Toxicities of butoxyethanol ester and propylene glycol butyl ether ester formulations of 2,4-dichlorophenoxy acetic acid (2,4-D) to juvenile salmonids

Continuous-flow toxicity tests were conducted to determine acute toxic effects of butoxy-ethanol ester (BOEE) and propylene glycol butyl ether ester (PGBEE) formulations of 2,4-D on juvenile chinook salmon (Oncorhynchus tshawytscha) and steelhead-rainbow trout (Salmo gairdneri). A chronic toxicity test with chinook salmon egg-to-fry was conducted to determine effects of BOEE on survival and growth. The hydrolysis in water of 2,4-D esters to 2,4-D acid was influenced by the presence of fish. Median lethal concentrations (96-hr LC50 values) indicated that PGBEE (170 to 355 g/L) was slightly more toxic (37 to 57%) than BOEE (303 to 525 g/L). The LC50 values also indicated that chinook salmon were generally more sensitive than steelhead-rainbow trout and that fry and smolts were equally sensitive to the 2,4-D esters. Static tests substantially underestimated BOEE toxicity when compared to dynamic tests. Based on reduced survival and growth of chinook salmon alevins and fry, the estimated maximum safe chronic exposure concentration under these test conditions is 40 g/L BOEE.     

Field evaluation of triclopyr ester toxicity to fish

Two field experiments were conducted to assess the predictions of laboratory time-toxicity tests regarding lethal effects of triclopyr butoxyethyl ester (TBEE) on fish in standing and flowing water bodies. Large lake enclosures were treated with TBEE by backpack sprayer at concentrations of 0.25–7.6 mg/L, expressed as acid equivalents. Median dissipation times for TBEE in lake water ranged from 4–8 d.Effects of the treatments on survival and growth of caged rainbow trout were measured. All trout died by 3 d at initial concentrations of 0.69–7.6 mg/L. There was 43% mortality of rainbow trout in the enclosure treated at 0.45 mg/L, and no mortality in the 0.25 mg/L enclosure or the controls. The treatments at the two lower concentrations had significant adverse effects on the growth rates of surviving trout. TBEE was applied to sections of a forest headwater stream at nominal concentrations of 0.8 mg/L and 2.7 mg/L. These concentrations represent maximum-expected environmental concentrations in 50- and 15-cm deep bodies of water, respectively, when directly oversprayed at an application rate of 3.84 kg/ha. Concentrations of TBEE were rapidly dissipated (as much as 70% decline within 55 m) and exposure periods at concentrations above 0.1 mg/L varied from 25 min in the low-concentration area to 55 min in the high-concentration area. The applications of TBEE at both initial test concentrations did not result in any mortality of resident brook trout. There were no significant effects of the herbicide treatments on the growth of 1+ and 2+ brook trout, but there were indications that the growth of 0+ trout was reduced as a result of exposure to TBEE in the stream. These results were in general agreement with the predictions of laboratory time-toxicity tests.     

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.     

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.     

Effects of the herbicides hexazinone and triclopyr ester on aquatic insects.

Experiments were conducted to measure acute lethal response of aquatic insects to hexazinone (Velpar L) and triclopyr ester (Garlon 4) in flow-through laboratory bioassays, and to determine lethal and behavioral effects of these herbicides on insects in outdoor stream channels. No significant mortality (chi 2 P greater than 0.05) occurred in 13 test species exposed to hexazinone in laboratory flow-through bioassays (1-hr exposure, 48-hr observation) at the maximum test concentration of 80 mg/liter. The survival of insects exposed to 80 mg/liter hexazinone in outdoor stream channels was likewise unaffected. Significant drift (chi 2 P less than 0.001) of Isonychia sp. occurred during a hexazinone treatment of the stream channels, but only at the maximum concentration of 80 mg/liter, and survival of the displaced Isonychia sp. was not affected. In flow-through bioassays with triclopyr ester, 10 of 12 test species showed no significant mortality at concentrations greater than 80 mg/liter. Survival of Isogenoides sp. and Dolophilodes distinctus was significantly affected at less than 80 mg/liter. Lethal concentrations were estimated by probit analysis of concentration-response data (1-hr exposure, 48-hr observation) for Simulium sp. (LC50 = 303 mg/liter), Isogenoides sp. (LC50 = 61.7 mg/liter), and D. distinctus (LC50 = 0.6 mg/liter). Triclopyr ester applications to the stream channels resulted in significant drift and mortality of D. distinctus at 3.2 mg/liter (no effects at 0.32 mg/liter), Isogenoides sp. at 32 mg/liter, and Hydropsyche sp. and Epeorus vitrea at 320 mg/liter. The risk to aquatic insects of these herbicides used in forest vegetation management is discussed.     

