Comparison of chlorine and chlorine dioxide toxicity to fathead minnows and bluegill

The comparative toxicity of total residual chlorine (TRC) and chlorine dioxide (ClO₂) was evaluated by conducting 96 h flow-through bioassays with three types of fish. The fish were subjected to an intermittent exposure regime in which biocide residuals were present for approx. 2-h periods beginning at 0, 24, 48 and 72 h into the tests. These conditions simulated the antifouling procedure (1 h day⁻¹ biocide addition) used to control biofouling of nuclear reactor heat exchangers at the Savannah River Plant near Aiken, South Carolina. LC₅₀ values showed that ClO₂ was approx. 2–4 times more toxic than TRC to: (1) juvenile and 1-year-old fathead minnows (Pimphales promelas); and (2) young-of-the-year bluegill (Lepomis macrochirus).The TRC mean 96-h LC₅₀ values were: 0.08 mg l⁻¹ for juvenile fathead minnows, 0.35 mg l⁻¹ for adult fathead minnows and 0.44 mg l⁻¹ for young-of-the-year bluegills. The ClO₂ mean LC₅₀ values were: 0.02 mg l⁻¹ for juvenile fathead minnows, 0.17 mg l⁻¹ for adult fathead minnows and 0.15 mg l⁻¹ for young-of-the-year bluegills.     

The toxic effects of trinitrotoluene (TNT) and its primary degradation products on two species of algae and the fathead minnow

The effects of alpha trinitrotoluene (alpha TNT) and its primary degradation product (TNTcc), commonly referred to as “pink water”, were determined on members of two trophic levels. The growth responses of the algae Selenastrum capricornutum and Microcystis aeruginosa were examined through static bioassays. Death and behavioral responses of the fathead minnow (Pimephales promelas) were determined using a proportional diluter. Alpha TNT and TNTcc were both more toxic to the fathead minnow than to either species of alga. Five and 15 mg l⁻¹ alpha TNT inhibited S. capricornutum and M. aeruginosa growth, respectively. TNTcc inhibited S. capricornutum growth at concentrations above 9 mg l⁻¹; it was lethal to M. aeruginosa at 50 mg l⁻¹, but stimulated growth at lower concentrations. The 96-h lc₅₀ values based on the death response of the fathead minnow to alpha TNT and TNTcc were 2.58 and 1.60 mg l⁻¹, respectively. The 96-h ec₅₀ values based on the behavioral responses were 0.46 and 0.64 mg l⁻¹, respectively. There was no response to concentrations of 0.05 mg l⁻¹ alpha TNT and 0.07 mg l⁻¹ TNTcc.     

Acute and chronic toxicity of copper to the fathead minnow in a surface water of variable quality

Acute and chronic toxicity tests conducted with the fathead minnow and copper used as the source of dilution water a natural stream to which a sewage treatment plant upstream contributed a variety of materials known to affect acute copper toxicity. Nominal total copper 96-h median tolerance limit values (96-h TL50), determined with static testing procedures, ranged from 1.6 to 21 mg l⁻¹. Dissolved copper 96-h TL50 values ranged from 0.60 to 0.98 mg l⁻¹. The maximum acceptable toxicant concentration (MATC) based on survival, growth, reproduction, and hatchability of eggs was between 0.066 and 0.118 mg l⁻¹.     

A comparison of toxicity tests conducted in the laboratory and in experimental ponds using cadmium and the fathead minnow (Pimephales promelas)

Acute toxicity tests were conducted in the laboratory with fathead minnows (Pimephales promelas) to determine the 96-h LC₅₀ of cadmium under three conditions: (1) in laboratory water, (2) in water from experimental ponds, and (3) in pond water underlain by sediment. Cadmium was then applied at doses equivalent to the estimated LC₅₀ values to 0.07-ha ponds containing caged fathead minnows. A cadmium ion selective electrode, ultrafiltration, and equilibrium calculations were used to determine cadmium speciation, and several water quality characteristics were measured to correlate differences in mortality between test systems (laboratory and field) with observed differences in water quality. The LC₅₀ estimates (mg l⁻¹) for the bioassays were 4.39 for the laboratory water, 3.52 for the pond water with sediment, and 2.91 for the pond water. Concentrations of Cd²⁺ decreased and those of cadmium in the particulate (> 1.2 μm) and 300,000 mol. wt (0.018–1.2 μm) fractions increased over the 96-h; cadmium in these fractions was believed to consist of colloidal sized CdCO₃ precipitates. Concentrations of Cd²⁺ decreased at different rates between test systems, regulated by the degree of CdCO₃(s) supersaturation which in turn depended on pH and total metal concentrations. Differences in toxicity in the laboratory tests were attributed to differences in water hardness and Cd²⁺ concentrations. Mortality of fathead minnows was low (0–10%) during the 96-h test period in the ponds due to the higher pH, which produced supersaturated conditions resulting in the rapid formation of nontoxic CdCO₃ precipitates and a more rapid decrease in Cd²⁺ concentrations as compared to the laboratory bioassays.     

