Acute toxicity of hydrogen cyanide to freshwater fishes.

Acute toxicity of hydrogen cyanide was determined at various temperatures from 4 degrees to 30 degrees C and oxygen concentrations of 3.36 to 9.26 mg/L on different life history stages of five species of fish: fathead minnow, Pimephales promelas Refinesque; bluegill, Lepomis macrochirus Rafinesque; yellow perch, Perca flavescens (Mitchill); brook trout, Salvelinus fontinalis (Mitchill); and rainbow trout, Salmo gairdneri Richardson. Median lethal threshold concentrations and 96-hr LC50's were established by flow-through type biassays. Acute toxicity varied from 57 microgram/L for juvenile rainbow trout to 191 microgram/L for field stocks of juvenile fathead minnows. Juvenile fish were more sensitive at lower temperatures and at oxygen levels below 5 mg/L. For most species juveniles were most sensitive and eggs more resistant.     

A bioavailability model predicting the toxicity of nickel to rainbow trout (Oncorhynchus mykiss) and fathead minnow (Pimephales promelas) in synthetic and natural waters

The effects of Ca, Mg and pH on the toxicity of Ni to juvenile rainbow trout (Oncorhynchus mykiss) were examined during 17-26-day exposures to Ni in 15 synthetic test solutions. Higher chemical activities of Ca2+, Mg2+ and H+ reduced Ni toxicity, as demonstrated by increased 17-day median lethal concentrations expressed as Ni2+ activity (17-d LC50(Ni2+)). A non-linear increase of the 17-d LC50(Ni2+) with increasing H+ suggested that the effect of pH could not be appropriately described by single-site competition between Ni(2+) and H+ for sensitive sites on the fish gill. Instead, a linear increase of pNi2+ (=-log 17-d LC50(Ni2+)) with increasing pH was observed with a slope of 0.32. This slope was used as the basis for modelling the effect of pH. The effects of Ca and Mg were modelled according to single-site competition with logK(CaBL)=logK(MgBL)=3.6, both assumed to be independent of pH. The effect of pH was superimposed on this competition effect and was also assumed to be independent of Ca and Mg concentrations. The model was able to predict 17-d LC50s (expressed as dissolved Ni) in most synthetic test waters within a factor 2 deviation from observed toxicity. The model's predictive capacity was also evaluated using results of similar laboratory toxicity tests with juvenile rainbow trout in Ni-spiked European natural surface waters. For most of these waters, predicted 17-d LC50s did not deviate more than a factor 2 from observed toxicity. The same model, calibrated to account for sensitivity differences between species, life stages and/or exposure durations, was able to accurately predict 96-h LC50s for larval and juvenile fathead minnow (Pimephales promelas) and juvenile rainbow trout, based on data taken from literature. Although the developed model seems very promising, the uncertainty around the role of alkalinity and the exact mechanisms by which Ca, Mg and pH modify Ni toxicity need to be further explored.     

Relative sensitivity of bull trout (Salvelinus confluentus) and rainbow trout (Oncorhynchus mykiss) to acute copper toxicity

Bull trout (Salvelinus confluentus) were recently listed as threatened in the United States under the federal Endangered Species Act. Past and present habitat for this species includes waterways contaminated with heavy metals released from mining activities. Because the sensitivity of this species to copper was previously unknown, we conducted acute copper toxicity tests with bull and rainbow trout (Oncorhynchus mykiss) in side-by-side comparison tests. Bioassays were conducted using water at two temperatures (8 degrees C and 16 degrees C) and two hardness levels (100 and 220 mg/L as CaCO3). At a water hardness of 100 mg/L, both species were less sensitive to copper when tested at 16 degrees C compared to 8 degrees C. The two species had similar sensitivity to copper in 100-mg/ L hardness water, but bull trout were 2.5 to 4 times less sensitive than rainbow trout in 220-mg/L hardness water. However, when our results were viewed in the context of the broader literature on rainbow trout sensitivity to copper, the sensitivities of the two species appeared similar. This suggests that adoption of toxicity thresholds that are protective of rainbow trout would be protective of bull trout; however, an additional safety factor may be warranted because of the additional level of protection necessary for this federally threatened species.     

