Acute toxicity of copper to the threespine stickleback, Gasterosteus aculeatus

This study focuses on characterizing the acute toxicity of copper in freshwater to the threespine stickleback, Gasterosteus aculeatus, a small and widely distributed euryhaline fish. The threespine stickleback is used as an effluent monitoring species in both Canada and the United States, yet in some locations natural populations are listed as threatened or endangered. Four 96-h static renewal acute toxicity tests were performed in moderately hard water using U.S. EPA methods with adult fish (mean wet weight = 0.41 g/fish). The geometric mean of the 24-, 48-, 72- and 96-h LC(50)s based on measured concentrations of total copper (estimated dissolved copper in parentheses) in the test solutions were 382.2 (366.9), 278.7 (267.6), 256.6 (246.3), and 227.2 (218.1) microg Cu/L, respectively. Conservative estimates of acute toxicity thresholds, made using LC1 values, for adult threespine sticklebacks over 24-, 48-, 72- or 96-h exposure periods in moderately hard water are approximately 114.3 (109.7), 78.3 (75.2), 67.0 (64.3), and 52.4 (50.3) microg Cu/L, respectively. Test results were normalized to a range of water hardness from very soft to very hard using two U.S. EPA methods, the water hardness and the Biotic Ligand Model normalization procedures. Subsequently, interspecies sensitivity comparisons were made with aquatic animal species used in both the current and proposed U.S. EPA copper water quality criteria documents. Information reported in this study may be useful in effluent toxicity identification evaluations, ecological risk assessments and criteria development where copper is a concern.     

Estimation of toxicity to marine species with structure-activity models developed to estimate toxicity to freshwater fish

Structure-activity models which were developed to estimate toxicity of chemicals to freshwater fish were tested for use with an estuarine fish (Cyprinodon variegatus) and mysids (Mysidopsis bahia). Significant linear and polynomial relationships that correlated well existed between reported 96-h LC₅₀ values for each marine species and log P (log octanol/water partition coefficient). Good linear relationships were obtained when the 96-h LC₅₀ values for C. variegatus and M. bahia were regressed on water solubility (μmol/l). These models were compared to models developed for freshwater fish using log P and log S. Models using log P to estimate acute toxicity for two freshwater fish produced 96-h LC₅₀ values similar to those measured for C. variegatus and M. bahia, whereas, those models developed with water solubility produced 96-h LC₅₀ values similar to those for C. variegatus, but not for M. bahia. The data indicated that models developed with log P for freshwater fish can be used to estimate toxicity to C. variegatus for a minimum of 58% of the chemicals, whereas models using water solubility estimated toxicity to C. variegatus for a minimum of 77% of the chemicals within an order of magnitude for screening purposes. The calculated 96-h LC₅₀ values were compared to the measured values for each marine species and those measured for Pimephales promelas (fathead minnow) and Poecilia reticulata (guppy). Tests indicated generally that calculated 96-h LC₅₀ values were overestimates of the measured 96-h LC₅₀ values when models for freshwater fish were used to estimate toxicity to each marine species. More data are required for marine species to determine if highly significant relationships between marine and freshwater fish exist with comparisons using larger sample sizes.     

Influence of temperature and dissolved oxygen on the acute toxicity of profenofos to fathead minnows (Pimephales promelas)