Comparative toxicity of ten organic chemicals to ten common aquatic species

The susceptibilities of 10 aquatic organisms to 10 organic chemicals were determined using lethality tests. The species included six fishes, two crustaceans, a chironomid and an amphibian. The chemicals were selected to span the toxicity range from 26 g l⁻¹ to 1 μg l⁻¹ and include chemicals which were lethal by four modes of toxic action. There was no consistent relative susceptibility among the test species because the sensitivity to specific modes of toxic action varied among the chemicals. Nonetheless, the toxicities of the chemicals to any given species were highly correlated to the toxicities to other species, particularly among fishes. The 96-h median lethal concentration (LC₅₀) of the chemicals to rainbow trout (Salmo gairdneri) could be estimated from the 96-h LC₅₀ with fathead minnows (Pimephales promelas) with a correlation coefficient greater than 0.99. Equations for estimating the lethal concentration of chemicals with each species from the 96-h LC₅₀ for fathead minnows are presented.     

Effects of pH increases and sodium chloride additions on the acute toxicity of 2,4-dichlorophenol to the fathead minnow

The observable toxic effects produced by short-term exposure of fathead minnows (Pimephales promelas) to 2,4-dichlorophenol were reduced when the pH of the test water was increased by the addition of NaOH. After exposure for 192 h to 7.43 mg 2,4-dichlorophenol l^-1, the average survival of fathead minnows ranged from 28% at pH 7.57 to 100% at pH 9.08. Normal schooling behaviour was completely disrupted, and the equilibrium of most fish was affected after a 24-h exposure to 7.43 mg 2,4-dichlorophenol 1^-1 at pH 7.57, but neither schooling nor equilibrium were affected even after 192 h at pH 8.68 and 9.08. Schooling and swimming behaviour of fathead minnows exposed to 12.33 mg 2,4-dichlorophenol l^-1 were affected at all pH levels. Survival of these fish after 24 h ranged from 0% at pH 7.84–46% at pH 8.81. Sodium chloride in concentrations ranging from 0 to 13.9 mg l^-1 had no observable effects on the acute toxicity of 2,4-dichlorophenol to fathead minnows.     

An appraisal of the effect of biological treatment on the environmental quality of high-yield mechanical pulping effluents

Before biological treatment, the effluents from one CTMP (chemi-thermomechanical pulping) and three TMP (thermomechanical pulping) mills were acutely lethal to fathead minnows (Pimephales promelas) and the water flea Ceriodaphnia with 48-h LC₅₀ values of 2.2 to > 50%. The effluents also caused chronic effects at concentrations of 0.01–5.3%. After biological treatment, effluents from the three TMP mills were not acutely lethal to either test species. Biotreated effluents from the CTMP mill were also not acutely lethal to minnows but were lethal to Ceriodaphnia (48-h LC₅₀: 54–80%). The chronic effects of biotreated effluents occurred at concentrations of 47 to > 100% for fathead minnows and at 5–37% for Ceriodaphnia. Biological treatment also reduced the levels of BOD (>80%), COD (>60%) and wood extractives (>99%).     

The effects of depressed pH on flagfish reproduction, growth and survival

Breeding communities of flagfish, Jordanella floridae, were exposed to northern Ontario lake water (hardness 28 mg l⁻¹ CaCo₃) adjusted to depressed pH levels of 6.0, 5.5, 5.0 and 4.5. Control water (pH 6.8) received no acid treatment. Egg production, egg fertility and fry growth was impaired (P < 0.05) at all exposure levels. Flagfish fry survival was reduced (P < 0.05) at pH 5.5 and 5.0 and no fry survived at pH 4.5. Variability of hatching in all treatments precluded any identifiable hatching response to depressed pH. Reduction in the reproductive processes monitored indicated the following order of sensitivity: egg production > fry survival > fry growth > egg fertility.Results of this study coincide with reproductive investigations on brook trout and fathead minnows indicating the “no effect” level of pH depression for successful reproduction to be pH 6.5.     

