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.     

The effect of calcium and magnesium ratios on the toxicity of copper to five aquatic species in freshwater

While it is generally accepted that water hardness affects copper toxicity, the major ions that contribute to water hardness (calcium [Ca] and magnesium [Mg]) may affect copper toxicity differently. This is important because the Ca:Mg ratio in standard laboratory-reconstituted waters often differs from the ratio in natural surface waters. Copper toxicity was assessed for five different aquatic species: rainbow trout (RBT), fathead minnow (FHM), Ceriodaphnia dubia, Daphnia magna, and an amphipod (Gammarus sp.) under different Ca:Mg ratios (4:0, 3:1, 1:1, 1:3, and 1:4 mass basis) at a common hardness (180 mg/L as CaCO3) and alkalinity (120 mg/L as CaCO3). Copper toxicity increased at lower Ca:Mg ratios for RBT but increased at higher Ca:Mg ratios for D. magna. Fathead minnows (<24 h old) were more sensitive to copper in 1:1 Ca:Mg waters compared to 3:1 Ca:Mg waters. The toxicity of copper did not vary under different Ca:Mg ratios for Gammarus sp., C. dubia, and 28-d-old FHM. The effect of Ca:Mg ratios on copper toxicity changed for D. magna in softer water (90 mg/L as CaCO3) compared with hard water studies.     

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.     

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.     

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.     

Relative sensitivity of early life stages of Arctic grayling, Coho salmon, and rainbow trout to nine inorganics.

The acute toxicity of nine inorganics associated with placer mining sediments to early life stages of Arctic grayling (Thymallus arcticus), coho salmon (Oncorhynchus kisutch), and rainbow trout (O. mykiss) was determined in soft water (hardness, 41 mg liter-1 CaCO3) at 12 degrees C. The relative toxicities of the inorganics varied by four orders of magnitude; from most toxic to least toxic, the rank order was cadmium, silver, mercury, nickel, gold, arsenite, selenite, selenate, and hexavalent chromium. In general, juvenile life stages of the three species tested were more sensitive to these inorganics than the alevin life stage. Among juveniles, no single species was consistently more sensitive to the inorganics than another; among alevins, Arctic grayling were generally more sensitive than coho salmon and rainbow trout. Based on the results of the present study, estimated no-effect concentrations of arsenic and mercury, but not cadmium, chromium, gold, nickel, selenium, or silver, are close to their concentrations reported in streams with active placer mines in Alaska. Thus, arsenic (as arsenite(III)) and mercury may pose a hazard to Arctic grayling and coho salmon in Alaskan streams with active placer mines.     

Acute and chronic toxicity of zinc to the mottled sculpin Cottus bairdi

The acute and chronic toxicity of zinc to wild mottled sculpin (Cottus bairdi) was measured with 13-d and 30-d flow-through toxicity tests, respectively. Exposure water hardness was 48.6 mg/L as CaCO3 and 46.3 mg/L as CaCO3 in the acute and chronic tests, respectively; pH was slightly above neutral; and temperature near 12 degrees C. The median lethal concentration (LC50) after 96 h was 156 microg Zn/L, but decreased with exposure duration to a median incipient lethal level (ILL50) of 38 microg Zn/L after 9 d, the lowest zinc LC50 reported for any fish species. The 30-d chronic no-effect and lowest-effect concentrations were 16 microg Zn/L (no mortality) and 27 microg Zn/L (32% mortality), respectively. The ILL50 was 32 microg Zn/L. No sublethal growth differences were observed during the chronic test. Analysis of the results from these tests suggested that mottled sculpin may experience acute and chronic toxicity at zinc concentrations lower than any other fish species tested to date. Protection of aquatic communities in stream reaches contaminated by metals seem to require determination of zinc toxicity to lotic species other than trout and other species amenable to aquaculture.     