The purpose of this study was to investigate the influence of temperature and dissolved oxygen levels on the acute toxicity of profenofos to fathead minnows (Pimephales promelas). Exposure conditions were as follows: normal temperature and normal dissolved oxygen (NTNO; 20 +/- 2 degrees C and 6.0-9.0 mg/L, respectively); normal temperature and low dissolved oxygen (NTLO; 20 +/- 2 degrees C and 1.7-2.6 mg/L, respectively); high temperature and normal dissolved oxygen (HTNO; 30 +/- 2 degrees C and 6.6-6.9 mg/L, respectively); high temperature and low dissolved oxygen (HTLO; 30 +/- 2 degrees C and 1.5-3.0 mg/L, respectively). Initial 96-h acute toxicity studies with profenofos were conducted at NTNO and HTLO exposure conditions. The 96-h LC50 at NTNO was 333 micrograms/L with 95% confidence limits ranging from 244 to 558 micrograms/L. However, the 96-h LC50 at HTLO was significantly lower at 21.5 micrograms/L with 95% confidence limits ranging from 17.4 to 28.8 micrograms/L. Acetylcholinesterase (AChE) activity was measured in the head and torso of surviving fish at 96-h. A weak dose-related decrease in AChE was observed at NTNO but no dose-response relationship was observed at HTLO exposure condition. Additional experiments were conducted using 50 micrograms/L profenofos at NTNO, NTLO, HTNO, and HTLO exposure conditions. Mortality, sublethal effects (erratic and hyperactive swimming), and AChE activity in the head and torso were measured at 2, 4, and 12-h following exposure to profenofos. No mortality or significant sublethal effects were observed in controls or profenofos-treated groups in NTNO and NTLO exposure conditions. However, significant mortality and sublethal effects were observed in profenofos-treated fish in HTNO at 12 h and at all time points in HTLO. Both high temperature and low dissolved oxygen, as well as combinations of high temperature and low dissolved oxygen significantly decreased AChE activity in control fish. Exposure to 50 micrograms/L profenofos in all exposure conditions further decreased AChE activity, but no apparent correlations between mortality and AChE activity were observed. These results suggest that the acute toxicity of profenofos to fathead minnows may be exacerbated during summer conditions in southern U.S. aquatic ecosystems.     

Preliminary investigation of multi-biomarker responses in three-spined stickleback (<Emphasis Type="Italic">Gasterosteus aculeatus</Emphasis> L.) sampled in contaminated streams

Recently, the three-spined stickleback (Gasterosteus aculeatus L.) has been proposed as a suitable fish species for detecting both androgen- and estrogen-induced endocrine disruption by environmental pollutants. This relatively pollution-tolerant fish is present in most European streams and small rivers but also coastal and estuarian areas. The purpose of the present field study was to determine the extent to which multiple biomarkers in this fish species could distinguish between streams with different pollution levels. Sticklebacks were sampled in French rivers characterised by various urban, industrial or agricultural contaminations and in outdoor lotic mesocosms as reference site. Physiological parameters including condition factor and liver somatic index, biotransformation enzymes such as 7-ethoxyresorufin-O-deethylase (EROD) and glutathione-S-transferase, antioxidant enzymes including glutathione peroxidase and total glutathione (GSH) content and lipoperoxidation (as TBARS) showed several differences between sites. For example, fish from an heavily contaminated stream exhibited a 9-fold EROD induction associated to a decrease of GSH and a 3-fold increase of TBARS content in comparison to fish from uncontaminated sites. When fish were transferred from polluted river to clean water, some of these biomarkers rapidly returned to basal levels found in fish in the reference site while others, like TBARS levels were still high after 2 weeks of depuration. Based on multivariate analyses, the battery of biomarkers proved to differentiate all sites, with a very good classification rate for highly contaminated streams. Influence of fish gender and sampling period on biomarker responses was also observed and is discussed. The results of this field study provide additional support for the use of stickleback for in situ multi-biomarker assessment.     

Toxicity of perfluorooctane sulfonate and perfluorooctanoic acid to plants and aquatic invertebrates

Acute toxicities of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were tested on four freshwater species and three plant species. PFOS was more toxic than PFOA for all species tested in this study. Similar time-response patterns of PFOS and PFOA toxicity were observed for each tested species. Values of the 48-h LC(50) of PFOS for all test species ranged from 27 to 233 mg/L and values of the 96-h LC(50) for three of the species ranged from 10 to 178 mg/L. Values of the 48-h LC(50) of PFOA for all test species ranged from 181 to 732 mg/L and values of the 96-h LC(50) for three of the species ranged from 337 to 672 mg/L. The most sensitive freshwater species to PFOS was green neon shrimp (Neocaridina denticulate) with a 96-h LC(50) of 10 mg/L. Of the aquatic organisms tested, the aquatic snail (Physa acuta) always has the highest resistance to PFOS or PFOA toxicity over each exposure period. Both PFOS and PFOA had no obvious adverse effect on seed germination for all three plant species. Five-day EC(50) of root elongation was more sensitive to LC(50) of seed germination in this study. Based on EC(10), EC(50), and NOECs, the 5-day root elongation sensitivity of test plants to both PFOS and PFOA was in the order of lettuce (Lactuca sativa) > pakchoi (Brassica rapa chinensis) > cucumber (Cucumis sativus). Based on the results of this study and other published literature, it is suggested that current PFOS and PFOA levels in freshwater may have no acute harmful ecological impact on the aquatic environment. However, more research on the long-term ecological effects of PFOS and PFOA on aquatic fauna are needed to provide important information to adequately assess ecological risk of PFOS and PFOA.     