The interaction of treated bleached kraft mill effluent and dissolved oxygen concentration on the survival of the developmental stages of the sheepshead minnow (Cyprinodon variegatus)

The interactions of treated bleached kraft mill effluent (BKME) and dissolved oxygen concentration (DO) on the survival of the embryo, fry, juvenile and adult stages of the sheepshead minnow, Cyprinodon variegatus, were studied under continuous-flow 96 h bioassay conditions. Embryo survival was dependent on effluent concentration only and showed no interaction at nominal DO concentrations of 1.0, 3.0 and 5.0 mg l⁻¹. Survival of the fry was related solely to DO concentration with no interaction with BKME concentrations up to 100%. Juvenile sheepshead minnows showed increased sensitivity to BKME at a nominal DO concentration of 1.0 mg l⁻¹. Adult fish were not affected by BKME at any of the DO concentrations tested. This study shows that the acute toxicity of BKME effluent to sheepshead minnows is a function of the developmental stage of the organism and DO concentration in the receiving stream.     

Acute toxicity of 12 industrial chemicals to freshwater and saltwater organisms

Aquatic animal toxicity is a major criterion used by the U.S. EPA to designate and classify hazardous substances other than oil. This research developed basic toxicity data for twelve industrial chemicals with which little or no previous testing had been done. Static 96h toxicity tests were performed with one freshwater species (fathead minnow, Pimephales promelas) and one saltwater species (grass shrimp, Palaemonetes pugio or white shrimp, Penaeus setiferus) on the following chemicals: ammonium fluoride, arsenic trisulfide, benzoyl chloride, benzyl chloride, cupric acetate, o-dichlorobenzene, p-dichlorobenzene, mercuric acetate, mercuric thiocyanate, resorcinol, sodium hypochlorite and toluene-2,4-diisocyanate (TDI). As defined by 96 h LC50's ≤ 500 mg l⁻¹, all 12 chemicals were hazardous to freshwater minnows, and all but TDI were hazardous to saltwater shrimp. The physicochemical behaviors of the compounds greatly influenced their aquatic toxicities.     

Lethal and sublethal exposure and recovery effects of ozone-produced oxidants on adult white perch (Morone americana Gmelin)

Adult white perch (Morone americana), acclimated to 15°C, were exposed to a series of ozone-produced oxidant (OPO) concentrations for 96 h using continuous flow bioassay techniques. Toxicity data were analyzed using both response surface modeling and standard probit regression. White perch were also exposed to a series of near and sublethal OPO concentrations, selected from the acute toxicity study, for 96 h and then placed in clean non-ozonated water for 14 days. Blood pH, hematocrit and gill histopathology were analyzed during exposure at 24, 48 and 96 h and after 4 and 14 days in the recovery period. Blood pH and hematocrit levels were analyzed statistically using standard ANOVA and multiple range tests. Histopathological effects were examined using both light microscopy and scanning electron microscopy. The 24-, 48- and 96-h LC₃₀'s were 0.38, 0.26 and 0.20 mg OPO l⁻¹, respectively. Blood pH was significantly reduced at concentrations 0.15 mg OPO l⁻¹ but not at 0.10 mg l⁻¹ or lower concentrations. Hematocrit significantly increased at concentrations 0.10 mg OPO l⁻¹. Histopathological examination revealed minimal effects on gill tissue at 0.01 mg OPO l⁻¹, moderate epithelial sloughing and heavy mucus production at 0.05 mg OPO l⁻¹ and extreme tissue damage at concentrations 0.10 mg l⁻¹. Results from both the acute toxicity and the exposure and recovery study were compared with the effects of chlorine-produced oxidants (CPO) obtained from the literature. Both OPO and CPO appear to have similar effects on adult white perch.     

Factors influencing acute toxicity estimates of hydrogen sulfide to freshwater invertebrates

Acute bioassay tests of hydrogen sulfide were run on Assellus militaris Hay, Crangonyx richmondensis laurentianus Bousfield. Gammarus pseudolimnacus Bousfield. Bactis vagans McDonough. Ephemera simulans Walker and Hexagenia limbata (Serville). Size and type of test chamber, type of substrate for barrowing forms or those seeking shelter in gravel, oxygen concentration, pH, and season of collection influenced the sensitivity of organisms. Hydrogen sulfide exposure at sublethal levels reduced feeding activity of Gammarus. Data indicate that test conditions should approximate natural habitat conditions as closely as practical. The most acceptable 96-h LC₅₀ hydrogen sulfide concentrations for the various species are: Assellus 1.07 mg 1⁻¹Crangonyx 0.84 mg 1⁻¹. Gammarus 0.059 mg 1⁻¹. Baetis 0.020 mg 1⁻¹. Ephemera 0.316 mg 1⁻¹, and Hexagenia, 0.111 mg 1⁻¹. Chronic exposure tests now in progress suggest that the no-effect levels are 8–12 per cent of the 96-h LC₅₀.     

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.     

