that facilitates the observation of toxicity effects under an anatomical microscope. Lastly, as vital producers in the aquatic environment, microalgae are an indispensable object in the study of aquatic ecology that are often used to evaluate the health of aquatic ecosystems. The effects of pollutants on microalgae could manifest in many ways, such as effects on growth, cell morphology and structure, photosynthesis, intracellular REDOX balance, and active enzyme levels [15]. Comparisons of biomagnification of individual PFAS compounds in primary consumers (e.g., mussels) and top predators (e.g., fishes) showed that the transfer and bioaccumulation of PFASs in the aquatic ecosystem increases their toxicity, highlighting the subsequent potential health risks to humans through the consumption of PFAS-contaminated fish [16].
PFASs released from emissions can reach the sea and oceans through the air and rivers. Due to the large emission volume and high solubility of ionic PFASs, river discharge is a major concern as it is the main pathway for pollutant transmission from land to sea, including the deep sea [3]. Continuous emissions and the long persistence of PFASs have caused aquatic/marine sediments to become major collection points for PFAS pollution from multiple sources [17]. Thus, it is imperative to gain more complete and updated knowledge of the adverse effects of PFASs and their substitutes on various aquatic invertebrates, planktons, and microorganisms on different levels, such as at the genetic, cell, tissue, organ, individual, species, and colony levels. Based on the results of such investigations, reliable reference resources for the subsequent development and application of environmental remediation and management policies could be provided to governments. Moreover, accurate biological testing methods should be used, and sensitive subjects should be screened to clarify the potential toxicity of aquatic pollutants quickly, accurately, and comprehensively.

2. Toxicity of Per- and Polyfluoroalkyl Substances to Aquatic Invertebrates

2.1. Bivalvia

2.1.1. Green Mussel (Perna viridis)

The green mussel (P. viridis) belongs to the phyllobranchia group of molluscs and has been widely used in environmental monitoring due to its sedentary lifestyle, filter feeding characteristics, high accumulation capacity for a variety of pollutants, and its easy identification and collection [18]. With a 96 h LC50 of 68.3 mg/L (Table 1), exposure to PFOS solution caused oxidative stress, including alteration of SOD activity and short-term changes in GSH, MDA, and GSH content in the coat and visceral mass of P. viridis [18][19]. PFOS, PFOA, PFNA, and PFDA all induced dose-dependent and bioaccumulation-correlated oxidative damage as well as DNA damage (e.g., DNA strand breaks and fragmentation, chromosomal breaks, and apoptosis), membrane instability, and reduced body weight in green mussels [20][21][22].

2.1.2. Pearl Mussel (Hyriopsis cumingii)

Hyriopsis cumingii, a typical benthic bivalve, filter feeds on bacteria, phytoplankton, protozoa, rotifers, small cladhorns, small copepods, and organic debris. Therefore, it is more frequently exposed to PFOS than other aquatic organisms. In addition, as one of the main freshwater hyridae widely distributed across major water systems in China, its habits and structure have been studied in depth [23]. PFOS exposure caused significant oxidative compression of the gill tissue (increased SOD activity) and hepatopancreas (alteration of the activity of GSH, SOD, GST, ALT, and AST), aggravated the lipid peroxidation reaction (increased MDA content in the gill and hepatopancreas), induced the activation of apoptosis signal proteins (upregulation of caspase-3 and caspase-9), aggravated the apoptosis of cells in the tissue, and impacted the structure and function of the tissue [23] (Table 2). Further, rapid triggering of cellular detoxification and oxidative stress in the antioxidant system in the hepatopancreas of H. cumingii was detected during PFOS treatment; however, blockage of toxic metabolic pathways and the accumulation of oxidants may have been the origin of such cellular damage [24].