Mechanistic analysis of acute, Ni-induced respiratory toxicity in the rainbow trout (Oncorhynchus mykiss): an exclusively branchial phenomenon

In moderately hard Lake Ontario water (approximately 140 mg L(-1) as CaCO3) waterborne Ni (9.7-10.7 mg Ni L(-1)) is acutely toxic to adult rainbow trout (Oncorhynchus mykiss) exclusively via branchial mechanisms. Ventilation in resting trout (evaluated using a ventilatory masking technique) was adversely affected, as ventilation rate (VR), ventilation volume (VG), opercular stroke volume (VSV) and resting oxygen consumption (MO2) were all increased, and oxygen extraction efficiency (U%) decreased over 48 h of Ni exposure. Extensive gill Ni accumulation (41-fold over control levels) during 82 h of waterborne Ni exposure resulted in marked ultrastructural damage to the respiratory epithelium of the gill, including swelling of the secondary lamellae evidenced by changes to both the lamellar region (increased secondary lamellar tissue volume (VSL/V(LR), and to the secondary lamellae themselves (increased volume of tissue lying outside the pillar system (VOPS/VSL). Additionally, decreased lamellar height and increased lamellar width indicated a reduction in lamellar surface area available for gas diffusion. The relative diffusing capacity of experimental fish was only 59% of that of control fish. Infusion of Ni into the blood, achieving a similar time course and magnitude of plasma [Ni] elevation to that during waterborne exposure, failed to elicit any signs of respiratory toxicity typically diagnostic of acute, high level waterborne Ni exposure. Infusion of Ni into the blood for 96 h resulted in only minor accumulation of Ni in the gill, suggesting that acute Ni-induced respiratory toxicity is related to accumulation of high levels of Ni in the gill from the water. Additionally, infusion of Ni into the bloodstream led to significant extrabranchial Ni accumulation only in the kidney. White muscle, heart, liver, stomach, and intestine did not significantly accumulate Ni following infusion into the bloodstream and trapped plasma analysis revealed that, with the exception of the kidney, a substantial portion of Ni accumulated in tissues following infusion could be accounted for by extracellular (blood-bound) Ni.     

Renal function in the freshwater rainbow trout (Oncorhynchus mykiss) following acute and prolonged exposure to waterborne nickel

Renal function was investigated in adult rainbow trout following acute and prolonged exposure to waterborne Ni in moderately hard Lake Ontario water (approximately 140 mgL(-1) as CaCO3). Fish were exposed for 36 days to a sublethal concentration of 442 microg Ni L(-1), followed by 96 h of exposure to 12,850 microg Ni L(-1) (approximately 33% of the 96 h LC50). Prolonged exposure markedly affected only the renal handling of Ni, with no substantial effect on the plasma concentration, urinary excretion rate (UER) or clearance ratio (CR) of Na+, Cl-, K+, Ca2+, Mg2+, inorganic phosphate (P(i)), glucose, lactate, total ammonia (T(amm)), protein and free amino acids (FAA). Glomerular filtration rate (GFR) was reduced by 75% over 96 h of acute Ni challenge in both fish previously exposed to Ni and naive fish, with no significant change in urine flow rate (UFR), suggesting a substantial reduction in water reabsorption to maintain urine flow and water balance. Renal Mg2+ handling was specifically impaired by acute Ni challenge, leading to a significantly increased UER(Mg2+) and significantly decreased plasma [Mg2+] only in naive fish. Previously-exposed fish were well-protected against Ni-induced Mg2+ antagonism, indicating true acclimation to Ni. Only in naive, acutely challenged fish was there an increased UER of titratable acidity (TA-HCO3), net acidic equivalents, P(i), T(amm) and K+. Again, all of these parameters were well-conserved in previously-exposed fish during acute Ni exposure, strongly suggesting that prolonged, sublethal exposure protected against acute Ni-induced respiratory toxicity.     