Heavy metal toxicity to fish and the influence of water hardness

Toxicity tests with rainbow trout confirm that cadmium is less toxic in hard water (96 hr LC50=2.6 mg Cd/L) than in soft water (96 hr LC50=1.3 mg Cd/L). Water quality studies indicate that this is not due to a chemical reduction of available cadmium in hard water and no significant differences in cadmium uptake were detected between fish from the two levels of hardness. Possible explanations for the effect of hardness on heavy metal toxicity to fish are discussed.     

Effects of chronic Cd exposure via the diet or water on internal organ-specific distribution and subsequent gill Cd uptake kinetics in juvenile rainbow trout (Oncorhynchus mykiss)

New regulatory approaches to metal toxicity (e.g., biotic ligand model [BLM]) focus on gill metal binding and tissue-specific accumulation of waterborne metals; the dietary route of exposure and dietary/waterborne interactions are not considered, nor are the consequences of chronic exposure by either route. Therefore, we studied the effect of the same gill Cd load (approximately 2.5 microg/g), achieved by a chronic, 30-d exposure to Cd either via the diet (1,500 mg/kg) or the water (2 microg/L), on tissue-specific Cd distribution and subsequent uptake of waterborne Cd in juvenile rainbow trout (Oncorhynchus mykiss). These two exposure regimes resulted in a branchial Cd load that had been taken up across either apical gill membranes (waterborne Cd) or basolateral gill membranes (through the bloodstream for dietary Cd). The BLM characteristics of the gills (i.e., short-term Cd uptake kinetics) were altered: affinity (log K(Cd Gill) [95% confidence level]) decreased from 7.05 (6.75-8.76) for control to 6.54 (6.32-7.03) for waterborne Cd and 5.92 (5.83-6.51) for dietary Cd, whereas binding capacity (Bmax) increased from 3.12 (2.14-4.09) to 4.80 (3.16-6.43) and 5.50 (2.86-8.17) nmol x g(-1) for control, waterborne, and dietary Cd, respectively. Fish exposed to dietary Cd accumulated a much greater overall chronic Cd body burden relative to fish exposed to waterborne Cd or control fish. The carcass accumulated the greatest percentage of total body Cd in control and waterborne-exposed fish, whereas the intestinal tissue accumulated the greatest percentage in dietary-exposed fish. Tissue-specific Cd burdens were highest in the kidney in both dietary and waterborne treatments. We conclude that chronic Cd exposure alters Cd uptake dynamics, and that the route of Cd exposure, whether waterborne or dietary, results in differences of internal Cd accumulation and branchial Cd uptake characteristics. These factors should be considered in future BLM development.     

Effects of water hardness on toxicological responses to chronic waterborne silver exposure in early life stages of rainbow trout (Oncorhynchus mykiss)

Rainbow trout embryos and larvae were exposed to 0, 0.1, and 1 microg/L total silver (as AgNO3) in water of three different hardnesses (soft water [2 mg/L as CaCO3], moderately hard water [150 mg/L], and hard water [400 mg/L]) in a flow-through system from fertilization to swim-up (64 d). The objective of the study was to investigate the effects of water hardness on chronic silver toxicity. In the absence of silver, elevating hardness had a positive effect on early life stage survival and development, significantly decreasing mortality and accelerating time to 50% swim-up. Following hatch, exposure to 1 microg/L Ag significantly increased mortality relative to exposure to 0 microg/L Ag. No significant effects of silver on time to 50% hatch were observed; however, time to 50% swim-up was delayed, and 50% swim-up was not achieved over the course of the experiment during some exposures to 1 microg/L Ag. These results suggest that the current Canadian Water Quality Guideline (http://www.ccme.ca/assets/pdf/e1_062.pdf) of 0.1 microg/L Ag is sufficient in preventing mortality and altered development in early life stages of rainbow trout. Increasing water hardness from 2 to 150 or 400 mg/L was modestly protective against the mortality and delays in time to 50% swim-up associated with exposure to 1 microg/L Ag. The 150- and 400-mg/L hardnesses were equally protective against mortality, but 150-mg/L was more protective than 400-mg/L hardness against the delays in time to 50% swim-up. Overall, the protective effects of hardness on chronic silver toxicity in early life stages of rainbow trout are modest but similar to the protection afforded to acute silver toxicity in juvenile and adult rainbow trout.     

