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.     

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.     

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).     

Effects of naphthalene and benzene on fathead minnows and rainbow trout

Fathead minnows (FHM) and rainbow trout (RBT) were used in flow-through bioassays to determine the acute toxicity of benzene and naphthalene, and to determine the embryo-larval effects of naphthalene on FHM. On an acute basis, naphthalene was more toxic than benzene (naphthalene LC₅₀ values were 1.6 mg/L for RBT and 7.9 mg/L for FHM; benzene LC₅₀ values were 5.3 mg/L for RBT and >15.1 mg/L for FHM). In the embryo-larval test naphthalene significantly (= 0.05) reduced FHM growth at concentrations as low as 0.85 mg/L. The highest concentration producing no effect was 0.45 mg/L naphthalene, which was 5.7% of the FHM 96-hr LC₅₀. Based upon long-term no-effects naphthalene concentration, the best estimate of the maximum acceptable toxicant concentration (MATC) was >0.45 to <0.85 mg/L naphthalene.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     

Chronic toxicity of dietary disodium arsenate heptahydrate to juvenile rainbow trout (Oncorhynchus mykiss)

Juvenile rainbow trout were fed semi-purified diets containing graded levels of disodium arsenate heptahydrate (DSA) for 12–24 weeks under standard laboratory conditions to define the maximum acceptable toxicant concentration (MATC) and to correlate signs of toxicity with diet and tissue arsenic concentrations. The MATC for DSA was between 13 and 33 g As/g diet or 0.281–0.525 mg As/kg body weight/day. The most sensitive and reliable indicator of chronic dietary DSA toxicity in rainbow trout was chronic inflammation of the gallbladder wall. Chronic inflammatory changes in the sub-epithelial tissues of the gallbladder wall were evident in 71% of rainbow trout exposed to 33 g As/g diet for 24 weeks, and 100% of rainbow trout exposed to 65 g As/g diet for 24 weeks or 49 g As/g diet for 12 weeks. No fish exposed to 13 g As/g diet or less for up to 24 weeks showed any demonstrable gallbladder lesions or any other ill effect of arsenic exposure. Other signs of chronic dietary DSA toxicity to rainbow trout included decreased growth rate, mild to moderate anemia, and, at higher levels of exposure, active feed refusal leading to decreased feed consumption. Mild nephrocalcinosis was noted in one experiment where kidney arsenic residues exceeded 14 g As/g tissue dry weight.Supported by the Natural Sciences and Engineering Research Council of Canada and the Ontario Ministry of Agriculture and FoodPortions of this material were presented at the 29th Annual Meeting of the Canadian Federation of Biological Societies, June 16–20, 1986, Guelph, Ontario, and the 14th Annual Aquatic Toxicity Workshop, November 2–4, 1987, Toronto, Ontario, Canada     

Use of Behavioral Responses of Rainbow Trout <Emphasis Type="Italic">Oncorhynchus mykiss</Emphasis> in Identifying Sublethal Exposure to Hexavalent Chromium

Laboratory tests were conducted in a flow-through apparatus on 1-year-old rainbow trout Oncorhynchus mykiss to evaluate the sensitivity of a number of their behavioral responses to hexavalent chromium (Cr⁶⁺). Test fish were exposed to Cr⁶⁺ concentrations corresponding to 0.001–1 parts of the rainbow trout 96-h LC50 (0.029–28.5 mg Cr/L, respectively) in short-term (15 min) tests. Sensitivity parameter responses could be arranged into the following sequence: latent period of detection response = locomotor activity > gill ventilation frequency > coughing rate. All the rainbow trout responses were sensitive behavioral indicators of sublethal exposure. Behavioral responses meet the criteria as rapid tools for bioassay testing and could be easily standardized using Cr⁶⁺ as a reference toxicant.     

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 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.     

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.     

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.     

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.     

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.     

