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.     

Toxicity of the herbicide glyphosate and several of its formulations to fish and aquatic invertebrates

Studies were initiated to determine the acute toxicity of technical grade glyphosate (MON0573), the isopropylamine salt of glyphosate (MON0139), the formulated herbicide Roundup^® (MON02139), and the Roundup^® surfactant (MON0818) to four aquatic invertebrates and four fishes: daphnids (Daphnia magna), scuds (Gammarus pseudolimnaeus), midge larvae (Chironomous plumosus), mayfly nymphs (Ephemerella walkeri), Rainbow trout (Salmo gairdneri), fathead minnows (Pimephales promelas), channel catfish (Ictalurus punctatus), and bluegills (Lepomis macrochirus). Acute toxicities for Roundup ranged from 2.3 mg/L (96-h LC50, fathead minnow) to 43 mg/L (48-h EC50, mature scuds). Toxicities of the surfactant were similar to those of the Roundup formulation. Technical glyphosate was considerably less toxic than Roundup or the surfactant; for midge larvae, the 48-h EC50 was 55 mg/L and for rainbow trout, the 96-h LC50 was 140 mg/L. Roundup was more toxic to rainbow trout and bluegills at the higher test temperatures, and at pH 7.5 than at pH 6.5. Toxicity did not increase at pH 8.5 or 9.5. Eyed eggs were the least sensitive life stage, but toxicity increased markedly as the fish entered the sac fry and early swim-up stages. No changes in fecundity or gonadosomatic index were observed in adult rainbow trout treated with the isopropylamine salt or Roundup up to 2.0 mg/L. The aging of Roundup test solutions for seven days did not reduce toxicity to midge larvae, rainbow trout or bluegills. In avoidance studies, rainbow trout did not avoid concentrations of the isopropylamine salt up to 10.0 mg/L; mayfly nymphs avoided 10.0 mg/L of Roundup, but not 1.0 mg/L. In a simulated field application, midge larvae avoided 2.0 mg/L of Roundup. Application of Roundup, at recommended rates, along ditchbank areas of irrigation canals should not adversely affect resident populations of fish or invertebrates. However, spring applications in lentic situations, where dissolved oxygen levels are low or temperatures are elevated, could be hazardous to young-of-the-year-fishes.     

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.     

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.     

Acute and embryo-larval toxicity of phenolic compounds to aquatic biota

Because of the prevalence of phenolic compounds in various types of effluents, both acute and embryo-larval bioassays were performed on eight phenolic compounds with rainbow trout, fathead minnows andDaphnia pulicaria. In flow-through bioassays, the 96-hr LC₅₀ values for rainbow trout and fathead minnows ranged from <0.1 mg/L for hydroquinone to >100 mg/L for resorcinol.Daphnia pulicaria was consistently the least sensitive species tested as measured in 48-hr bioassays, while fathead minnows and rainbow trout varied in their relative sensitivity to phenolics as measured in 96-hr tests. Fathead minnows were more sensitive to phenol at 25°C than at 14°C.In embryo-larval bioassays with phenol, fathead minnow growth was significantly reduced by 2.5 mg/L phenol, while rainbow trout growth was significantly reduced by 0.20 mg/L phenol. For both species the embryolarval effects concentration was 1.1% of the 96-hr LC₅₀. Another embryolarval bioassay was attempted withp-benzoquinone, a highly toxic phenolic compound found in fossil fuel processing wastewaters, which was discontinued because the compound was rapidly degraded chemically or biologically in the headtank and aquaria.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.     

Oil dispersion increases the apparent bioavailability and toxicity of diesel to rainbow trout (Oncorhynchus mykiss)