Distribution and elimination of a polychlorinated biphenyl after acute dietary exposure in yellow perch and rainbow trout

Distribution and elimination of a single polychlorinated biphenyl isomer (2,5,2,5-tetrachloro[¹⁴C]biphenyl, 4-CB) were compared in a nonfatty fish (yellow perch) and a fatty fish (rainbow trout). Adult fish were exposed acutely to 4-CB (0.8 g/fish) by the oral or intraperitoneal route and were killed at designated times thereafter for one month. Whole body elimination of 4-CB was similar in both species with 20 to 30% of the radioactive 4-CB being eliminated in the first 3 to 4 days after treatment, but very little thereafter. Also, the same extent of elimination was seen when the compound was given orally or intraperitoneally. Tissue distribution of 4-CB residues was different in the two species. Perch relied on viscera and carcass as main 4-CB distribution sites and skeletal muscle, skin and scales as minor sites. In rainbow trout, on the other hand, skeletal muscle and carcass were major distribution sites, whereas viscera and skin were minor sites. This species difference in 4-CB distribution was not due to a difference in sexual maturity of the perch and trout, because a build-up of eggs or sperm was not present in the peritoneal cavity of either species.Supported in part by the University of Wisconsin Sea Grant College Program, NIEHS Grant ES01332, and NIEHS Aquatic Biomedical Center Grant ES01985.     

Metal toxicity to embryos and larvae of eight species of freshwater fish-II: copper

Fish larvae and early juveniles of all species tested (brook trout, rainbow trout, brown trout, lake trout, northern pike, white sucker, herring, and smallmouth bass) were more sensitive to copper than the embryos. Embryo survival was affected only at the higher concentrations tested, for all species except the rainbow trout. The concentrations of copper that caused significant effects on the larval standing crop were similar for all species (31.7-43.5 microgram Cu/1) except the northern pike, which seemed to be considerably more resistant (104.1 microgram Cu/1). Copper concentrations shown to have no significant effects on the early developmental stages of these species are considered close estimates of the copper concentrations that would have no measurable adverse effects during a complete life cycle toxicity test under similar test conditions.     

Acute toxicity of hydrogen cyanide to freshwater fishes

Acute toxicity of hydrogen cyanide was determined at various temperatures from 4° to 30°C and oxygen concentrations of 3.36 to 9.26 mg/L on different life history stages of five species of fish: fathead minnow,Pimephales promelas Refinesque; bluegill,Lepomis macrochirus Rafinesque yellow perch,Perca flavescens (Mitchill); brook trout,Salvelinus fontinalis (Mitchill); and rainbow trout,Salmo gairdneri Richardson. Median lethal threshold concentrations and 96-hr LC50's were established by flow-through type bioassays. Acute toxicity varied from 57μg/L for juvenile rainbow trout to 191μg/L for field stocks of juvenile fathead minnows. Juvenile fish were more sensitive at lower temperatures and at oxygen levels below 5 mg/L. For most species juveniles were most sensitive and eggs more resistant. Paper No. 9954, Scientific Journal Series,Minnesota Agricultural Experiment Station, St. Paul, Minnesota. Research supported by theU.S. Environmental Protection Agency, Environmental Research Laboratory, Duluth, Minnesota, under Grant No. R802914.     