The effects of low hardness and pH on copper toxicity to Daphnia magna

The majority of metal toxicity data available for freshwater organisms have been generated in laboratory water at pH > 6.5 and hardness > 50 mg/L as CaCO3. Extrapolation of these results to soft surface waters (i.e., hardness < or = 40 mg/L as CaCO3), similar to predominant conditions in the southeastern United States, may prove challenging. For example, South Carolina has surface waters that average 20 mg/L as CaCO3, and exist at extremes of 1 and 600 mg/L as CaCO3. This research characterized the acute toxicity of Cu to Daphnia magna in waters with low hardness and low pH. The 48-h total Cu median lethal concentrations were related to water hardness over a hardness range of 8 to 51 mg/L as CaCO3. Although toxicological differences existed between water hardness of 7 and 20 mg/L as CaCO3 (p = 0.0001), differences in pH (range 5.5-8.5) did not influence acute Cu toxicity. Results of these laboratory studies will provide the data needed to more accurately predict organism response to Cu in waters with low pH and low hardness.     

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.     

Influence of water chemistry on the acute toxicity of copper and zinc to the cladoceran Ceriodaphnia cf dubia

This study determined the influence of key water chemistry parameters (pH, alkalinity, dissolved organic carbon [DOC], and hardness) on the aqueous speciation of copper and zinc and its relationship to the acute toxicity of these metals to the cladoceran Ceriodaphnia cf dubia. Immobilization tests were performed for 48-h in synthetic or natural waters buffered at various pH values from 5.5 to 8.4 (other chemical parameters held constant). The toxicity of copper to C. cf dubia decreased fivefold with increasing pH, whereas the toxicity of zinc increased fivefold with increasing pH. The effect of DOC on copper and zinc toxicity to C. cf dubia was determined using natural fulvic acid in the synthetic water. Increasing DOC was found to decrease linearly the toxicity of copper, with the mean effect concentration of copper that immobilized 50% of the cladocerans (EC50) value 45 times higher at 10 mg/L, relative to 0.1 mg/L DOC at pH 6.5. In contrast, the addition of 10 mg/L DOC only resulted in a very small (1.3-fold) reduction in the toxicity of zinc to C. cf dubia. Copper toxicity to C. cf dubia generally did not vary as a function of hardness, whereas zinc toxicity was reduced by a factor of only two, with an increase in water hardness from 44 to 374 mg CaCO3/L. Increasing bicarbonate alkalinity of synthetic waters (30-125 mg/L as CaCO3) decreased the toxicity of copper up to fivefold, which mainly could be attributed to the formation of copper-carbonate complexes, in addition to a pH effect. The toxicity of copper added to a range of natural waters with varying DOC content, pH, and hardness was consistent with the toxicity predicted using the data obtained from the synthetic waters.     

Evaluation of acute copper toxicity to larval fathead minnows (Pimephales promelas) in soft surface waters

The hardness-based regulatory approach for Cu prescribes an extrapolation of the toxicity-versus-hardness relationship to low hardness (< or =50 mg/L as CaCO3). Hence, the objective of the present research was to evaluate the influences of water quality on acute Cu toxicity to larval fathead minnow (Pimephales promelas) in low-hardness surface waters. Seasonal water sampling was conducted at 24 sites throughout South Carolina, USA, to determine the site-specific influences of soft surface-water conditions on acute Cu toxicity. Concurrent toxicity tests in laboratory water, matched for hardness and alkalinity (modified method), also were conducted to allow calculation of water-effect ratios (WERs). In addition, tests were conducted at recommended hardness levels (recommended method) for comparison of WER methodology in soft water. Surface-water conditions (average+/-standard deviation, n = 53) were hardness of 16+/-8 mg/L as CaCO3, alkalinity of 18+/-11 mg/L as CaCO3, and dissolved organic carbon of 6+/-4 mg/L. Dissolved Cu 48-h median lethal concentration (LC50) values varied nearly 45-fold across the dataset and greater than four-fold at individual sites. Spatial (p < 0.0001) and seasonal (p = 0.026) differences among LC50 values were determined for eight sites that had multiple toxicity results for one year. All modified WERs were greater than 1.0, suggesting that the site waters were more protective of Cu toxicity than the matched laboratory water. Some WERs generated using recommended methods were less than 1.0, suggesting limited site-specific protection. Based on these observations, extrapolation of the hardness-based equation for Cu at 50 mg/L or less as CaCO3 would adequately protect fathead minnow populations in soft surface waters. The WER results presented here demonstrate the inconsistency between hardness-based criteria and the methodology for deriving site-specific water-quality criteria in low-hardness waters.     