INFLUENCE OF TEMPERATURE AND DISSOLVED OXYGEN ON THE ACUTE TOXICITY OF PROFENOFOS TO FATHEAD MINNOWS (PIMEPHALES PROMELAS)

ABSTRACT

The purpose of this study was to investigate the influence of temperature and dissolved oxygen levels on the acute toxicity of profenofos to fathead minnows (Pimephales promelas). Exposure conditions were as follows: normal temperature and normal dissolved oxygen (NTNO; 20 ± 2°C and 6.0–9.0 mg/L, respectively); normal temperature and low dissolved oxygen (NTLO; 20 ± 2°C and 1.7–2.6 mg/L, respectively); high temperature and normal dissolved oxygen (HTNO; 30 ± 2°C and 6.6–6.9 mg/L, respectively); high temperature and low dissolved oxygen (HTLO; 30 ± 2°C and 1.5–3.0 mg/L, respectively). Initial 96-h acute toxicity studies with profenofos were conducted at NTNO and HTLO exposure conditions. The 96-h LC₅₀ at NTNO was 333 µg/L with 95% confidence limits ranging from 244 to 558 µg/L. However, the 96-h LC₅₀ at HTLO was significantly lower at 21.5 µg/L with 95% confidence limits ranging from 17.4 to 28.8 µg/L. Acetylcholinesterase (AChE) activity was measured in the head and torso of surviving fish at 96-h. A weak dose-related decrease in AChE was observed at NTNO but no dose–response relationship was observed at HTLO exposure condition. Additional experiments were conducted using 50 µg/L profenofos at NTNO, NTLO, HTNO, and HTLO exposure conditions. Mortality, sublethal effects (erratic and hyperactive swimming), and AChE activity in the head and torso were measured at 2, 4, and 12-h following exposure to profenofos. No mortality or significant sublethal effects were observed in controls or profenofos-treated groups in NTNO and NTLO exposure conditions. However, significant mortality and sublethal effects were observed in profenofos-treated fish in HTNO at 12 h and at all time points in HTLO. Both high temperature and low dissolved oxygen, as well as combinations of high temperature and low dissolved oxygen significantly decreased AChE activity in control fish. Exposure to 50 µg/L profenofos in all exposure conditions further decreased AChE activity, but no apparent correlations between mortality and AChE activity were observed. These results suggest that the acute toxicity of profenofos to fathead minnows may be exacerbated during summer conditions in southern U.S. aquatic ecosystems.     

Acute toxicity to freshwater organisms of antiparasitic drugs for veterinary use

The acute toxicity of five antiparasitic drugs used in the veterinary field-amprolium hydrochloride (APH), bithionol (BT), levamisole hydrochloride (LVH), pyrimethamine (PYM) and trichlorfon (TRC)-to the aquatic organisms Oryzias latipes, Daphnia magna, and Brachionus calyciflorus was examined. The toxicity test with O. latipes was conducted in accordance with the OECD Guidelines for the Testing of Chemicals (1993) to determine the 24-, 48-, 72-, and 96-h LC(50) values. In addition, 24- and 48-h EC(50) values for D. magna and a 24-h EC(50) for B. calyciflorus were determined with the DAPHTOXKIT F(trade mark) magna (Creasel, Belgium) and the ROTOXKIT F(trade mark) (Creasel, Belgium), respectively. High-performance liquid chromatographic analysis revealed that APH, LVH, and PYM were stable in water, but BT was unstable, decreasing by 84% on average at 24 h. TRC rapidly decomposed, with only 0.7% of the initial concentration remaining after 96 h, forming dichlorvos. The toxicity of TRC to O. latipes was determined in two ways: exposure to the same medicated water for 96 h (static test) and exposure to medicated water replaced every 24 h (semistatic test). AMP, LVM, and PYM were tested in the static condition, and BT was tested in the semistatic condition. BT was most toxic to O. latipes, with a 96-h LC(50) of 0.24 mg L(-1), followed by PYM, with a 96-h LC(50) of 5.6 mg L(-1). The 24-, 48-, 72-, and 96-h LC(50) values of TRC in the static test were 92.0, 45.2, 29.5, and 17.6 mg L(-1), respectively, which tended to be lower than those in the semistatic test, especially late in the observation period. D. magna was the most susceptible to TRC, with a 48-h EC(50) as low as 0.00026 mg L(-1). The 48-h EC(50) values of BT, PYM, and LVH for D. magna were 0.3, 5.2, and 64.0 mg L(-1), respectively. B. calyciflorus was the most susceptible to BT, with an EC(50) of 0.063 mg L(-1), followed by PYM, with an EC(50) of 15.0 mg L(-1). Among the test compounds, APH was the least toxic to all the freshwater organisms tested, with a 96-h LC(50) of >600 mg L(-1) for O. latipes, a 48-h EC(50) of 227 mg L(-1) for D. magna, and an EC(50) of 403 mg L(-1) for B. calyciflorus.     

