Biological half-lives of eight polycyclic aromatic hydrocarbons (PAHs) in rainbow trout (Salmo gairdneri)

Adult rainbow trout were exposed to a single oral dose containing a mixture of eight PAHs, and fish were sampled at intervals between 5–48 days after exposure. Regression analyses on whole fish indicate levels declined significantly in four of the compounds monitored. Their biological half-lives were estimated as 9 days for phenanthrene, 7 days for fluorene and anthracene and 6 days for fluoranthene. No reliable estimates could be derived for benzo[a]pyrene, benz[a]anthracene, chrysene or pyrene because of low or nondetectable concentrations at the first sample interval although it could be suggested that their half-lives would be less than several days. The data also suggested that these PAHs are poorly absorbed by trout.     

Avoidance response of rainbow trout (Salmo gairdneri) to single-dose chlorination in a power plant discharge canal

Rainbow trout (Salmo gairdneri) were exposed to 20 min single-dose chlorine additions designed to achieve maximum total residual chlorine (TRC) concentrations of 0.04, 0.2, 0.6, and 1.0 mg l⁻¹. First retreats from the chlorine front occurred at 0.05 mg l⁻¹ TRC. Approximately 95% of the fish had moved downstream when TRC reached 0.5 mg l⁻¹, well before cumulative time-dose exposure approached lethal limits. Percentage of fish remaining near the discharge decreased linearly as TRC concentration rose, suggesting that a rapid rise in receiving water chlorine level might be beneficial in reducing cumulative time-dose exposure. Rainbow trout demonstrated the initial sensitivity to avoid lethal chlorine exposure, but complete assessment of the utility of the avoidance response must also consider distribution throughout chlorination and the potential for repeated exposure.     

Lethal toxicity of permethrin (NRDC-143) to rainbow trout, salmo gairdneri, in relation to body weight and water temperature

Lethal toxicity of permethrin varied inversely with water temperature and body weight. The 96 h LC 50 (median lethal concentration) for 1 g trout increased by an order of magnitude from 0.62 to 6.43 μg 1⁻¹ between 5 and 20°C. However between 5 and 10°C the 96 h LC 50 changed little from 0.6 μg 1⁻¹. Large trout (200 g) were considerably more tolerant to permethrin than small fish. Thus, the 96 h LC 50s for 1 and 200 g trout were 3.17 and 314 μg 1⁻¹ respectively at 15°C. The size effect was most pronounced between 1 and 50 g.It is to be noted that the application of permethrin for insect control coincides with the usual period of emergence of rainbow trout fry subsequent to a spawning period of April to late June.     

Acute lethality, and sub-lethal effects of acetone, ethanol, and propylene glycol on the cardiovascular and respiratory systems of rainbow trout Salmo gairdneri

Acute lethality and sub-lethal effects of acetone, ethanol, and propylene glycol on the cardiovascular and respiratory systems of rainbow trout (Salmo gairdneri) were examined. The 24 h LC₅₀ values for acetone and ethanol in a flow-through bioassay system at 10°C ± 0.5, are 6100 mg l⁻² and 11,200 mg l⁻¹, respectively. No mortality to fingerling trout was produced by propylene glycol at 50,000 mg l ⁻¹ during a 24 h exposure period in a static system.Acetone and ethanol, at about 0.48 and 0.26 of the fingerling LC₅₀, respectively, affected cardiovascular/respiratory parameters in adult rainbow trout. Acetone produced an increase in ventilation rate to a maximum of 158% of control values, as well as an increase in buccal pressure amplitude attaining a maximum of 410% of control values. Ethanol exposed fish exhibited a slight depression in ventilation rate and buccal pressure amplitude during initial stages of the 24 h exposure period. Ethanol had no effect on heart rate, despite a significant decrease in Q-T interval. Propylene glycol, at less than 0.08 of a concentration not producing apparent stress in fingerlings, had a mildly stimulatory effect on ventilation rate, and heart rate in adults. It is concluded that of the three solvents employed in this study, propylene glycol is most suitable for use as a solvent in fish toxicity tests.     