Influence of water quality and age on nickel toxicity to fathead minnows (Pimephales promelas)

This research characterized the effects of water quality and organism age on the toxicity of nickel (Ni) to fathead minnows (Pimephales promelas) to facilitate the accurate development of site-specific water-quality criteria. Nickel sulfate hexahydrate (NiSO4 x 6H2O) was used as the Ni source for performing acute toxicity tests (median lethal concentration after 96-h exposure [96-h LC50]) with < 1-d-old and 28-d-old P. promelas under varying regimes of hardness, pH, alkalinity, and natural organic matter (NOM). The toxicity of Ni was inversely related to water hardness between hardness values of 20 and 150 mg/L (as CaCO3). Below 30 mg/L alkalinity, Ni toxicity was related to alkalinity. The effect of pH was confounded by hardness and the presence of NOM. In the absence of NOM, the toxicity of Ni increased as pH increased at high hardness and alkalinity. In general, 28-d-old fish were less sensitive than < 1-d-old fish to Ni. This lower sensitivity ranged from 12-fold at low hardness and alkalinity (20 and 4 mg/L, respectively) to 5-fold at high hardness and alkalinity (100 and 400 mg/L, respectively). The presence of NOM (10 mg/L as dissolved organic carbon [DOC]) reduced Ni toxicity by up to 50%, but this effect appeared to be saturated above DOC at 5 mg/L. Incubating Ni with the NOM solution from 1 to 17 days had no effect on Ni toxicity. When using multivariate analysis, the 96-h LC50 for Ni was a function of fish age, alkalinity, hardness, and NOM (96-h LC50 = -0.642 + 0.270(fish age) + 0.005(alkalinity) + 0.018(hardness) + 0.138(DOC)). When using this model, we found a strong relationship between measured and predicted 96-h LC50 values (r2 = 0.94) throughout the treatment water qualities. The biotic ligand model (BLM) did not accurately predict Ni toxicity at high or low levels of alkalinity. Results of our research suggest that the BLM could be improved by considering NiCO3 to be bioavailable.     

Toxicity of Copper to Early-life Stage Kootenai River White Sturgeon, Columbia River White Sturgeon, and Rainbow Trout

White sturgeon (Acipenser transmontanus) populations throughout western North America are in decline, likely as a result of overharvest, operation of dams, and agricultural and mineral extraction activities in their watersheds. Recruitment failure may reflect the loss of early-life stage fish in spawning areas of the upper Columbia River, which are contaminated with metals from effluents associated with mineral-extraction activities. Early-life stage white sturgeon (A. transmontanus) from the Columbia River and Kootenai River populations were exposed to copper during 96-h flow-through toxicity tests to determine their sensitivity to the metal. Similar tests were conducted with rainbow trout (RBT [Oncorhynchus mykiss]) to assess the comparative sensitivity of this species as a surrogate for white sturgeon. Exposures were conducted with a water quality pH 8.1-8.3, hardness 81-119?mg/L as CaCO(2), and dissolved organic carbon 0.2-0.4?mg/L. At approximately 30?days posthatch (dph), sturgeon were highly sensitive to copper with median lethal concentration (LC(50)) values ranging from 4.1 to 6.8?μg/L compared with 36.5?μg/L for 30?dph RBT. White sturgeon at 123-167?dph were less sensitive to copper with LC(50) values ranging from 103.7 to 268.9?μg/L. RBT trout, however, remained more sensitive to copper at 160?dph with an LC(50) value of 30.9?μg/L. The results indicate that high sensitivity to copper in early-life stage white sturgeon may be a factor in recruitment failure occurring in the upper Columbia and Kootenai rivers. When site-specific water-quality criteria were estimated using the biotic ligand model (BLM), derived values were not protective of early-life stage fish, nor were estimates derived by water-hardness adjustment.     