Ecotoxicoproteomics in gills of the sentinel fish species, Cottus gobio, exposed to perfluorooctane sulfonate (PFOS)

The environmental persistence, bioaccumulative tendency and potential toxicity of perfluorooctane sulfonate (PFOS) have generated great concern. This study aimed at evaluating the toxicity of short-term PFOS exposure in gills of the European bullhead Cottus gobio, a candidate sentinel species, by monitoring the response of some enzymes (citrate synthase CS, cytochrome c oxidase CCO, and lactate dehydrogenase LDH), and by undertaking a proteomic analysis using 2D-DIGE. First, a 96-h exposure to 1mg PFOS/L significantly altered the activity of mitochondrial CS and CCO. Second, 2D-DIGE gels were used to compare gills from the control fish group with tissues from fish exposed for 96h to either 0.1 or 1mg PFOS/L. From the 27 protein spots displaying significant changes in abundance following PFOS exposure, a total of 20 different proteins were identified using nano LC-MS/MS and the Peptide and Protein Prophet of Scaffold software. The differentially expressed proteins that were identified are involved in the general stress response, ubiquitin-proteasome system, energy metabolism, and actin cytoskeleton, which provide clues on the cellular pathways and components mainly affected by PFOS. Moreover, our results showed that most proteins were differentially expressed at the low but not at the high PFOS concentration. This work provides insights into the biochemical and molecular events in PFOS-induced toxicity in gill tissue, and suggests that further studies on the identified proteins could provide crucial information to better understand the mechanisms of PFOS toxicity in fish.     

The biotransformation of three 14C-labelled phenolic compounds in twelve species of freshwater fish

1. The urinary and biliary excretion of 14C-labelled m-cresol, 1-naphthol and o-chlorophenol were investigated in 12 species of freshwater fish (bitterling, Rhodeus sericeus amarus; bream, Abramis brama; crucian carp, Carassius carassius; goldfish, Carassius auratus; gudgeon, Gobio gobio; guppy, Poecilia reticulata; minnow, Phoximus phoximus; perch, Perca fluviatilis; roach, Rutilus rutilus; rudd, Scardinius erythropthalmus; three-spined stickleback, Gasterosteus aculeatus; tench, Tinca tinca) when immersed in sub-lethal concentrations of the compounds in the aquarium water for 48 h. 2. The sulphate and glucuronic acid conjugates of 1-naphthol and o-chlorophenol were detected in both the aquarium water and the bile of all the fish species. 3. The oxidation product of m-cresol, m-hydroxybenzoic acid, and the sulphate conjugate of the phenol, were excreted into the aquarium water of all species except the guppy, which did not excrete m-hydroxybenzoic acid. In addition to these two metabolites, the glucuronic acid conjugate of m-cresol was found in the bile of all species, except for guppies whose small size precluded study of biliary excretion.     

Aquatic toxicity of four alkylphenols (3-tert-butylphenol, 2-isopropylphenol, 3-isopropylphenol, and 4-isopropylphenol) and their binary mixtures to microbes, invertebrates, and fish