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).     

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.     

Sublethal and acute toxicity of the ethylene glycol butyl ether ester formulation of triclopyr to juvenile coho salmon (Oncorhynchus kisutch)

The toxicity of Garlon^®4, the ethylene glycol butyl ether ester formulation of the herbicide tryclopyr, to juvenile coho salmon (Oncorhynchus kisutch) was investigated at several lethal and sublethal concentrations. Fish behavior, random activity and oxygen uptake were monitored. Coho salmon exhibited three distinct responses related to concentration and duration of exposure: (1) at concentrations greater than 0.56 mg/L fish were initially lethargic, then regressed to a highly distressed condition characterized by elevated oxygen uptake and finally death, (2) at 0.32–0.43 mg/L fish were lethargic throughout the exposure period with reduced oxygen uptake, and (3) at concentrations 0.10 mg/L fish were hypersensitive to stimuli, exhibiting elevated activity and oxygen uptake levels during photoperiod transitions. Whole body residue analysis showed that uptake of the ester and subsequent hydrolysis to the acid form in the fish was rapid, with significant accumulation of the acid in the tissues. This suggests that some threshold tissue concentrations were associated with the observed results. For juvenile coho salmon the 96-hr LC₅₀ of Garlon^®4 was 0.84 mg/L.     

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.     

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.     

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.     

Organochlorine concentrations in Laurentian Great Lakes salmonines: Implications for fisheries management

To assess species-specific differences in organochlorine (OC) concentrations and sport harvest of Lake Michigan salmonines, and how this may affect human exposure to OC compounds, creel survey and OC analysis data for salmon and trout collected from the western waters of Lake Michigan in 1985 and 1990 were examined. In all species, total concentrations of polychlorinated biphenyls (PCBs) attained the highest concentration of the OC compounds quantified in both study years. DDT and metabolites attained the second highest concentration of OC compounds, in those species in which these compounds were quantified, followed by chlordane and its constituents and dieldrin, respectively. The relative concentrations of PCBs and OC pesticides remained constant between study years in all species, except for brook trout as limited 1990 data prevented analysis. For the mean lengths of each species of salmonines taken by anglers in 1985, lake trout showed the highest concentrations of OC compounds followed by brown trout, chinook salmon, brook trout, rainbow trout, and coho salmon, respectively. In 1990 lake trout again had the highest concentration of OCs followed by chinook salmon, brown trout, rainbow trout, and coho salmon. Brook trout were not in the analysis. Chinook salmon contributed the greatest proportion of OCs to the 1985 sport catch because of its dominance in total biomass of fish harvested. Lake trout contributed the greatest proportion of OCs to the 1990 sport catch, although the second highest in biomass harvested, because of the higher concentration of OC compounds in this species. The concentrations of PCBs declined between study years in all species except brook trout becaused limited 1990 data prevented this comparison. Study results indicate salmonine stocking policies can significantly influence the exposure of sport fish consumers in the Great Lakes region to OC compounds.     

Altering cytochrome P4501A activity affects polycyclic aromatic hydrocarbon metabolism and toxicity in rainbow trout (Oncorhynchus mykiss)