Effects of medetomidine on hepatic EROD activity in three species of fish

Medetomidine, an antifouling candidate, was investigated for its effects on cytochrome P4501A (CYP1A) activity in fish. Rainbow trout (Oncorhynchus mykiss), turbot (Psetta maxima), and Atlantic cod (Gadus morhua) were exposed to medetomidine either via i.p. injection (<5 micromol (1mg)/kg) or via water (<50 nM). Enzyme activity was measured as ethoxyresorufin-O-deethylase (EROD) activity in liver microsomes. There was a small (2-7-fold) increase in EROD activity in rainbow trout. In turbot, EROD activity increased (4-fold) after injection, while a non-significant (50%) decrease was observed after water exposure. No effects on EROD activities were observed in Atlantic cod. In vitro inhibition studies of EROD activities in liver microsomes from all three species showed that medetomidine was a very potent CYP1A inhibitor. Thus, median inhibition values (IC(50)) were 35+/-10nM for rainbow trout, 47+/-17 nM for turbot, and 111+/-70 nM for Atlantic cod. These observed effects suggest that medetomidine interferes with CYP1A-dependent metabolism of xenobiotics in these fish species.     

Effects of dissolved organic carbon concentration and source, pH, and water hardness on chronic toxicity of copper to Daphnia magna

The effects of pH (5.3-8.7), water hardness (CaCO3 at 25-500 mg/L), dissolved organic carbon (DOC) concentration (1.6-18.4 mg/L), and DOC source on the chronic toxicity of copper to Daphnia magna were investigated by using a multifactorial, central composite test design. Natural dissolved organic matter (DOM) was collected at three sites in Belgium and The Netherlands by using reverse osmosis. For a total number of 35 toxicity tests performed, 21-d no-observed-effect concentrations (NOECs) of copper based on reproduction ranged from 29.4 to 228 microg/L and 21-d concentrations of copper causing 50% reduction of reproduction (EC50s) ranged from 41.5 to 316 microg/L. Statistical analysis revealed that DOC concentration and pH had a significant effect on copper toxicity but hardness (at the levels tested) did not. In general, an increase in pH or DOC resulted in a linear increase of 21-d NOEC and EC50 values. All DOMs (originating from three different sources) reduced copper toxicity to the same extent. Multiple linear regression analysis on the results of all 35 toxicity tests revealed that DOC concentration is the most important factor for chronic toxicity of copper to D. magna, explaining about 60% of the observed variability, whereas pH only explained about 15% of the observed variability. Regression models were developed (with DOC and pH as parameters) that were capable of predicting NOECs and EC50s within a factor of 1.9 from observed NOEC and EC50 values obtained with eight natural surface waters spiked with copper. Until future research further elucidates the mechanisms underpinning the observed bioavailability relations, these empirical regression models can become a first simple tool for regulatory applications.     