Sensitivity of mottled sculpins (Cottus bairdi) and rainbow trout (Onchorhynchus mykiss) to acute and chronic toxicity of cadmium, copper, and zinc

Studies of fish communities of streams draining mining areas suggest that sculpins (Cottus spp.) may be more sensitive than salmonids to adverse effects of metals. We compared the toxicity of zinc, copper, and cadmium to mottled sculpin (C. bairdi) and rainbow trout (Onchorhynchus mykiss) in laboratory toxicity tests. Acute (96-h) and early life-stage chronic (21- or 28-d) toxicity tests were conducted with rainbow trout and with mottled sculpins from populations in Minnesota and Missouri, USA, in diluted well water (hardness = 100 mg/L as CaCO3). Acute and chronic toxicity of metals to newly hatched and swim-up stages of mottled sculpins differed between the two source populations. Differences between populations were greatest for copper, with chronic toxicity values (ChV = geometric mean of lowest-observed-effect concentration and no-observed-effect concentration) of 4.4 microg/L for Missouri sculpins and 37 microg/L for Minnesota sculpins. Cadmium toxicity followed a similar trend, but differences between sculpin populations were less marked, with ChVs of 1.1 microg/L (Missouri) and 1.9 microg/L (Minnesota). Conversely, zinc was more toxic to Minnesota sculpins (ChV = 75 microg/L) than Missouri sculpins (chronic ChV = 219 microg/L). Species-average acute and chronic toxicity values for mottled sculpins were similar to or lower than those for rainbow trout and indicated that mottled sculpins were among the most sensitive aquatic species to toxicity of all three metals. Our results indicate that current acute and chronic water quality criteria for cadmium, copper, and zinc adequately protect rainbow trout but may not adequately protect some populations of mottled sculpins. Proposed water quality criteria for copper based on the biotic ligand model would be protective of both sculpin populations tested.     

Relative sensitivity of bull trout (Salvelinus confluentus) and rainbow trout (Oncorhynchus mykiss) to acute exposures of cadmium and zinc

Bull trout (Salvelinus confluentus) were recently listed as threatened in the United States under the federal Endangered Species Act. Present and historical habitat of this species includes waterways that have been impacted by metals released from mining and mineral processing activities. We conducted paired bioassays with bull trout and rainbow trout (Oncorhynchus mykiss) to examine the relative sensitivity of each species to Cd and Zn independently and as a mixture. A total of 15 pairs of acute toxicity bioassays were completed to evaluate the effects of different water hardness (30 or 90 mg/L as CaCO3), pH (6.5 or 7.5), and temperature (8 or 12 degrees C) on Cd and Zn toxicity. For both species, the acute toxicity of both Cd and Zn was greater than previously observed in laboratory studies. Bull trout were about twice as tolerant of Cd and about 50% more tolerant of Zn than were rainbow trout. Higher hardness and lower pH water produced lower toxicity and slower rates of toxicity in both species. Elevated temperature significantly increased the sensitivity of bull trout to Zn but decreased the sensitivity (not significantly) of rainbow trout to Zn. At a hardness of 30 mg/L, the toxicity values (i.e., median lethal concentration; 120-h LC50) for both species were lower than the current U.S. national water quality criteria for protection of aquatic life, indicating that current national criteria may not be protective of sensitive salmonids--including the threatened bull trout--in low calcium waters.     

Toxicity of anin situ oil shale process water to rainbow trout and fathead minnows

Anin situ oil shale process water, designated Omega-9 water, was used in flow-through bioassays with fathead minnows, rainbow trout and rainbow trout eggs. Of the two fish species, rainbow trout were more sensitive to acute exposure to Omega-9 water with 96-hour LC₅₀ dilutions of 0.51% and 0.41% in two independent determinations. In embryo-larval studies, the length of fry from eggs hatched and maintained in 0.16% process water was significantly less than that of eggs hatched in control water. A solution of the 13 major inorganic constituents of Omega-9 water, with a 96-hour LC₅₀ of 0.56% for rainbow trout, showed that inorganics accounted for most of the acute toxicity of Omega-9 water.Work funded under an Interagency Agreement between the U.S. Department of Energy and the U.S. Environmental Protection Agency under Contract No. DE-AS20-79 LC 01761 to the Rocky Mountain Institute of Energy and Environment, University of Wyoming.     