The polycyclic aromatic hydrocarbons (PAHs) phenanthrene and retene (7-isopropyl-1-methyl phenanthrene) are lethal to rainbow trout (Oncorhynchus mykiss) larvae during chronic exposures. Phenanthrene is a low-toxicity, non-cytochrome P4501A (CYP1A)-inducing compound that accumulates in fish tissues during exposure to lethal concentrations in water. Retene is a higher toxicity CYP1A-inducing compound that is not detectable in tissue at lethal exposure concentrations. The metabolism, excretion, and toxicity of retene and phenanthrene were examined in juvenile and larval rainbow trout during coexposure to the model CYP1A inducer beta-naphthoflavone (betaNF), or to the inducer-inhibitor piperonyl butoxide to determine if modulating CYP1A activity affected PAH metabolism and toxicity. Phenanthrene metabolism, excretion rate, and toxicity increased with coexposure to betaNE Piperonyl butoxide inhibited phenanthrene metabolism and reduced the excretion of all phenanthrene metabolites. As a consequence, embryo mortality rates increased but rates of sublethal effects did not. Coexposure of trout to retene and betaNF caused no change in retene metabolism and excretion, but retene toxicity increased, perhaps due to additivity. Piperonyl butoxide inhibited retene metabolism, decreased the excretion of some retene metabolites while increasing the excretion of others, and increased the toxicity of retene. These results support the role of CYP1A activity in PAH metabolism and excretion, and the role ofthe CYP1A-generatedmetabolites of PAHs in chronic toxicity to larval fish.     

A test system to evaluate the susceptibility of Oregon, USA, native stream invertebrataes to triclopyr and carbaryl

The susceptibility of six indigenous macroinvertebrate species representative of U.S. Pacific Northwest streams (Ameletus sp., Brachycentrus americanus, Calineuria californica, Cinygma sp., Lepidostoma unicolor, Psychoglypha sp. early and late instar) to formulated triclopyr ester (herbicide) and carbaryl (insecticide) was determined using laboratory bioassays. Acute toxicity was expressed as the lethal concentration to 50% (LC50) and 1% (LC1) of the test population based on a 96-h exposure duration. Carbaryl was found to be 1,000 times more toxic than triclopyr for all the organisms tested. The LCI values (7.5, 28.8, 9.0, 3.0, 9.5, 14.8, 33.8 microg/L, respectively, for carbaryl and 1.8, 3.9, 4.0, 4.2, 29.0, 16.1 mg/L, respectively, for triclopyr) were used in the calculation of hazardous concentration to 5% of the stream macroinvertebrate community (HC5) based on the lower 95% confidence limit (HC5/95). The hazardous concentration (HC5/95) for triclopyr was 0.11 mg/L and for carbaryl ranged from 0.43 to 0.66 microg/L, respectively. Triclopyr and carbaryl symptomology were analyzed for two organisms, C. californica and Cinygma sp. Carbaryl symptomology included knockdown and moribund states with severity and time of appearance being a function of dose. In triclopyr poisoning, death occurred suddenly with little or no symptomology. Time to 50% mortality (LT50) values were consistently higher for C. californica than for Cinygma sp. exposed to both chemicals at similar concentrations.     

Immunocompetence of juvenile chinook salmon against Listonella anguillarum following dietary exposure to polycyclic aromatic hydrocarbons

Juvenile chinook salmon (Oncorhynchus tschawytscha) were fed a mixture of 14 polycyclic aromatic hydrocarbon (PAH) compounds that reflected the PAH composition of salmon stomach contents in an urban estuary of Puget Sound, Washington (USA). Following a 28-d dietary exposure, a standardized Listonella anguillarum challenge model was used to determine whether PAH exposure (16, 64, and 252 mg/kg wet wt feed) causes reduced disease resistance under the conditions examined in this study. To assess innate immunity, five replicate groups of fish per dose were acclimated for one week, exposed to a lethal concentration 60 of bacteria, and monitored for 14 d. In a parallel experiment, the effects of PAH exposure on the acquired immune response were examined by immersion vaccinating fish against L. anguillarum and allowing specific immunity to develop for three weeks prior to challenge. All mortalities were aseptically sampled to confirm L. anguillarum infections. No significant differences in fish length, weight, or coefficient of condition were observed. These controlled laboratory experiments suggest that dietary exposures to an environmentally relevant mixture of PAH compounds do not alter the immunocompetence or growth of juvenile chinook salmon.     

Joint toxicity of mercury and selenium in salmonid eggs

Toxic interactions between mercury and selenium in fertilized eggs of rainbow trout (Salmo gairdneri) and lake trout (Salvelinus namaycush) were investigated and compared to the pronounced synergistic effect previously reported in carp (Cyprinus carpio) eggs. Mercury produced concentration-dependent decreases in median survival times and caused decreases in median hatch times. Selenium, at concentrations up to 10 mg Se/L, had no effect on hatching times, and did not produce mortality, and had no effect on mercury toxicity. At concentrations of 100 mg Se/L and higher, an apparent protective effect of selenium on mercury toxicity was observed in lake trout eggs. Requirements for additional research are discussed with emphasis on predictions of region-wide damage to freshwater fish populations due to atmospheric deposition of these chemical elements.     