Using accelerated life testing procedures to compare the relative sensitivity of rainbow trout and the federally listed threatened bull trout to three commonly used rangeland herbicides (picloram, 2,4-D, and clopyralid)

We conducted 96-h static acute toxicity studies to evaluate the relative sensitivity of juveniles of the threatened bull trout (Salvelinus confluentus) and the standard cold-water surrogate rainbow trout (Onchorhyncus mykiss) to three rangeland herbicides commonly used for controlling invasive weeds in the northwestern United States. Relative species sensitivity was compared using three procedures: standard acute toxicity testing, fractional estimates of lethal concentrations, and accelerated life testing chronic estimation procedures. The acutely lethal concentrations (ALC) resulting in 50% mortality at 96 h (96-h ALC50s) were determined using linear regression and indicated that the three herbicides were toxic in the order of picloram acid > 2,4-D acid > clopyralid acid. The 96-h ALC50 values for rainbow trout were as follows: picloram, 41 mg/L; 2.4-D, 707 mg/L; and clopyralid, 700 mg/L. The 96-h ALC50 values for bull trout were as follows: picloram, 24 mg/L; 2.4-D, 398 mg/L; and clopyralid, 802 mg/L. Fractional estimates of safe concentrations, based on 5% of the 96-h ALC50, were conservative (overestimated toxicity) of regression-derived 96-h ALC5 values by an order of magnitude. Accelerated life testing procedures were used to estimate chronic lethal concentrations (CLC) resulting in 1% mortality at 30 d (30-d CLC1) for the three herbicides: picloram (1 mg/L rainbow trout, 5 mg/L bull trout), 2,4-D (56 mg/L rainbow trout, 84 mg/L bull trout), and clopyralid (477 mg/L rainbow trout; 552 mg/L bull trout). Collectively, the results indicated that the standard surrogate rainbow trout is similar in sensitivity to bull trout. Accelerated life testing procedures provided cost-effective, statistically defensible methods for estimating safe chronic concentrations (30-d CLC1s) of herbicides from acute toxicity data because they use statistical models based on the entire mortality:concentration:time data matrix.     

Effects of sodium chloride on chronic silver toxicity to early life stages of rainbow trout (Oncorhynchus mykiss)

The chronic (early life stage) toxicity of silver to rainbow trout (Oncorhynchus mykiss) was determined in flow-through exposures. Rainbow trout embryos were exposed to silver (as AgNO3) from 48 h or less postfertilization to 30 d postswimup in soft water in the presence and absence of 49 mg/L of NaCl (30 mg/L of Cl). The studies determined effect levels for rainbow trout exposed throughout an extended development period and assessed possible protective effects of sodium chloride. Lowest-observed-effect concentrations were greater than 1.25 microg/L of dissolved silver for survival, mean day to hatch, mean day to swimup, and whole-body sodium content in both studies. Whole-body silver concentrations increased significantly at 0.13 microg/L of dissolved silver in unmodified water and at 1.09 microg/L of dissolved silver in amended water. The maximum-acceptable toxicant concentration for growth was greater than 1.25 microg/L of dissolved silver in unmodified water and 0.32 microg/L of dissolved silver in amended water. Whole-body silver concentrations were more sensitive than survival and growth end points in unmodified water. Interpretation of sodium chloride effects on chronic silver toxicity to rainbow trout was complicated by differences in measured effect levels that were potentially the result of strain differences between test organisms in the two studies.     

An Ecological Risk Assessment of the Acute and Chronic Toxicity of the Herbicide Picloram to the Threatened Bull Trout (<Emphasis Type="Italic">Salvelinus confluentus</Emphasis>) and the Rainbow Trout (<Emphasis Type="Italic">Onchorhyncus mykiss</Emphasis>)