Mechanism of NTA degradation by a bacterial mutant

Transport of nitrilotriacetic acid (NTA) into the cytoplasm of a bacterial mutant was an active process. The mutant was able to degrade NTA from an initial concentration of 290,000 μg l⁻¹ of NTA to less than 50 μg l⁻¹ in 45 min, representing a rate of 486 μg NTA degraded per hour per mg dry weight of cells. This extremely fast rate of NTA utilization was substantiated by kinetic studies in which a Km of 82 μg l⁻¹ and a V_max of 370 μg h⁻¹ (mg dry weight cells)⁻¹ were found. The maximal temperature for NTA degradation was 50°C. The ability of the mutant to metabolize NTA resided mainly in the cell membrane fraction. Exchange diffusion technique showed that glycine and acetic acid were the metabolic products of NTA degradation. No iminodiacetic acid (IDA), succinate or citrate could be detected.     

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.     

Effect of temperature and dissolved oxygen on biodegradation of nitrilotriacetate

The effect of temperature and dissolved oxygen on the rate of biodegradation of nitrilotriacetate (NTA) was examined in water samples collected from the Rur River. Biodegradation of NTA was first order with respect to NTA concentration over a concentration range of 50–1000 μg l⁻¹. First order rate constants showed a typical temperature dependency (temperature coefficient, Q₁₀ = 2) and biodegradation of NTA was observed over a temperature range of 2–24°C. The effect of temperature on the rate of NTA biodegradation was described by the Arrhenius equation, with calculated activation energies in the range reported for ordinary enzyme reactions. Biodegradation of NTA was also observed at low dissolved oxygen concentrations (0.3 mg l⁻¹), although at reduced rates compared to high oxygen concentrations (13 mg l⁻¹). Biodegradation of NTA was oxygen-dependent, suggesting an obligate oxygen requirement for the initial steps in NTA metabolism by natural microbial communities in surface waters. In general, our results indicate that NTA biodegradation will occur in natural waters under conditions of low temperature and low dissolved oxygen and also at low NTA concentrations.     

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.     

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.     

Chronic toxicity of vanadium to flagfish

The 96-h LC50 of vanadium to adult American flagfish (Jordanella floridae) was 11.2 mg l⁻¹ in very hard water. Larvae showed 28-day LC50's of 1.13 and 1.88 mg l⁻¹ of vanadium with larger larvae being more resistant. These appeared to be thresholds of lethality. During continuous exposure for 96 days, larval growth and survival were the most sensitive indicators of vanadium toxicity and were marginally reduced at 0.17 mg l⁻¹. At 0.041 mg l⁻¹, there were no deleterious sublethal effects but there was definite stimulation of growth in females and of reproductive performance. The threshold for chronic toxicity was judged to be about 0.08 mg l⁻¹. The “safe”-to-lethal ratio was 0.007 and this could be used as an application factor for other species. There was no clear evidence that vanadium had any long-term cumulative toxicity.     

Influence sur la survie jusqu'a eclosion des embryons de carpe commune (cyprinus carpio l.) apres traitement, pendant la fecondation et le developpement precoce, par le carbendazime, un fongicide antimitotique de synthese

The toxicity of the systemic antimitotic fungicide carbendazim, a benzimidazol compound, was studied both by trout and common carp insemination, as well as on the early development of the common carp.The toxicity is several grades of magnitude higher for these stages of the vital cycle compared with the effect on the adult stages: whereas The Pesticide Manual states that for the adult Carp, an LC₁₀₀ (24 h) > 1000 mg 1⁻¹ we find, during insemination at pH 9: LC₁₀₀ (30 min) < 5 mg l⁻¹ and during insemination at pH 7: LC₁₀₀ (30 min) <2.5 min l⁻¹.During early development we find, for instance, LC₁₀₀ (30 min) < 5 mg 1⁻¹ before the end of activation and LC₁₀₀ (24 h) < 1 mg l⁻¹ before the end of epiboly.In the course of insemination, the egg is more sensitive to carbendazim at pH 7 than at pH 9: this difference may be attributed to a greater solubility of the non ionic form of the molecule in the biological membranes.The resistance of the embryo to short treatment grows at the end of activation. This may be attributed to the decrease of the shell permeability during activation.Before the end of activation, the resistance to short intoxication seems to be able to fluctuate, which perhaps corresponds to the existence of sensitive stages in the mitotic cycle.The resistance to an over 24-h exposure increases abruptly at the end of epiboly, which could correspond to a protective part played by the enveloping layer.We suggest the possibility of classifying aquatic pollutants by correlating their physiological mode of action to the resistance profile of the fish embryo.The carp egg seems to be a favourable biological model for studying the effects of aquatic pollutants.