Diesel is a complex mixture containing polycyclic aromatic hydrocarbons, which persist after a spill, pass readily from water into tissues, and are toxic to early life stages of fish. The bioavailability and chronic toxicity of hydrocarbons dissolved into water from floating diesel (water-accommodated fraction) and chemically dispersed diesel (chemically enhanced water-accommodated fraction) were measured by the extent of ethoxyresorufin-O-deethylase (EROD) induction in juvenile rainbow trout (Oncorhynchus mykiss) and by the severity of blue sac disease in embryos. The water-accommodated fraction of floating diesel was virtually nontoxic to embryos at nominal concentrations up to 1,000 mg/L, causing only small weight changes. Liver EROD induction in juvenile trout was only observed at the highest nominal water-accommodated fraction concentration (10,000 mg/L). Chemical dispersion increased the bioavailability and toxicity of diesel to trout by 100-fold. Diesel chemically enhanced water-accommodated fraction induced EROD activity, caused blue sac disease, and impaired development and growth of embryonic trout at nominal concentrations as low as 10 mg/L; 88% mortality occurred at 100 mg/L. However, when total hydrocarbon concentrations were measured, differences between dispersed and undispersed diesel disappeared, with a median lethal concentration of 8 mg/L of total hydrocarbons and sublethal median effective concentrations ranging from 1.3 to 6.1 mg/L. Dispersion of diesel by high-energy mechanical mixing was recently reported to cause acute lethality to juvenile trout between 40 and 200 mg/L. Therefore, dispersion of oil by any means increases the bioavailability and apparent toxicity of diesel to fish embryos without changing the toxicity of its components. Nevertheless, in an actual spill, dispersion of diesel increases the effects of oil on fish populations.     

An Ecological Risk Assessment of the Exposure and Effects of 2,4-D Acid to Rainbow Trout (<Emphasis Type="Italic">Onchorhyncus mykiss</Emphasis>)

Numerous state and federal agencies are increasingly concerned with the rapid expansion of invasive, noxious weeds across the United States. Herbicides are frequently applied as weed control measures in forest and rangeland ecosystems that frequently overlap with critical habitats of threatened and endangered fish species. However, there is little published chronic toxicity data for herbicides and fish that can be used to assess ecological risk of herbicides in aquatic environments. We conducted 96-h flowthrough acute and 30-day chronic toxicity studies with swim-up larvae and juvenile rainbow trout (Onchorhyncus mykiss) exposed to the free acid form of 2,4-D. Juvenile rainbow trout were acutely sensitive to 2,4-D acid equivalent at 494 mg/L (95% confidence interval [CI] 334–668 mg/L; 96-h ALC₅₀). Accelerated life-testing procedures, used to estimate chronic mortality from acute data, predicted that a 30-day exposure of juvenile rainbow trout to 2,4-D would result in 1% and 10% mortality at 260 and 343 mg/L, respectively. Swim-up larvae were chronically more sensitive than juveniles using growth as the measurement end point. The 30-day lowest observable effect concentration (LOEC) of 2,4-D on growth of swim-up larvae was 108 mg/L, whereas the 30-day no observable effect concentration (NOEC) was 54 mg/L. The 30-day maximum acceptable toxicant concentration (MATC) of 2,4-D for rainbow trout, determined as the geometric mean of the NOEC and the LOEC, was 76 mg/L. The acute:chronic ratio was 6.5 (i.e., 494/76). We observed no chronic effects on growth of juvenile rainbow trout at the highest concentration tested (108 mg/L). Worst-case aquatic exposures to 2,4-D (4 mg/L) occur when the herbicide is directly applied to aquatic ecosystems for aquatic weed control and resulted in a 30-day safety factor of 19 based on the MATC for growth (i.e., 76/4). Highest nontarget aquatic exposures to 2,4-D applied following terrestrial use is calculated at 0.136 mg/L and resulted in a 30-day safety factor of 559 (e.g., 76/0.163). Assessment of the exposure and response data presented herein indicates that use of 2,4-D acid for invasive weed control in aquatic and terrestrial habitats poses no substantial risk to growth or survival of rainbow trout or other salmonids, including the threatened bull trout (Salvelinus confluentus).     

Acute toxicity of selenium dioxide to freshwater fishes.

Acute toxicity tests of selenium dioxide were conducted for 96 to 336 hr in intermittent-flow bioassay systems using six species of freshwater fish. The decreasing order of species sensitivity was: fathead minnow, flagfish, brook trout, channel catfish, goldfish, and bluegil. Curves relating median lethal concentration to exposure time for each species exposed for more than 168 hr were sigmoid in shape and were characterized by a change in slope indicating a more rapid mortality rate after 96 to 168 hr toxicant exposure. The 96-hr LC50 estimates ranged from 2.9 mg/L SeO2 for fathead minnow fry to 40.0 mg/L for bluegill juveniles. Effects of brief toxicant exposure (24 hr) on fathead minnow and flagfish juveniles included limited delayed mortality and no effects on growth over a 28-day period.     

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.     