The acute and chronic toxicity of four simple alkylphenols with butyl and propyl substitutions was evaluated with aquatic microbes, invertebrates, and fish. These alkylphenols-3-tert-butylphenol, 2-isopropylphenol, 3-isopropylphenol, and 4-isopropylphenol-have been detected in various environmental media, but their impact on aquatic fauna has seldom been evaluated. Relative susceptibility to each phenolic varied by test species. The marine bacterium Vibrio fischeri was the most susceptible to the alkylphenols, up to 3 orders of magnitude more sensitive than species of higher trophic levels. For 4-isopropylphenol, the 5-min Microtox EC(50) value was 0.01 mg/L, whereas the EC(50) for Ceriodaphnia after a 48-h exposure was 10.1 mg/L. Notable differences in sensitivity to the alkylphenols was also observed with the Microtox assay: 4-isopropylphenol was > 200 times more toxic to V. fischeri than was 2-isopropylphenol (EC(50) = 2.72 mg/L). For V. fischeri, the mixture toxicity of the alkylphenols was additive in nature and was predicted by a concentration addition model. The energy of the lowest unoccupied molecular orbital (ELUMO) explained the observed toxicity of the individual alkylphenols to V. fischeri (r(2) = 0.92, p < 0.05). These results suggest that the mode of action of polar narcotic alkylphenols to V. fischeri is different than that of other test organisms, possibly because of the differences in the cell structure of the prokaryotic V. fischeri.     

Is Cl- protection against silver toxicity due to chemical speciation?

In freshwater teleosts, the primary mechanism of acute silver toxicity is inhibition of Na(+)/K(+) ATPase and carbonic anhydrase at the gill, leading to net Na(+) and Cl(-) loss due to the continued diffusion of these ions into the hypoosmotic external environment. External Cl(-) has been shown to protect rainbow trout (Oncorhychus mykiss) against silver toxicity presumably by complexation to form AgCl. However, Cl(-) does not appear to greatly influence silver toxicity to at least two other species, the European eel (Anguilla Anguilla) and the fathead minnow (Pimephales promelas). We hypothesized that differences in protective effects of Cl(-) at the gill were due to differing requirements or mechanisms for Cl(-) uptake among fish species. To test this hypothesis, we exposed Fundulus heteroclitus, which does not take up Cl(-) across the gills, and Danio rerio and P. promelas, which do rely on Cl(-) uptake across the gills, to Ag(+) in waters of varying Cl(-) concentration. The 96-h LC50s of F. heteroclitus exposed to Ag(+) in soft water with 10 microM Cl(-), 1mM KCl, and 0.5mM MgCl(2) were 3.88, 1.20, and 3.20 microg/L, respectively, and not significantly different. The 96-h LC50s for D. rerio exposed to Ag(+) in soft water with 10 microM Cl(-) and 1mM KCl were 10.3 and 11.3 microg/L, respectively and P. promelas exposed under the same conditions were 2.32 and 2.67 microg/L, respectively. Based on these results, increasing external Cl(-) concentration by as much as 1mM (35.5mg/L) did not offer protection against Ag(+) toxicity to any fish species tested. Although previous results in our laboratory have demonstrated that P. promelas do take up Cl(-) at the gill, a mechanism of uptake has not been identified. Additional experiments, investigating the mechanisms of Na(+) and Cl(-) influx at the gill of P. promelas and the influence of silver, demonstrated that Cl(-) uptake in P. promelas acclimated to soft water occurs through both a Na(+):K(+):2Cl(-) co-transporter and a Cl(-)/HCO(3)(-) exchanger, but is not dependent on carbonic anhydrase. Further, acclimation water chemistry was found to greatly influence subsequent branchial silver accumulation, but Cl(-) uptake was not sensitive to 10 microg/L Ag(+).     

Acute waterborne nickel toxicity in the rainbow trout (Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism

The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard ( approximately 140 mg l(-1) as CaCO(3)) Lake Ontario water, where the 96-h LC(50) for juvenile trout (1.5-3.5 g) was 15.3 mg (12.7-19.0, 95% C.L.) dissolved Ni l(-1). No marked impact of Ni exposure on average unidirectional or net fluxes of Na(+), Cl(-), or Ca(2+) was observed in juvenile trout exposed for 48-60 h to 15.6 mg Ni l(-1) as NiSO(4). Furthermore, when adult rainbow trout (200-340 g) were fitted with indwelling dorsal aortic catheters and exposed for 117 h to 11.6 mg Ni l(-1) as NiSO(4), plasma ions (Na(+), Cl(-), Ca(2+), and Mg(2+)) were all well conserved. However, mean arterial oxygen tension dropped gradually to approximately 35% of control values. This drop in P(aO(2)) was accompanied by an acidosis primarily of respiratory origin. P(aCO(2)) rose to more than double control values with a concomitant drop in arterial pH of 0.15 units. Acute respiratory toxicity was further evidenced by a significant increase in hematocrit (Ht), and plasma lactate, and a significant decrease in spleen hemoglobin (Hb). Following 117 h of exposure to 11.6 mg Ni l(-1), the gill, intestine, plasma, kidney, stomach, and heart accumulated Ni significantly, with increases of 60, 34, 28, 11, 8, and 3-fold, respectively. Brain, white muscle, liver, and bile did not significantly accumulate Ni. Plasma Ni exhibited a remarkable linear increase with time to levels approximately 30-fold higher than controls. We conclude that in contrast to most other metals, Ni is primarily a respiratory, rather than an ionoregulatory, toxicant at exposure levels close to the 96-h LC(50). The implications of a waterborne metal as an acute respiratory toxicant (as opposed to ionoregulatory toxicants such as Cu, Ag, Cd, or Zn) with respect to toxicity modeling are discussed.     