Toxic effects of hexavalent chromium on brook trout (Salvelinus fontinalis) and rainbow trout (Salmo gairdneri)

Exposing brook trout to various concentrations of chromium [Cr(VI)] for up to 22 months (including reproduction) significantly increased alevin mortality at 0.35 mg Cr l⁻¹ and retarded growth of young brook trout at the lowest concentration tested (0.01 mg Cr l⁻¹). Eight month exposures of rainbow trout significantly increased alevin mortality at 0.34 mg Cr l⁻¹ and also retarded growth at the lowest concentration tested (0.10 mg Cr l⁻¹). Exposures of brook trout lasting 22 months showed, however, that growth was only temporarily affected, and therefore, it was not used as an end point to measure the affects of chromium on either species. Reproduction, and embryo hatchability of brook trout were unaffected at Cr(VI) concentrations that affected survival of newly hatched alevins. The maximum acceptable toxicant concentration (MATC) for brook and rainbow trout exposed to Cr(VI) in water with a hardness of 45 mg l⁻¹ (as CaCO₃) and a pH range of 7–8 lies between 0.20 and 0.35 mg Cr l⁻¹. The 96-h lc₅₀ for brook and rainbow trout was 59 and 69 mg Cr l⁻¹, respectively: therefore, the application factor (MATC/96-h lc₅₀) for both species lies between 0.003 and 0.006.     

The effect of sublethal concentrations of copper and zinc on ventilatory activity. Blood oxygen and pH in rainbow trout (Salmo gairdneri)

Changes in buccal and opercular pressure amplitude, as well as ventilation and coughing frequency were monitored in rainbow trout using catheterization of respiratory cavities and pressure transducers. One or more of the ventilatory parameters measured were found to change under toxicant stress at concentrations of copper or zinc at or below the LC 50. Possible synergistic effects were indicated when the two metal ions were tested together.Serial analyses of arterial P_O2 and pH in fish exposed to copper and zinc individually at concentrations approximating the LC 50 showed that environmental zinc produced a sharp decrease in both P_O2 and pH. Copper, however, caused little effect other than a transient increase in pH. The toxic action of the two metals in low concentrations thus may not be the same.     

Toxicity of silver to rainbow trout (Salmo gairdneri)

The mean 96-h LC₅₀'s of silver with rainbow trout were 6.5 μg l⁻¹ and 13.0 μg l⁻¹ in soft water (approximately 26 mg l⁻¹ hardness as CaCO₃) and hard water (350 mg l⁻¹ hardness as CaCO₃), respectively. The long-term, “no effect” concentration for silver, added to the water as silver nitrate, was between 0.09 and 0.17 μg l⁻¹ after 18 months exposure in soft water. The “no effect” concentration is that concentration range which defines no observed effect. Based on mortalities different from the control, no mortalities attributable to silver occurred at 0.09 μg Ag l⁻¹, whereas 17.2% mortality occurred to fish exposed to 0.17 μg ll⁻¹. The “no effect” concentration does not reflect possible effects of silver on spawning behavior or reproduction, since female rainbow trout will not generally reach sexual maturity before 3 yr. At silver concentrations of 0.17 μg l⁻¹ or greater, silver caused premature hatching of eggs and reduced growth rate in fry. In one experiment, the eggs were completely hatched within 10 days of exposure; whereas, control eggs completed hatching after 42 days. The prematurely erupted fry were not well developed and frequently died. The growth rate of surviving fry was greatly reduced.     

The acute toxicity of vanadium and copper to eyed eggs of rainbow trout (Salmo gairdneri)

The effects of vanadium (25–595 mg l⁻¹) and of copper (0.03–4.78 mg l⁻¹) on embryonic survival and hatching of eyed eggs of rainbow trout, Salmo gairdneri, were investigated. Copper was approx. 300-fold more toxic than vanadium (96-h LC₅₀ = 0.4 and 118 mg l⁻¹, respectively) but had little effect on the timing of hatch. Vanadium induced premature hatching of eyed eggs at concentrations from 44 to 595 mg l⁻¹. Concentrations of copper required to produce lethality in eyed eggs were similar to concentrations required to produce mortality in juveniles. Vanadium concentrations approx. 15 times higher were required to produce mortality in eyed eggs than in juveniles. Therefore, acute exposure of eyed rainbow trout eggs to vanadium is not a sensitive toxicity test for use in establishing water quality criteria or maximum acceptable toxicant concentrations.     

A QSAR model for predicting toxicity (LC50) to rainbow trout

A fragment constant method for prediction of toxicity (LC50) to rainbow trout was developed based on the experimental LC50 values of 258 chemicals obtained from the literature. The dataset was randomly divided into a training set and a validation set for purposes of model development and validation. The final model was established using all of the experimental LC50 values by pooling the two sets together. The coefficient of the determination for the final model was 0.9495 with a mean residual of 0.42 log-units. The model's robustness was tested using jackknife tests.     