Influence of dietary sodium on waterborne copper toxicity in rainbow trout,Oncorhynchus mykiss

Juvenile rainbow trout were fed diets containing control (0.26 mmol/g) or elevated (1.3 mmol/g) dietary Na+ in combination with either background (19 nmol/L) or moderately elevated levels (55 or 118 nmol/L) of waterborne Cu for 21 d. Unidirectional waterborne Na+ uptake rates (measured with 22Na) were up to four orders of magnitude higher than those of Cu (measured with 64Cu). Chronic exposure to elevated dietary Na+ alone or in combination with elevated waterborne Cu decreased whole-body uptake rates of waterborne Na+ and Cu. Accumulation of new Cu and Na+ at the gills was positively and highly significantly correlated and responded to the experimental treatments in a similar fashion, suggesting that Na+ and Cu have common branchial uptake pathways and that dietary Na+ preexposure modifies these pathways. Chronic exposure to elevated waterborne Cu significantly increased Cu concentrations in the liver but caused only modest increases in total Cu concentrations in the whole body and gill. Chronic exposure to elevated dietary Na+ slightly decreased whole-body Cu concentration on day 14 and greatly reduced liver Cu concentration on days 14 and 21; new Cu accumulation in whole-body, gill, and internal organs was reduced on all days. Chronic exposure to elevated waterborne Cu or dietary Na+ alone reduced short-term gill Cu binding at low waterborne Cu concentrations. At high waterborne Cu concentrations, chronic exposure to elevated waterborne Cu had no effect, while elevated dietary Na+ increased Cu binding to the gills. Combined chronic exposure to elevated dietary Na+ and waterborne Cu decreased gill Cu binding over the entire range of Cu concentrations tested. Clearly, chronic exposure to elevated dietary Na+ and waterborne Cu appears to modify gill Cu-binding characteristics and may be important considerations in future development of a chronic biotic ligand model for Cu.     

Copper Speciation and Accumulation in the Gill Microenvironment of Carp (Cyprinus carpio) in the Presence of Kaolin Particles

Carp were exposed to copper adsorbed on kaolin particles at various concentrations (0–2.4 mg/L), and net accumulation due to elevated adsorbed copper in the surrounding water was observed. Copper speciation in the water and fish gill microenvironment was modeled in the presence and absence of kaolin using a chemical speciation program (MINTEQA2). The adsorption affinity constants of kaolin for copper at various pH values used in the speciation calculations were experimentally determined, and the quantitative relationship between the affinity constant and pH was modeled. Copper accumulations in fish gills exposed to kaolin-adsorbed copper was then observed. The results indicate that desorption occurred in the fish gill microenvironment due to both mucus competition of copper and slight increase in water pH. Furthermore, the available copper species increased as a result of desorption, causing a net accumulation of Cu by the gills. Received: 15 June 2001/Accepted: 2 November 2001     

Acute and chronic toxicity of nickel to rainbow trout (Oncorhynchus mykiss)