2.2. Other Bivalves

Understanding the effects of contaminants on freshwater mussels is critical to conservation efforts and environmental risk assessments because they are often among the species most sensitive to aquatic contaminants [25]. Concerning the two life stages of Fatmucket (Lampsilis siliquoidea), glochidia are 8–25 times more sensitive to PFOS exposure than juveniles, and PFOS reduced the duration of glochidia viability and probability of metamorphosis at concentrations 3000 times lower than the most sensitive acute endpoint (24 h EC50) [25]. PFOS caused oxidative damage to the gills of Anodonta woodiana by altering the activity of SOD, CAT, and POD [26]. The Asian clam, Corbicula fluminea (Müller, 1774), a freshwater benthic organism, has been used to evaluate the effects of toxic pollutants such as ammonia, metal(loid)s, POPs, and pharmaceuticals owing to its highly sensitive morphology, behavior, and biochemical indices, including changes in enzymatic activity and gene expression in response to chemical exposure [27]. PFOS caused a decrease in filtration rates and significant changes in the enzyme activity response of the antioxidant system (ROS promotion) in C. fluminea [27]. The zebra mussel (Dreissena polymorpha), a commonly occurring invasive species in rivers and lakes with a long life cycle (2–3 years), has been used to assess the levels of several toxicants including metals, polycyclic aromatic hydrocarbons, and polychlorinated biphenyls. It was concluded that the accumulation of these contaminants in zebra mussel tissue represents a potential hazard to organisms (i.e., fish and birds) that feed on them [28]. Although PFOS and PFOA have low bioaccumulation potential in zebra mussels [28], PFOS shows high genotoxicity, which increases with exposure concentration and time [22]. Ruditapes philippinarum, a beach shellfish widely occurring in coastal areas.
Table 1. EC50/LC50 values of target PFASs and some substitutes on aquatic invertebrates.
Invertebrate Life Stage Pollutant Effect Indicator Value Refs
Perna viridis Adult PFOS LC50 96 h lethal 68.3 mg/L [18][19]
PFOS EC50 Integrated genotoxicity 33 (29–37) μg/L [22]
PFOA 594 (341–1036) μg/L
PFNA 195 (144–265) μg/L
PFDA 78 (73–84) μg/L
Fatmucket Juvenile PFOS EC50 48 h, 96 h lethal 158.1, 158.1 mg/L [25]
Black sandshell 158.1, 141.7 (80.4–249.6) mg/L
Fatmucket Glochidia PFOS EC50 24 h, 48 h lethal 16.5 (8.0–33.9), 17.7 (7.2–43.5) mg/L
PFOA 164.4 (116.0–232.8), 162.6 (130.6–202.3) mg/L
Black sandshell PFOS 13.5 (5.7–31.8), 17.1 (9.4–31.1) mg/L
PFOA 161.0 (135.8–191.0), 161.3 (135.0–192.7) mg/L
Perinereis nuntia Adult PFOS LC50 96 h lethal 64 mg/L [29]
Dugesia japonica Adult PFOS, PFOA LC50 24 h lethal 34 (30–38), 352 (331–374) mg/L [30]
48 h lethal 27 (24–31), 345 (325–366) mg/L
72 h lethal 26 (23–29, 343 (324–364) mg/L
96 h lethal 23 (20–25), 337 (318–357) mg/L
Neocaridina denticulate PFOS, PFOA 24 h lethal >200, >1000 mg/L
48 h lethal 57 (43–75), 712 (663–764) mg/L
72 h lethal 20 (17–24), 546 (502–594) mg/L
96 h lethal 10 (9–12), 454 (418–494) mg/L
Physa acuta PFOS, PFOA 24 h lethal 271, 856 (768–954) mg/L
48 h lethal 233 (226–241), 732 (688–779) mg/L
72 h lethal 208 (197–219), 697 (661–735) mg/L
96 h lethal 178 (167–189), 672 (635–711) mg/L
Gammarus insensibilis Adult PFOS LC50 48 h lethal 9.99 mg/L [31]
Macrobrachium rosenbergii Adult PFOS LC50 96 h lethal 0.68 ± 0.22 mg/L [32]
Paracentrotus lividus Adult PFOS, PFOA LC50 72 h lethal 0.11, 110 mg/L [33]
Siriella armata 6.9, 15.5 mg/L
Limnodrilus hoffmeisteri Adult PFOS EC50 48 h lethal pH 6.2 23.81 ± 1.14 mg/L [34][35]
48 h lethal pH 7.0 35.89 ± 0.49 mg/L
48 h lethal pH 8.0 39.80 ± 1.15 mg/L
PFOS LC50 24 h lethal pH 5.0 45.26 mg/L [35]