Cardiovascular-respiratory responses of rainbow trout (Salmo gairdneri) during chronic exposure to sublethal concentrations of cadmium

The effects of exposure to 3.6 and 6.4 μg l⁻¹ cadmium for periods up to 178 days on cardiac and ventilatory rates, hematocrit, hemoglobin concentration and erythrocyte adenosine triphosphate concentration in adult rainbow trout, Salmo gairdneri, were investigated. Except for slight transitory responses, 3.6 μg l⁻¹ cadmium had no effect on any of the cardiovascular/respiratory parameters. Significant increases in cardiac and ventilatory rates, blood hematocrit and hemoglobin were observed in fish exposed to 6.4 μg l⁻¹ Cd over the entire exposure period while erythrocyte ATP concentration declined during the last stages of exposure. Further experiments on the responses of fish exposed to 6.4 μg l⁻¹ Cd for 30 days demonstrated an impairment of oxygen transfer across the gill. The results are discussed in terms of possible gill impairment and hyperactivity as toxic responses to cadmium.     

Some physiological responses of rainbow trout (Salmo gairdneri) to intermittent monochloramine exposure

Rainbow trout (Salmo gairdneri) were exposed for 2.5 h to monochloramine (NH₂Cl) at an average concentration of 0.16 or 0.23 mg l⁻¹ (and with peak concentrations of 0.4 or 0.6 mg l⁻¹) three times daily. This simulates conditions in the outfall area of many electric power plants. Heart rate, opercular movement, cough frequency, arterial PO₂, lactate, hemoglobin and methemoglobin were monitored. The trout responded to chloramine pulses with slight increases in opercular movement, bradycardia, and a large increase in cough rate. These factors approached control rates between periods of exposure to a peak concentration of 0.4 mg l⁻¹, but not when the peak was 0.6 mg l⁻¹. Neither hemoglobin or lactate changed, while arterial PO₂ decreased slightly but not significantly. Methemoglobin concentration increased markedly at the end of each period of exposure with some recovery between them. In contrast to free chlorine, which causes acute hypoxemia due to gill damage, chloramine at these concentrations causes little if any hypoxemia. The elevated methemoglobin levels, not seen following exposure to free chlorine, indicate that perhaps chloramine is entering the blood stream to an extent that does not occur with free chlorine. Methemoglobinemia is probably not the proximate cause of death.     

Acute and chronic toxicity of lead to rainbow trout salmo gairdneri, in hard and soft water

Lead was found to be highly toxic to rainbow trout in both hard water (hardness 353 mg l⁻¹ as CaCO₃) and soft water (hardness 28 mg l⁻¹. Analytical results differ greatly with methods of analysis when measuring concentrations of lead in the two types of water. This is exemplified in LC50's and maximum acceptable toxicant concentrations (MATC's) obtained when reported as dissolved lead vs total lead added in hard water. Two static bioassays in hard water gave 96-h LC50's of 1.32 and 1.47 mg l⁻¹ dissolved lead vs total lead LC50's of 542 and 471 mg l⁻¹, respectively. In a flow-through bioassay in soft water a 96-h LC50 of 1.17 mg l⁻¹, expressed as either dissolved or total lead, was obtained. From chronic bioassays, MATC's of lead for rainbow trout in hard water were between 18.2 and 31.7 μg l⁻¹ dissolved lead vs 120–360 μg l⁻¹ total lead. In soft water, where exposure to lead was initiated at the eyed egg stage of development, the MATC was between 4.1 and 7.6 μg l⁻¹. With exposure to lead beginning after hatching and swim-up of fry, the MATC was between 7.2 and 14.6 μg l⁻¹. Therefore, fish were more sensitive to the effects of lead when exposed as eggs.     

Chronic toxicity of water-borne and dietary lead to rainbow trout (Salmo Gairdneri) in lake Ontario water

Rainbow trout (Salmo gairdneri) exposed to lead in Lake Ontario water demonstrated a 21-day LC₅₀ of 2.4 mg l⁻¹ lead. At lead concentrations ranging from 3 to 120 μg l⁻¹, log₁₀ of lead concentrations in most tissues of exposed fish appeared linearily related to log₁₀ of lead concentrations in water. Highest concentrations occurred in opercular bone followed by gill and kidney. Lead accumulation by brain was not clearly demonstrated. Exposure to lead in water at concentrations as low as 13 μg l⁻¹ caused significant increases in red blood cell (RBC) numbers, decreases in RBC volumes, decreases in RBC cellular iron content and decreases in RBC δ-amino levulinic acid dehydratase activity. No changes were observed in hematocrit or whole blood iron content. The changes indicated increased erythropoiesis to compensate for inhibition of hemoglobin production and increased mortality of mature red blood cells. After 32 weeks exposure to 120 μg l⁻¹ lead in water, 30% of remaining fish exhibited black tails, an early indication of spinal deformities. Lead added to food was not available for lead uptake by fish. Lead content of fish exposed to dietary lead was not elevated above control levels and the majority of lead consumed could be accounted for in the faeces. Dietary lead may have slightly inhibited uptake of dietary iron.     