Of the fish species tested in chronic Ni exposures, rainbow trout (Oncorhynchus mykiss) is the most sensitive. To develop additional Ni toxicity data and to investigate the toxic mode of action for Ni, we conducted acute (96-h) and chronic (85-d early life-stage) flow-through studies using rainbow trout. In addition to standard toxicological endpoints, we investigated the effects of Ni on ionoregulatory physiology (Na, Ca, and Mg). The acute median lethal concentration for Ni was 20.8 mg/L, and the 24-h gill median lethal accumulation was 666 nmol/g wet weight. No effects on plasma Ca, Mg, or Na were observed during acute exposure. In the chronic study, no significant effects on embryo survival, swim-up, hatching, or fingerling survival or growth were observed at dissolved Ni concentrations up to 466 microg/L, the highest concentration tested. This concentration is considerably higher than the only other reported chronic no-observed-effect concentration (<33 microg/L) for rainbow trout. Accumulation of Ni in trout eggs indicates the chorion is only a partial barrier with 36%, 63%, and 1% of total accumulated Ni associated with the chorion, yolk, and embryo, respectively. Whole-egg ion concentrations were reduced by Ni exposure. However, most of this reduction occurred in the chorion rather than in the embryos, and no effects on hatching success or larval survival were observed as a result. Plasma ion concentrations measured in swim-up fingerlings at the end of the chronic-exposure period were not significantly reduced by exposure to Ni. Nickel accumulated on the gill in an exponential manner but plateaued in trout plasma at waterborne Ni concentrations of 118 microg/L or greater. Consistent with previous studies, Ni did not appear to disrupt ionoregulation in acute exposures of rainbow trout. Our results also suggest that Ni is not an ionoregulatory toxicant in long-term exposures, but the lack of effects in the highest Ni treatment precludes a definitive conclusion.     

Comparison of relative binding affinities of endocrine active compounds to fathead minnow and rainbow trout estrogen receptors

Twelve chemicals were tested for binding affinity to rainbow trout liver estrogen receptor (rbtER) and fathead minnow liver ER (fhmER). The chemicals included estradiol (E2), diethylstilbestrol (DES), ethinylestradiol (EE2), estrone (El), estriol, tamoxifen (TAM), genistein (GEN), p-nonylphenol (PNP), p-tert-octylphenol (PTOP), methoxychlor (MXC), testosterone, and methyltestosterone (MT). Relative binding affinity (RBA) was calculated for each chemical as a function of E2 binding to the receptor. The estrogens DES, EE2, and E1 bound with high affinity to both receptors, with respective RBAs of 583, 166, and 28% (fathead minnow) and 179, 89, and 5% (rainbow trout). Relative binding affinity of E3, TAM, and GEN for both fhmER and rbtER were moderate, with values between 0.3 and 5%. The alkylphenols had weak affinity for the ERs with RBAs for the fhmER of 0.1 and 0.01 for PNP and PTOP, respectively. Corresponding values for the rbtER are 0.027 and 0.009. Estradiol ([3H]E2) only partially was displaced from both the fhmER and the rbtER by MXC, T, and MT. Comparison of RBAs of the chemicals tested for fhmER and rbtER indicates that the rank order of RBAs essentially are the same for both species.     

Acute toxicity of copper, ammonia, and chlorine to glochidia and juveniles of freshwater mussels (Unionidae)

The objective of the present study was to determine acute toxicity of copper, ammonia, or chlorine to larval (glochidia) and juvenile mussels using the recently published American Society for Testing and Materials (ASTM) Standard guide for conducting laboratory toxicity tests with freshwater mussels. Toxicity tests were conducted with glochidia (24- to 48-h exposures) and juveniles (96-h exposures) of up to 11 mussel species in reconstituted ASTM hard water using copper, ammonia, or chlorine as a toxicant. Copper and ammonia tests also were conducted with five commonly tested species, including cladocerans (Daphnia magna and Ceriodaphnia dubia; 48-h exposures), amphipod (Hyalella azteca; 48-h exposures), rainbow trout (Oncorhynchus mykiss; 96-h exposures), and fathead minnow (Pimephales promelas; 96-h exposures). Median effective concentrations (EC50s) for commonly tested species were >58 microg Cu/L (except 15 microg Cu/L for C. dubia) and >13 mg total ammonia N/L, whereas the EC50s for mussels in most cases were <45 microg Cu/L or <12 mg N/L and were often at or below the final acute values (FAVs) used to derive the U.S. Environmental Protection Agency 1996 acute water quality criterion (WQC) for copper and 1999 acute WQC for ammonia. However, the chlorine EC50s for mussels generally were >40 microg/L and above the FAV in the WQC for chlorine. The results indicate that the early life stages of mussels generally were more sensitive to copper and ammonia than other organisms and that, including mussel toxicity data in a revision to the WQC, would lower the WQC for copper or ammonia. Furthermore, including additional mussel data in 2007 WQC for copper based on biotic ligand model would further lower the WQC.     