Parental exposure to methyl methane sulfonate of three-spined stickleback: contribution of DNA damage in male and female germ cells to further development impairment in progeny

Data regarding the link between DNA integrity of germ cells and the quality of progeny in fish exposed to genotoxicant are scarce although such information is of value to understand genotoxic effects of contaminants in aquatic fauna. This work aimed at studying the consequences of a parental exposure during the breeding season on offspring quality in three-spined stickleback. After in vivo exposure of adult fish to methyl methane sulfonate, a model alkylating compound, a clear increase in DNA damage was observed in erythrocytes of both genders, here used as a biomarker of exposure. MMS exposure significantly affected sperm DNA integrity but neither female fecundity nor fertilization success. In order to understand the contribution of each sex to potential deleterious effects in progeny due to parental exposure, mating of males and females exposed or not to MMS, was carried out. Exposure of both males and females or of males alone led to a significant increase in both mortality during embryo–larval stages and abnormality rate at hatching that appeared to be sensitive stages. Thus, in accordance with recent studies carried out in other freshwater fish species, such development defects in progeny were clearly driven by male genome, known to be devoid of DNA repair capacity in spermatozoa. The next step will be to investigate the link between DNA damage in stickleback sperm and reproductive impairment in natural populations exposed to complex mixture of genotoxicants.     

Hazard Assessment of Resmethrin: I. Effects and Fate in Aquatic Systems

A comparative aquatic hazard assessment of resmethrin was conducted to investigate the need for its restricted use classification by the US. EPA as an adult mosquito control agent. This paper describes the environmental fate and aquatic toxicity of resmethrin. The following paper compares resmethrin to the alternative insecticides. Environmental fate studies indicate that resmethrin has a short photolytic half-life in water (< 1h). Furthermore, it is immobile in soil and biodegradable (half-life=36.5d) under aerobic conditions. Laboratory studies with constant 48- to 96-h exposures show it is acutely toxic to fish and invertebrates in the 0.22–15.0g/L range. Daphnia magna, pink shrimp (Penaeus duorarum) and rainbow trout (Oncorhynchus mykiss) are the most sensitive and mollusks are the least sensitive species. Chronic laboratory studies indicate that the maximum acceptable toxicant concentrations (MATCs) for resmethrin and D. magna, Pimephales promelas, O. mykiss, and Cyprinodon variegatus are 0.58, 0.52, 0.43, and 10.3g/L, respectively. The acute-to-chronic ratios (1.1–7.3) for all species studied indicate that chronic toxicity will not be an issue for resmethrin. Furthermore, the characteristics of acute exposures (48- to 96-h) used in the laboratory will not occur under field conditions because of the short half-life of resmethrin in fresh- and salt-water.     

Influence of acclimation and cross-acclimation of metals on acute Cd toxicity and Cd uptake and distribution in rainbow trout (Oncorhynchus mykiss)