Kinetics of dose-response relationship in the bimodal respiration of Colisa lalia (Hamilton-Buchanan) exposed to lindane (γ-BHC)

Acute bioassay tests were conducted with the organochlorine pesticide, lindane on Colisa lalia. LC50 and its 95% upper and lower confidence limits for different periods of exposure were determined. A toxicity curve was constructed from which is derived the lethal threshold concentration for Colisa to lindane. The fish were exposed to two selected concentrations viz., 0.1 and 0.37 mg 1^?1 for 96 and 6 h respectively and their behaviour and bimodal respiration were studied. Erratic behavioural responses were noticed at 0.37 mg 1^?1 whereas the response at 0.1 mg 1^?1 were orderly and adaptive. Total oxygen consumption of fish increased but the dependence on the type of respiration differed in the two concentrations, and this selective dependence at 0.1 mg 1^?1 is suggested to have survival value.     

Comparative toxicity of organotin compounds to rainbow trout (Oncorhynchus mykiss) yolk sac fry

The comparative toxicity of various organotin compounds was investigated in early life stages of the rainbow trout. Beginning with yolk sac fry, trout were continuously exposed for 110 days to tributyl- (TBTC), triphenyl- (TPhTC) or tricyclohexyltin chloride (TCHTC) at concentrations of 0.12-15 nM, to trimethyltin chloride (TMTC) at concentrations of 3-75 nM or to dibutyl- (DBTC) or diphenyltin chloride (DPhTC) at 160-4000 nM. The diorganotin compounds DBTC and DPhTC were about three orders of magnitude less toxic than the triorganotin homologs TBTC and TPhTC. Both for DBTC and DPhTC, a no-observable-effect concentration (NOEC) of 160 nM was established, corresponding to 40 and 60 ppb, respectively. Of the triorganotin compounds, TCHTC appeared to be the most toxic, inducing 100% mortality within 1 week at a concentration of 3 nM. Only a few trout survived exposure to 0.6 nM TCHTC for 110 days. TBTC and TPhTC caused acute mortality at a concentration of 15 nM. For both TBTC and TPhTC a NOEC of 0.12 nM was established, corresponding to water concentrations of 40 and 50 ppt, respectively. Histopathological examination revealed depletion of glycogen in liver cells of both di- and triorganotin exposed fish, except in the case of TMTC. No signs of toxicity were observed in fish exposed to up to 75 nM TMTC, the highest concentration tested. Atrophy of the thymus, the most prominent sign of toxicity of di- and tributyltin compounds in mammalian species, was not observed in early life stages of rainbow trout. Tail melanization was observed in the groups exposed to 3 nM TPhTC, 3 nM TBTC, 800 nM DBTC and 800 nM DPhTC. At the end of the exposure period, resistance to infection was examined by an intraperitoneal challenge with Aeromonas hydrophila, a secondary pathogenic bacterium to fish. Resistance of bacterial challenge was found to be decreased even at the lowest-effect concentration of both di- and triorganotin compounds.     

Long-term effects of treated domestic wastewater on brown trout

A 12-month bioassay was conducted to determine the effects of unchlorinated, treated, domestic wastewater on survival, growth, swimming performance, and gill tissue of brown trout (Salmo trutta). Ammonia was the toxicant of concern, because the facility's effluent periodically exceeded the U.S. Environmental Protection Agency's (EPA) recommended criterion. Juvenile brown trout (initial weight = 2 g), which were exposed to six concentrations (0–37%) of effluent, were fed a restricted ration, so that growth rates were similar to those of wild stream residents. At the highest effluent concentration, monthly mean concentrations of un-ionized ammonia ranged from 0.004 to 0.055 mg l⁻¹ NH₃---N (at. wt = 14); these concentrations exceeded the EPA criterion of 0.016 mg l⁻¹ about 40% of the time. There were no significant effects of effluent concentration on survival, growth, or swimming performance of brown trout, but the degree of damage to gills was directly related to effluent concentration.     