24 h lethal pH 6.0 46.23 mg/L
24 h lethal pH 7.0 60.70 mg/L
24 h lethal pH 8.0 64.48 mg/L
24 h lethal pH 9.0 65.74 mg/L
TFA, trifluoroace-tic acid; PFPrA, perfluoropropionic acid; PFBA, perfluorobutanoic acid; PFPeA perfluopentanoic acid; PFHxA, perfluorohexanoic acid.
Table 2. Toxicity effects of commonly detected single PFASs on aquatic invertebrates.
Classification Damage/Effect Impact Detail PFOS PFOA
Cumulative toxicity Accumulation Whole soft tissues Cf [27] Cv [36] Lh [34][35]  
Hepatopancreas Es [37]  
Muscle Es [37]  
Developmental toxicity Growth Body weight Pv [20]  
Relative condition factor Pv [20] Pv [20]
Oxidative toxicity Visceral mass SOD, GSH Pv [18][19]  
Mantle SOD, GSH Pv [18][19]  
Gill SOD, GSH, GR, GST, POD Hc [23] Aw [26] Mr [32]  
Hepatopancreas SOD, GSH, GR, GST Hc [23][24] Cv [36] Mr [32]  
Gastrointestinal tract SOD, CAT Mr [32]  
Humor SOD, CAT Gc [38]  
Whole soft tissues CAT, EROD, GSH, GPX, ROS, POD Pv [20][21] Cf [27] Dj [39] Pn [29] Gi [31] Lh [34][35] Pv [20][21] Rp [40] Dj [39]
Lipid peroxidation MDA Pv [18][19][21] Hc [23] Cf [27] Gi [31] Mr [32] Pv [21]
Genetic toxicity DNA damage Strand break Pv [20][21][22] Pn [29] Pv [21][22] Dj [41]
Point mutation Gc [38]  
Gene expression Antioxidant enzyme Cf [27] Mj [42]  
Immune related (heat shock protein) Cf [27] Dj [43]  
P450 and phase II enzymes Cf [27] Cv [36] Pn [29]  
Neurogenesis Dj [39] Dj [39]
Cytotoxicity Apoptosis Membrane damage Cv [36] Pv [20]
Caspase-3, -6 expression Hc [23]  
Organ toxicity Liver ALT, AST Hc [23][24]  
Digestive gland Histological alteration Cf [27]  
Gonad Histological alteration Cf [27]  
Hepatopancreas Histological alteration Es [37]  
Gill Histological alteration Es [37]  
Metabolic toxicity Whole body Oxygen consumption Dp [28] Dp [28]
Multixenobiotic transporter activity Dp [28] Dp [28]
Hepatopancreas Respiration Es [37]  
Glycogen Es [37]  
CCO, LDH Es [37]  
Behavioral toxicity Predation/Feeding Suppressed filtration rate Pv [20] Cf [27]  
Siphoning behavior inhibition Cf [27]  
Neurology toxicity Neurology system Abdominal nerve cord injury   Dj [39]
Cerebral ganglion Dj [39]  
Nerve of the tail Dj [39]  
Immune toxicity Critical enzyme ACP, ALP Hc [23] Mr [32] Gc [38]  
Heat shock protein Cf [27] Dj [43]  
Overall toxicity Enhanced integrated biomarker response Pv [22] Cf [27] Pv [22]
Pv, Perna viridis; Hc, Hyriopsis cumingii; Aw, Anodolffa woodiana; Cf, Corbicula fluminea; Dp, Dreissena polymorpha; Rp, Ruditapes philippinarum; Cv, Crassostrea virginica; Dj, Dugesia japonica; Pn, Perinereis nuntia; Mj, Macrophthalmus japonicus; Es, Eriocheir sinensis; Gi, Gammarus insensibilis; Mr, Macrobrachium rosenbergii; Gc, Glyptocidaris crenularis; Lh, Limnodrilus hoffmeisteri.
ALT, alanine transaminase; AST, aspartate aminotransferase; ACP, acid phosphatase; ALP, alkaline phosphatase; PFCAs, perfluorinated carboxylic acids; CCO, cytochrome c oxidase; LDH, lactate dehydrogenase.is highly sensitive to pollutants and, therefore, commonly used in research that focuses on their detection [40]. PFOA exposure triggered changes of antioxidant (SOD, CAT, and POD) and biotransformation enzymes (GST, EROD, and lipid peroxide) in R. philippinarum. As a result, it could be considered as a potential biomarker for PFOA pollution of marine ecosystems [40]. The Eastern oyster (Crassostrea virginica) is a stationary filter feeding organism that can bioaccumulate contaminants in contaminated particulate matter and the surrounding water [36]. PFOS caused significant cellular lysosomal damage in oysters (Cr. virginica) [36] and induced histopathological alterations in the gonads and digestive glands of freshwater clams (C. fluminea) [27].