The development of chronic metal toxicity models for fresh water fish is complicated by the physiological adjustments made by the animal during exposure which results in acclimation. This study examines the influence of a pre-exposure to a chronic sublethal waterborne metal on acclimation responses as well as the uptake and distribution of new metal into juvenile rainbow trout. In one series of tests, trout were exposed to either 20 or 60 microg/L Cu, or 150 microg/L Zn for a month in moderately hard water and then cross-acclimation responses to Cd were measured in 96 h LC(50) tests. Cu exposed trout showed a cross-acclimation response but Zn exposed trout did not. Using these results, a detailed examination of Cd uptake and tissue distribution in metal-acclimated trout was done. Trout were exposed to either 75 microg/L Cu or 3 microg/L Cd for 1 month to induce acclimation and subsequently, the uptake and distribution of new Cd was assessed in both Cd- and Cu-acclimated fish using (109)Cd. The pattern of accumulation of new metal was dramatically altered in acclimated fish. For example, in 3 h gill Cd binding experiments, Cd- and Cu-acclimated trout both had a higher capacity to accumulate new Cd but only Cu-acclimated fish showed a higher affinity for Cd compared to unexposed controls. Experiments measuring Cd uptake over 72 h at 3 microgCd/L showed that the Cd uptake rate was lower for Cd-acclimated fish compared to both Cu-acclimated fish and unexposed controls. The results demonstrate the phenomenon of cross-acclimation to Cd and that chronic sublethal exposure to one metal can alter the uptake and tissue distribution of another. Understanding how acclimation influences toxicity and bioaccumulation is important in the context of risk assessment. This study illustrates that knowledge of previous exposure conditions is essential, not only for the metal of concern, but also for other metals as well.     

Comparison of nickel toxicity to cladocerans in soft versus hard surface waters

The aims of the present study were to investigate (1) whether cladocerans living in soft water (operationally defined hardness < 10 mg CaCO(3)/L) are intrinsically more sensitive to Ni than cladocerans living in hard water (operationally defined hardness > 25 mg CaCO(3)/L) and (2) whether a single bioavailability model can be used to predict the protective effect of water hardness on the toxicity of Ni to cladocerans in both soft and hard water. To address these research questions, acute and chronic bioassays were conducted with 10 different cladoceran species collected in soft and hard water lakes in Sweden. Soft water organisms were tested in a 'soft' and a 'moderately hard' test water (nominal hardness = 6.25 and 16.3 mg CaCO(3)/L, respectively). Hard water organisms were tested in a 'moderately hard' and a 'hard' test water (nominal hardness = 16.3 and 43.4 mg CaCO(3)/L, respectively). The results of the toxicity tests in the 'moderately hard' test water revealed no significant differences between the intrinsic sensitivity of soft versus hard water organisms. Modeling exercises indicated that water hardness significantly reduced Ni toxicity to both the soft and the hard water organisms tested. Although predictions of chronic toxicity were sufficiently accurate using the same logK(CaBL) and logK(MgBL) (i.e. the model parameters describing the effect of hardness) for all organisms under consideration, predictions of acute toxicity were significantly more accurate when separate logK(CaBL) and logK(MgBL) values were derived for the soft and the hard water organisms tested. This is due to the fact that the relative decrease of acute Ni toxicity to soft water organisms in 'moderately hard' compared to 'soft' test water was significantly higher than for hard water organisms in 'hard' compared to 'moderately hard' test water.     

Comparative study on sensitivity of higher plants and fish to heavy fuel oil

Laboratory tests were conducted on higher plants [garden cress (Lepidium sativum), great duckweed (Spirodela polyrrhiza), and Tradescantia clone BNL 02] and fish [rainbow trout (Oncorhynchus mykiss) at all stages of development: eggs, larvae and adults] to estimate their sensitivity to heavy fuel oil (HFO). A number of biological indices (survival, growth, and physiological and morphological parameters) as well as the genotoxic impact (Tradescantia) of HFO was evaluated by acute and chronic toxicity tests. Fish were found to be more sensitive to the toxic effect of HFO than were higher plants. EC(50) values obtained for higher plants ranged from 8.7 g/L (L. sativum) to 19.8 g/L (Tradescantia), and maximum-acceptable-toxicant concentration (MATC) values ranged from 0.1 to 1.0 g/L of total HFO for L. sativum and Tradescantia, respectively. The 96-h LC(50) values ranged from 0.33 g/L, for larvae, to 2.97 g/L, for adult fish, and the MATC value for fish was found to be equal to 0.0042 g/L of total HFO. To evaluate and predict the ecological risk of the overall effects of oil spills, studies should be performed using a set of acute and chronic bioassays that include test species of different phylogenetic levels with the most sensitive morphological, physiological, and genotoxic indices.