Toxicity of sodium selenite to rainbow trout fry

In a study designed to examine the long-term effects of inorganic selenium (IV) on early life stages of rainbow trout (Salmo gairdneri), survival was significantly reduced at selenium concentrations of 47 and 100 μg l⁻¹ after 90 days of exposure. Length and weight were significantly reduced after 90 days of exposure to 100 μg l⁻¹. Whole-body residues of selenium increased with increasing exposure concentrations but appeared to decline between 30 and 90 days of exposure. Analyses of trout backbone indicated little change in bone development with exposure to selenium (IV) with one exception; calcium concentrations were significantly decreased in fish exposed to 12 μg l⁻¹ of selenium. Results of our study indicates that a recommended safe level of 10 μg l⁻¹ for inorganic selenium would not significantly affect growth and survival of rainbow trout; however, concentrations of selenium near this level can reduce the levels of calcium in the backbones of trout.     

The acute toxicity of pulse-dosed, para-substituted phenols to larval American flagfish (Jordanella floridae): a comparison with toxicity to photoluminescent bacteria and predicted toxicity using log Kow

The acute toxicity of nine para-substituted phenols was determined using a pulse-exposure testing protocol and 8-day-old larval American flagfish (Jordanella floridae). Relative tolerance was assessed by determining the 2-h pulse exposure concentration causing 20 and 50% mortality (PE LC20 and PE LC50) over the subsequent 94 h. Four bioassays were run for each phenol and yielded the following mean PE LC20 values (mg 1(-1)) in descending order of toxicity: p-aminophenol, 0.06; hydroquinone, 0.13; phenol, 0.70; p-nitrophenol, 0.81; p-cyanophenol, 3.0; p-chlorophenol, 3.3; p-hydroxyacetophenone, 4.2; p-hydroxybenzyl alcohol, 6.4; and p-hydroxybenzoic acid, 170. These toxicities did not correlate significantly with either previously reported toxicity values for the photoluminescent bacteria Photobacterium phosphoreum, or with the log octanol-water partition coefficient. For some of the compounds, however, sensitivities were quite close to previously reported rainbow trout chronic no-observed-effect concentrations based on continuous exposure. Caution is urged with respect to applying "low-level" biota techniques or simple quantitative structure-activity correlations such as Kow when attempting to predict the toxicity of specific chemicals to fish.     

The toxicity of various mining flotation reagents to rainbow trout (Salmo gairdneri)

Preliminary testing of eight collectors (xanthates) and four frothers in 96-h static and 28-day flow-through bioassays using rainbow trout as the test organism show a great disparity in the toxicity of the chemicals administered in these two ways.For the short-term tests, the relative toxicity of the compounds is expressed as an lc₅₀ or as a range of concentration in mg l⁻¹ in which the lc₅₀ is expected to fall. Of the collectors tested in this way sodium ethyl and potassium amyl xanthate were the most toxic, with lc₅₀'s in the range of 30–50 mg l⁻¹. Among the frothers, xylenol (cresylic acid) was found to be the most toxic (5.6 mg l⁻¹ >lc₅₀ > 3.2 mg l⁻¹) while polypropylene glycol was least toxic (lc₅₀ > 1000 mg l⁻¹).The long-term tests using potassium ethyl, sodium isopropyl, sodium ethyl, and potassium amyl xanthate indicated that in the flow-through system, the toxicity of the chemicals was in the order of 100 fold greater compared with the static bioassay results.     

Toxicological effects of dehydroabietic acid (DHAA) on the trout, Salmo gairdneri Richardson, in fresh water

Toxicological and physiological effects of dehydroabietic acid (DHAA), a major poison to fishes in pulp and paper mill effluents, were studied by two experiments with rainbow trout, Salmo gairdneri Richardson: in the first, fish were acutely exposed for 4 days to an average DHAA concentration of 1.2 mg l⁻¹ (Exp. I) and in the second for 30 days to an average of 20 μg DHAA l⁻¹ (Exp. II).Compared to the controls, fish of Exp. I displayed a decreased relative weight of liver, an increased blood haematocrit, and increased haemoglobin as well as plasma protein concentrations. The aspartate aminotransferase activity of heart muscle was significantly elevated, as was also the lactate dehydrogenase (LDH) of white muscle tissue. In the blood plasma, the proportion of muscle type LDH activity was simultaneously increased. UDP-glucuronyl-transferase activities of liver and kidney were strongly decreased. Results suggest an increased and altered use of body energy reserves, decreased plasma volume and impaired liver function.Fish of Exp. II showed an increased relative weight of spleen. In addition, liver and gill LDH shifted towards heart-type. We conclude that 20 μg l⁻¹ is close to the “minimum effective concentration” of DHAA to rainbow trout.