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.     

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.     

Comparison of the sensitivities of common in vitro and in vivo assays of estrogenic activity: application of chemical toxicity distributions

A number of contaminants in municipal effluent discharges are estrogen agonists to fish. Whereas several in vitro and in vivo techniques have been developed to assess the estrogenic activity of these compounds or ambient environmental samples, previous comparisons of the relative sensitivities of these approaches remain inconclusive. We employed a probabilistic hazard assessment approach using chemical toxicity distributions (CTDs) to perform a novel evaluation of relative sensitivities of six common in vitro and in vivo assays. We predicted that there was an 8.3% (human breast ademocarcinoma cell line, MCF-7, assay), 6.3% (yeast estrogen screen assay), or 1.9% (fish hepatocyte vitellogenin, VTG, assay) probability of detecting a compound in aquatic systems that will elicit an estrogenic response at concentrations at or below 0.1 microg/L, suggesting that the MCF-7 assay was the most sensitive in vitro assay evaluated in this study. The probabilities of eliciting the estrogenic response of VTG induction at a concentration less than 0.1 microg/L in rainbow trout, fathead minnow, and Japanese medaka were determined at 29.9, 26.2, and 18.8%, respectively. Thus, rainbow trout VTG induction was the most sensitive in vivo assay assessed. Subsequently, CTDs may provide a useful technique for hazard assessment of chemical classes for which exposure data are limited and for chemicals with common toxicological mechanisms and modes of action.     

Toxicity of selected priority pollutants to various aquatic organisms

Toxicity tests were conducted with selected compounds listed by the United States Environmental Protection Agency (EPA) as priority pollutants. Acute toxicity information was determined for acenaphthene, arsenic trioxide, cadmium chloride, mercury(II) chloride, silver nitrate, chlordane, endosulfan, and heptachlor. Acute tests were conducted using one or more of the following species: fathead minnows (Pimephales promelas), channel catfish (Ictalurus punctatus), rainbow trout (Salmo gairdneri), brown trout (Salmo trutta), brook trout (Salvelinus fontinalis), bluegills (Lepomis macrochirus), snails (Aplexa hypnorum), or chironomids (Tanytarsus dissimilis). Acute values from these tests ranged from a silver nitrate 96-hr LC50 of 6.7 micrograms/liter for fathead minnows to an arsenic trioxide 48-hr LC50 of 97,000 micrograms/liter for chironomids. In addition to acute tests, a fathead minnow embryo-larval exposure was conducted with silver nitrate to estimate chronic toxicity. The estimated maximum acceptable toxicant concentration for silver nitrate, based on fathead minnow survival, lies between 0.37 and 0.65 micrograms/liter.     

An Ecological Risk Assessment of the Acute and Chronic Effects of the Herbicide Clopyralid to Rainbow Trout (<Emphasis Type="Italic">Oncorhynchus mykiss</Emphasis>)

Clopyralid (3,6-dichloro-2-pyridinecarboxylic acid) is a pyridine herbicide frequently used to control invasive, noxious weeds in the northwestern United States. Clopyralid exhibits low acute toxicity to fish, including the rainbow trout (Oncorhynchus mykiss) and the threatened bull trout (Salvelinus confluentus). However, there are no published chronic toxicity data for clopyralid and fish that can be used in ecological risk assessments. We conducted 30-day chronic toxicity studies with juvenile rainbow trout exposed to the acid form of clopyralid. The 30-day maximum acceptable toxicant concentration (MATC) for growth, calculated as the geometric mean of the no observable effect concentration (68 mg/L) and the lowest observable effect concentration (136 mg/L), was 96 mg/L. No mortality was measured at the highest chronic concentration tested (273 mg/L). The acute:chronic ratio, calculated by dividing the previously published 96-h acutely lethal concentration (96-h ALC₅₀; 700 mg/L) by the MATC was 7.3. Toxicity values were compared to a four-tiered exposure assessment profile assuming an application rate of 1.12 kg/ha. The Tier 1 exposure estimation, based on direct overspray of a 2-m deep pond, was 0.055 mg/L. The Tier 2 maximum exposure estimate, based on the Generic Exposure Estimate Concentration model (GEENEC), was 0.057 mg/L. The Tier 3 maximum exposure estimate, based on previously published results of the Groundwater Loading Effects of Agricultural Management Systems model (GLEAMS), was 0.073 mg/L. The Tier 4 exposure estimate, based on published edge-of-field monitoring data, was estimated at 0.008 mg/L. Comparison of toxicity data to estimated environmental concentrations of clopyralid indicates that the safety factor for rainbow trout exposed to clopyralid at labeled use rates exceeds 1000. Therefore, the herbicide presents little to no risk to rainbow trout or other salmonids such as the threatened bull trout.     