2.3. Dugesia japonica

Living in springs, streams, and lakes with good water quality, the triploderm planarian, D. japonica, is very sensitive to toxic substances, teratogenic factors, and environmental pollutants. Hence, it can be used as an indicator species for water quality monitoring and as a model organism for toxicological research [39]. Furthermore, research indicated that PFOA rather than PFOS induced DNA damage [41], but the expression of hsp70 mRNA could be altered by PFOS to protect against toxicity and the accumulation of adverse effects [43]. Oxidative damage and neurotoxicity were caused by PFOS/PFOA exposure, but PFOA damaged the ventral nerve cord whereas PFOS mainly affected the cranial ganglion and caudal nerve to a certain dosage; at the gene expression level, PFOS exposure inhibited the expression of otxA and otxB [39]. Both PFOS and PFOA downregulated the expression of FoxD and upregulated the expression of nlg, although this effect was delayed after PFOS exposure. Regarding the expression of FoxG, PFOA primarily affected the trunk parenchyma whereas PFOS mainly affected the brain [39].

2.4. Perinereis nuntia

Polychaetes belong to the phylum Annelida (Polychaeta) and are among the highest number of highly abundant benthic species. Nereidae is one of the most diverse families of polychaeta [29]. Polychaetes live in sediments and move slowly. Unlike the infrequent exposure that self-swimming animals or reptiles will experience, the relatively stationary mode of life of Polychaetes can lead to chronic exposure to various environmental toxins, and any long-term changes in benthic health can be reflected in the polychaeta community. The 96 h LC50 value for PFOS in P. nuntia was at a medium level of 64 mg/L. PFOS interfered with the CYP pathway receptor, triggered the phase I detoxification reaction system, stimulated the internal production of ROS, and indirectly caused oxidative damage, such as lipid peroxidation, which was reflected by an increase in MDA. It also induced a response in antioxidant defense systems such as SOD, CAT, GSH, GR, and GSH-Px. Phase II detoxification systems, such as GST, were also involved in PFOS metabolism, and the accumulation of oxidative damage led to severe DNA damage, causing genotoxicity [29]. At the antioxidant defense system level, SOD and GR were sensitive to PFOS stress but the effects on GSH-PX and GST were delayed; on the DNA level, PFOS induced dose-dependent short-term DNA damage, which also caused oxidative damage. Lastly, EROD activity, expression of the CYP431A1 gene in CYP2 and the CYP424A1 gene in CYP4, GST enzyme activity, and GST omega gene alternation were caused by PFOS, with CYPs and GST playing an important role in the metabolism of PFOS in P. nuntia [29].