Polychlorinated Dibenzo-p-Dioxins (PCDDs) and Dibenzofurans (PCDFs) in Muscle and Eggs of Salmonid Fishes from the Great Lakes

Concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) were measured in dorsal muscle and eggs of coho salmon, lake trout, and chinook salmon collected from Lakes Superior, Michigan, and Huron (Michigan waters). Absolute and relative concentrations of PCDDs and PCDFs varied among sampling locations (inter- and intralake) and fish species. Fish collected from Bay City (Saginaw Bay) contained the greatest concentrations of PCDDs and PCDFs both in muscle and eggs. Among the three fish species, chinook salmon accumulated greater concentrations than did coho salmon or lake trout. Concentrations of PCDFs were greater than those of PCDDs in all fishes. OCDF and TCDF were the predominant congeners of PCDF, whereas OCDD and TCDD concentrations predominated in PCDDs. Homolog compositions of PCDDs and PCDFs suggested the existence of multiple local sources in various locations. Concentrations of PCDDs and PCDFs in eggs of fishes were significantly correlated with those in muscle. Received: 2 May 1998/Accepted: 20 December 1998     

Organochlorine concentration dynamics in Lake Michigan chinook salmon (Oncorhynchus tshawytscha)

To investigate how trophic level and physiological processes influence organochlorine (OC) chemical concentrations in chinook salmon (Oncorhynchus tshawytscha) and their offspring, data on polychlorinated biphenyl (PCB), and OC pesticides and metabolite concentrations in Lake Michigan chinook salmon muscle tissue, eggs, sac fry, and prey fish were analyzed. Total concentrations of PCBs in chinook salmon decreased exponentially from the mid-1970s to mid-1980s, but the concentrations have since shown an asymptotic response, a trend also seen in alewife (Alosa pseudoharengus), an exotic planktivore that is the principal prey of chinook salmon in western Lake Michigan, and bloater (Coregonus hoyi) an endemic planktivore. The total concentration of PCBs in chinook salmon were positively correlated with fish length. OC concentrations in chinook salmon eggs were positively correlated with the concentrations of these compounds in the muscle tissue of the gravid fish. Egg and sac fry OC concentrations were also positively correlated. Estimates of the quantities of various OCs in chinook salmon muscle tissue and eggs, reveal that between 22% and 40% of the quantities of these compounds are eliminated through spawning.     

Acute toxicity of cadmium, lead, zinc, and their mixtures to stream-resident fish and invertebrates

The authors conducted 150 tests of the acute toxicity of resident fish and invertebrates to Cd, Pb, and Zn, separately and in mixtures, in waters from the South Fork Coeur d'Alene River watershed, Idaho, USA. Field-collected shorthead sculpin (Cottus confusus), westslope cutthroat trout (Oncorhynchus clarkii lewisi), two mayflies (Baetis tricaudatus and Rhithrogena sp.), a stonefly (Sweltsa sp.), a caddisfly (Arctopsyche sp.), a snail (Gyraulus sp.), and hatchery rainbow trout (Oncorhynchus mykiss), were tested with all three metals. With Pb, the mayflies (Drunella sp., Epeorus sp., and Leptophlebiidae), a Simuliidae black fly, a Chironomidae midge, a Tipula sp. crane fly, a Dytiscidae beetle, and another snail (Physa sp.), were also tested. Adult westslope cutthroat trout were captured to establish a broodstock to provide fry of known ages for testing. With Cd, the range of 96-h median effect concentrations (EC50s) was 0.4 to >5,329 μg/L, and the relative resistances of taxa were westslope cutthroat trout ≈ rainbow trout ≈ sculpin < other taxa; with Pb, EC50s ranged from 47 to 3,323 μg/L, with westslope cutthroat trout < rainbow trout < other taxa; and with Zn, EC50s ranged from 21 to 3,704 μg/L, with rainbow trout < westslope cutthroat trout ≈ sculpin < other taxa. With swim-up trout fry, a pattern of decreasing resistance with increasing fish size was observed. In metal mixtures, the toxicities of the three metals were less than additive on a concentration-addition basis.