Lethal and Sublethal Toxicity of the Antifoulant Compound Irgarol 1051 to the Mud Snail <Emphasis Type="Italic">Ilyanassa obsoleta</Emphasis>

Irgarol 1051 is an algistatic compound used in copper-based antifoulant paints. It is a widespread and persistent pollutant of the estuarine environment. Ilyanassa obsoleta, the Eastern mud snail, is a common intertidal gastropod that inhabits mud flats and salt marshes along the east coast of North America. It is an important inhabitant of the estuarine environment; contributing to nutrient regeneration and regulating microbial processes in the sediments. The toxicity of irgarol to estuarine gastropods has not been previously examined, although they have the potential to be exposed to antifoulants through both aqueous and sediment routes. The objectives of this study were to evaluate irgarol’s effects on I. obsoleta survival, reproductive status (imposex occurrence and testosterone levels), chemoreceptive function, and cellular respiration (cytochrome-c oxidase activity). Irgarol was moderately toxic to I. obsoleta; adult aqueous 96-h LC₅₀ = 3.73 mg/L, larval aqueous 96-h LC₅₀ = 3.16 mg/L, and adult sediment 10-day LC₅₀ = 12.21 mg/kg. Larval snails were not significantly more sensitive to irgarol than adult snails. A chronic 45-day aqueous irgarol exposure (0.005–2.5 mg/L) did not induce imposex or affect free-testosterone levels. The 45-day chronic LC₅₀ of 1.88 mg/L was significantly lower than the 96-h acute value. A 96-h acute aqueous irgarol exposure (0.375–1.5 mg/L) caused a decrease in normal response to chemosensory cues such as the presence of food or predators. There was a significant increase in cytochrome-c oxidase activity at 2.5 mg/L, which might indicate irgarol’s disruption of the mitochondrial membrane and subsequently ATP synthesis. Although the toxicity values determined for I. obsoleta exceeded irgarol concentrations measured in surface waters, results from this toxicity assessment will provide valuable information to environmental resource managers faced with decisions regarding the use and regulation of antifoulant paints in the coastal zone.     

Chronic toxicity of hexavalent chromium to the fathead minnow (Pimephales promelas)

The chronic effects of hexavalent chromium on the fathead minnow (Pimephales promelas) were investigated. Survival was affected only at the high test concentration of 3.95 mg Cr/L. All chromium concentrations, including 0.018 mg/L, the lowest tested, retarded the early growth of first-generation fish, but this effect was only temporary. Growth of second-generation fish was not affected at concentrations of 1.0 mg/L or lower. Reproduction and hatchability of eggs were not affected at any chromium concentration tested.The maximum acceptable toxicant concentration (MATC) for fathead minnows in hard water (209 mg/L as CaCO₃ at pH 7.7) was based on survival and lies between 1.0 and 3.95 mg Cr/L, respectively. The application factor (MATC/96-hr LC50) is between 0.03 and 0.11.     

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.     

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.     

The chronic aquatic toxicity of a microbicide dibromonitrilopropionamide

The chronic aquatic toxicities of a microbicide dibromonitrilopropionamide (DBNPA) in Daphnia magna and rainbow trout were evaluated. DBNPA can significantly affect the reproduction and survival of D. magna. The lowest observed effective concentration (LOEC) and the no observed effective concentration (NOEC) of DBNPA to D. magna were 0.053 and 0.072 mg L(-1), respectively, and the intrinsic rate of natural increase (r) was significantly decreased (p < 0.05) at a concentration of 0.01 mg L(-1). Meanwhile, DBNPA affected the growth of juvenile rainbow trout at a concentration of 0.01875 mg L(-1) after 28-day exposure. The results showed that DBNPA has chronic deleterious effects on aquatic organisms.     

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.     

An Evaluation of Molybdenum Toxicity to the Oligochaete, <Emphasis Type="Italic">Tubifex tubifex</Emphasis>, and Early-Life Stages of Brown Trout, <Emphasis Type="Italic">Salmo trutta</Emphasis>

Limited data are available describing the aquatic toxicity of molybdenum in freshwater environments, making it difficult to assess the aquatic risk to freshwater organisms. In order to increase available information on the aquatic toxicity of molybdenum, a 96-h LC50 test with the oligochaete Tubifex tubifex and an 85-day development test using brown trout, Salmo trutta, were conducted. The T. tubifex test resulted in an LC50 value of 2782 mg/L. No adverse effects were observed on brown trout survival or length in the concentrations tested, however an IC10 value for growth (wet weight) was determined to be 202 mg/L. Whole body fish tissue concentrations for molybdenum increased in all treatment concentrations tested, although bioconcentration factors decreased at greater exposure concentrations, and ranged from 0.13 at an exposure concentration of 20 mg/L to 0.04 at an exposure of 1247 mg/L. A body burden of 26.0 mg/kg was associated with reduced wet weight.