2.5. Crustaceans

2.5.1. Crabs

Crabs play a key role in material cycling and energy flow in ecosystems. As detritivores, they primarily feed on detritus that is sifted from the surface sediment [42]. The intertidal mud crab, Macrophthalmus japonicus, a burrowing species widely distributed across Korea, Japan, northern China, Singapore, and Australia, is one of the most abundant macrobenthic animals in many intertidal mudflats and plays an important role in purification [42]. As a typical crustacean and eurhaline organism with high economic value, Eriocheir sinensis is often used as a model organism for salinity studies [37]. PFOS reduced the survival rate and enhanced the oxidative metabolism of the mud crab (M. japonicus) [42] and caused dose- and time-dependent microstructural damage to the hepatopancreas (e.g., the lumen of the hepatopancreas tubules increases in size until the basement membrane is ruptured) and gills (e.g., thickening of gill leaf, enlargement of blood cavity, and damage to the epithelial layer) of E. sinensis [37]. Additionally, it has been found that the interaction between salinity levels and PFOS exposure affects the hemolymph hemocyanin content and gill respiratory metabolic enzyme cytochrome C oxidase (CCO) in E. sinensis [37].

2.5.2. Shrimp

Besides planarians, freshwater shrimps are another pivotal detritus consumer in freshwater food webs and they play a vital role in energy and nutrient cycling in aquatic ecosystems [30]. The 96 h LC50 value for PFOS was 10 mg/L in green neon shrimp (Neocaridina denticulate) [30]. PFBA and PFBS exposure had a dose-response relationship with the enzyme activity of the antioxidant system in N. denticulate, and the SOD enzyme was found to be a more sensitive bioindicator than CAT and AChE [44]. In Gammarus insensibilis, PFOS exposure caused oxidative stress and cell damage but did not have any neurotoxic effects [31]. In Macrobrachium rosenbergii, the 96 h LC50 for PFOS stress was 0.68 ± 0.22 mg/L, resulting in oxidative damage reflected by MDA, SOD, CAT, and acid phosphatase (ACP) activity alterations. Additionally, in juvenile shrimp, 30 compounds in the gills, 19 compounds in the hepatopancreas, and 24 compounds in the gastrointestinal tract, all of which are involved in amino acid, fatty acid, and phospholipid metabolism, were adversely affected [32].

2.6. Echinidae

In Paracentrotus lividus, the acute EC50 values for PFOS and PFOA were 20 mg/L and 110 mg/L, respectively [33]. At the tissue level, morphological changes in Glyptocidaris crenularis included out stings and a dose-dependent increase of fluid inside the cell, a decrease in the number of red blood cells, short-term reduction of movement and feeding abilities, and antioxidant enzyme changes, for which SOD and ALP were sufficiently sensitive indicators. At the genetic level, low-dosage long-time exposure to PFOS increased methylation levels in G. crenularis, which may have subsequent genotoxic effects [38].

2.7. Tubifex

Exposure to Cd and PFOS caused severe damage to the antioxidant defense system of Limnodrilus hoffmeisteri, including effects on SOD activity, GSH levels, and MDA content alterations at pH 8.0 and pH 6.2, and the harmful effects of joint exposure were always a combination of the effects of single Cd and PFOS exposure [34]. Additionally, the pH value affected the toxicity of PFOS combinations with Cd2+ or Zn2+, especially the additive effects of bioaccumulation and oxidative stress when combined with Cd2+ under alkaline conditions [35].

This entry is adapted from the peer-reviewed paper 10.3390/ijerph192416729

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