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.     

Acute toxicity of selenium dioxide to freshwater fishes

Acute toxicity tests of selenium dioxide were conducted for 96 to 336 hr in intermittent-flow bioassay systems using six species of freshwater fish. The decreasing order of species sensitivity was: fathead minnow, flagfish, brook trout, channel catfish, goldfish, and bluegill. Curves relating median lethal concentration to exposure time for each species exposed for more than 168 hr were sigmoid in shape and were characterized by a change in slope indicating a more rapid mortality rate after 96 to 168 hr toxicant exposure. The 96-hr LC50 estimates ranged from 2.9 mg/L SeO₂ for fathead minnow fry to 40.0 mg/L for bluegill juveniles.Effects of brief toxicant exposure (24 hr) on fathead minnow and flagfish juveniles included limited delayed mortality and no effects on growth over a 28-day period.Research supported by the U. S. Environmental Protection Agency National Water Quality Laboratory, Duluth, Minnesota. (Contract No. 68-01-0748).     

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.     

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.     

Fate and biological effects of methyl parathion in outdoor ponds and laboratory aquaria. II. Effects

Methyl parathion (MEP) applied to three outdoor ponds at a nominal concentration of 100 micrograms liter-1 was toxic to some species of aquatic insects and crustaceans but not to fish. The spectrum of toxicity was similar to predictions based on a literature survey of data obtained from laboratory tests. Various secondary effects occurred that could not be predicted from laboratory toxicity tests. An increase in populations of Diaptomus in treated ponds was probably caused by mortality of predators and competitors. A bloom of filamentous algae which then collapsed, leading to severe depletion of dissolved oxygen and fish deaths, may have been triggered by mortality of herbivorous mayflies and daphnids. The growth of juvenile rainbow trout in treated ponds was significantly less than in untreated ponds. On the other hand their growth in laboratory aquaria was not affected when rainbow trout were exposed to higher concentrations of MEP than occurred in the outdoor ponds. It was concluded that growth of rainbow trout in the ponds was probably affected by mortality among aquatic insects and crustaceans on which they feed.     

Toxicity of underground coal gasification condenser water and selected constituents to aquatic biota

The acute and embryo-larval toxicity of the Laramie Energy Technology Center's Hanna-3 underground coal gasification (UCG) condenser water and its constituents were studied in continuous-flow bioassays. The 96-hr LC₅₀ dilution values for untreated Hanna-3 UCG condenser water were 0.1% for rainbow trout, 0.11% for fathead minnows and the 48-hr LC₅₀ dilution forDaphnia pulicaria was 0.18%. Separate 96-hr acute tests with phenol, ammonia, and ammonia plus phenol showed that these two constituents, acting synergistically, were the major constituents affecting the acute toxicity of this coal conversion effluent to fishDaphnia pulicaria, on the other hand, was relatively insensitive to phenol exposure; the primary constituent of Hanna-3 UCG condenser water affecting this species was ammonia.A previously described model was used for predicting the toxicity of effluents with high concentrations of phenol and ammonia to confirm our hypothesis that the acute toxicity of Hanna-3 UCG condenser water to fish was primarily due to the presence of phenol and ammonia. Using the Hanna-3 concentrations of phenol and ammonia in this formula, it was calculated that the 96-hr LC₅₀ values for rainbow trout and fathead minnows exposed to Hanna-3 condenser water would be 0.11% and 0.28%, respectively; values which are near the observed acute toxicity of Hanna-3 condenser water.In a 30-day embryo-larval exposure, fathead minnow egg hatchability, growth, and survival were significantly reduced at 0.04%, 0.02% and 0.01% Hanna-3 condenser water, respectively. At a Hanna-3 dilution of 0.01%, the phenol and un-ionized ammonia concentrations were calculated to be 0.23 mg/L and 0.14 mg/L, respectively. The phenol and un-ionized ammonia concentrations are within ranges expected to produce the long-term effects which were observed.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.