We conducted acute and chronic toxicity studies of the effects of picloram acid on the threatened bull trout (Salvelinus confluentus) and the standard coldwater surrogate rainbow trout (Oncorhynchus mykiss). Juvenile fish were chronically exposed for 30 days in a proportional flow-through diluter to measured concentrations of 0, 0.30, 0.60, 1.18, 2.37, and 4.75 mg/L picloram. No mortality of either species was observed at the highest concentration. Bull trout were twofold more sensitive to picloram (30-day maximum acceptable toxic concentration of 0.80 mg/L) compared to rainbow trout (30-day maximum acceptable toxic concentration of 1.67 mg/L) based on the endpoint of growth. Picloram was acutely toxic to rainbow trout at 36 mg/L (96-h ALC50). The acute:chronic ratio for rainbow trout exposed to picloram was 22. The chronic toxicity of picloram was compared to modeled and measured environmental exposure concentrations (EECs) using a four-tiered system. The Tier 1, worst-case exposure estimate, based on a direct application of the current maximum use rate (1.1 kg/ha picloram) to a standardized aquatic ecosystem (water body of 1-ha area and 1-m depth), resulted in an EEC of 0.73 mg/L picloram and chronic risk quotients of 0.91 and 0.44 for bull trout and rainbow trout, respectively. Higher-tiered exposure estimates reduced chronic risk quotients 10-fold. Results of this study indicate that picloram, if properly applied according to the manufacturer’s label, poses little risk to the threatened bull trout or rainbow trout in northwestern rangeland environments on either an acute or a chronic basis.     

Toxicity of cadmium to early life stages of brown trout (Salmo trutta) at multiple water hardnesses

Toxicity of cadmium to early life stages of brown trout (Salmo trutta) was determined at multiple water hardnesses. Increasing water hardness decreased cadmium toxicity. Postswimup fry were much more sensitive than embryos and larvae. Chronic values from early life stage tests initiated with eyed embryos were 3.52, 6.36, and 13.6 microg Cd/L at water hardnesses of 30.6, 71.3, and 149 mg/L, respectively. In tests initiated with 30-d postswimup fry, chronic values were 1.02, 1.83, and 6.54 microg Cd/L at water hardnesses of 29.2, 67.6, and 151 mg/L, respectively. Higher chronic values from the early life stage tests compared to tests initiated with swimup fry likely are caused by acclimation during cadmium-tolerant embryo and larval stages. Growth was not affected by cadmium in the early life stage tests but was negatively affected in tests initiated with fry at water hardnesses of 29.2 and 67.6 mg/L. Concentrations of cadmium that reduced growth were higher than those that increased mortality. Median lethal concentrations for swimup fry after 96 h were 1.23, 3.90, and 10.1 microg Cd/L at water hardnesses of 29.2, 67.6, and 151 mg/L, respectively. Test results enable prediction of acute mortality of brown trout swimup fry based on cadmium concentration and water hardness.     

Influence of exposure duration on the toxicity of triclopyr ester to fish and aquatic insects

Flow-through toxicity tests were conducted to determine the effects of exposure time on the toxicity of triclopyr butoxyethyl ester (Garlon^® 4) to fish (rainbow trout and chinook salmon) and stream insects (Hydropsyche sp. and Isonychia sp.). The toxicity of triclopyr ester to fish increased with exposure time, but the rate of increase in toxicity declined with increasing exposure duration. Median lethal concentrations for rainbow trout exposed for 1, 6, or 24 h were 22.5, 1.95, and 0.79 mg/L triclopyr ester (expressed as acid equivalent, nominal concentrations), respectively. Comparable values for chinook salmon were 34.6, 4.7, and 1.76 mg/L. The toxicity of triclopyr ester to aquatic insects also increased with increasing exposure time, but was considerably less than the toxicity to fish. There was no significant mortality (chi-square p>0.05) of insects following 3-h exposures to the maximum test concentration of approximately 110 mg/L. Median lethal concentrations following 9- and 24-h exposures were 14.9 and 4.0 ml/L for Hydropsyche sp., and 37.0 and 8.8 mg/L for Isonychia sp., respectively. At each exposure time in the toxicity tests, there was a sharp increase in mortality over relatively small increases in concentration, resulting in extremely steep slopes of the probit lines (6.3–33.8), and indicating an apparent response threshold. The herbicide exhibited delayed lethal effects, particularly in fish, but only at short term exposures to higher concentrations. The risk of adverse effects on fish and aquatic insects from triclopyr ester contamination, based on the results of these time-toxicity tests, is discussed.