Metal toxicity to embryos and larvae of eight species of freshwater fish—II: Copper

Fish larvae and early juveniles of all species tested (brook trout, rainbow trout, brown trout, lake trout, northern pike, white sucker, herring, and smallmouth bass) were more sensitive to copper than the embryos. Embryo survival was affected only at the higher concentrations tested, for all species except the rainbow trout. The concentrations of copper that caused significant effects on the larval standing crop were similar for all species (31.7–43.5 ug Cu/1) except the northern pike, which seemed to be considerably more resistant (104.1 g Cu/1). Copper concentrations shown to have no significant effects on the early developmental stages of these species are considered close estimates of the copper concentrations that would have no measurable adverse effects during a complete life cycle toxicity test under similar test conditions.     

A relationship between gill silver accumulation and acute silver toxicity in the freshwater rainbow trout: support for the acute silver biotic ligand model

Rainbow trout were exposed to a range of silver concentrations (as AgNO3) in flowing synthetic soft water (0.05 mM Na+, 0.05 mM Cl-, 0.05 mM Ca2+, 0.02 mM Mg2+, 0.02 mM K+, pH 7.0, approximately 0.7 mg C/L dissolved organic carbon, 10 mg CaCO3/L, 10 +/- 2 degrees C) to investigate a possible relationship between short-term gill silver accumulation (3 h or 24 h) and acute silver toxicity (96-h mortality). We also investigated potential relationships between gill silver accumulation and inhibition of Na+ uptake plus inhibition of gill Na+K(+)-adenosine triphosphatase (ATPase) activity. The 96-h median lethal concentration (LC50) values were 13.3 microg total Ag L(-1) and 3.3 microg dissolved Ag L(-1). A relationship was demonstrated between 3-h and 24-h gill silver accumulation and 96-h mortality. A relationship also was demonstrated between gill silver accumulation and inhibition of Na+ uptake at 24 h of exposure. No relationship between gill silver accumulation and inhibition of gill Na+K(+)-ATPase activity was found. The 96-h median lethal gill accumulation (LA50) values of 129 (at 3 h) and 191 ng g(-1) (at 24 h) and a conditional equilibrium binding constant of 8.0 for Ag+ binding to the gills were calculated. These observations support use of the silver biotic ligand model (BLM) as a regulatory tool to predict acute silver toxicity.     

Social interactions affect physiological consequences of sublethal copper exposure in rainbow trout,Oncorhynchus mykiss

The interactions of sublethal waterborne copper exposure and social dominance behavior were examined in juvenile rainbow trout. Dominance hierarchies were determined between pairs of fish by behavioral observations and among groups of 10 fish by the use of passive integrated transponder (PIT) tagging equipment. The present study is one of the first to utilize this novel PIT tag method for behavioral assessment. Feeding behavior was quantified by placing a PIT tag recorder at the entrance to the feeding area. Linear dominance hierarchies were documented based on these observations of feeding behavior. Dominance hierarchies established in control water were not altered by exposure to 30 microg/L of copper; however, physiological responses of fish to sublethal concentrations of copper were related to social rank. Subordinate fish exhibited a higher accumulation of copper in both gill and liver tissue. Subordinates of paired fish were also shown to have a higher uptake of sodium than dominant fish, and the uptake of sodium was correlated with uptake of copper from the water. Therefore, within a population of fish, it cannot be assumed that individuals of different social status will exhibit the same physiological responses to the presence of copper.