The Toxicity Of Cadmium To Several Aquatic Organisms Under Different Environmental Conditions

Cadmium(Cd)is an environmental pollutant that ranked eighth in the Top 20 Hazardous Substances Priority List.In recent years,Cd has received considerable attention because its concentration in water body has been markedly increased by human activities such as sewage treatment,production of pulp and paper,and processing of metals.Much of the Cd added to aquatic systems accumulates in sediments,and under certain conditions may reenter the water column.As a nonessential element,Cd may endanger the growth and development of aquatic life including benthic biota.Many studies have shown that that the toxicity of cadmium to an organism depends not only on the concentration of this metal,but also on the water chemistry.Environmental factors such as water hardness,salinity,pH,dissolved organic matter(DOM),complexants and other organic compounds may compete with cadmium cation for uptake sites or change Cd speciation through complexation with free ions,influencing Cd bioavailability and subsequent toxicity.Nanomaterials can also affect Cd uptake and toxicity by adsorption interactions.Moreover,the concentrations of Cd that result in acute or chronic toxicity vary over several orders of magnitude for different organisms.To the best of our knowledge,many shortcomings and gaps still exist in studies on the toxicity of Cd to aquatic organisms under different environmental conditions.For example,previous toxicity tests concerning the influence of water quality factors on Cd toxicity was either performed within a narrow pH range or was limited to only a single species;very little information is available on the combined toxicity of Cd and emerging environmental contaminants[e.g.,carbon nanotubes(CNTs)and perfluorooctane sulfonate(PFOS)]to aquatic organisms.Based on this background,the following research works were conducted to enhance understanding on cadmium toxicity in aquatic environment:(1)The toxicity of Cd to P.phosphoreum,D.magna and C.auratus was investigated under different pH levels.The acute toxicity of Cd to P.phosphoreum and D.magna across a relatively wide pH range(pH 5.0,6.0,7.0,8.0 and 9.0)was assessed by calculating EC50 values.It was found that Cd was least toxic under acidic conditions,and D.magna was more sensitive to the toxicity of Cd than P.phosphoreum.The activity of antioxidant enzymes[superoxide dismutase(SOD),catalase(CAT)and glutathione peroxidase(GPx)],the level of glutathione(GSH)and the malondialdehyde(MDA)content in the liver of C.auratus were measured to evaluate the effect of 0.01 and 0.1 mg/L Cd exposure on hepatic antioxidant system at three pH values(5.0,7.25,9.0).No test groups showed statistically significant changes in SOD,CAT and GPx activity,GSH level,or MDA content after 1 d exposure,whereas significantly suppressed antioxidant enzymes activities,decreased GSH level,and enhanced MDA content was observed in the fish liver after 7 d exposure to Cd at pH 9.0.Acute toxicity and oxidative stress test results shows that Cd was more toxic to the three test organisms in alkaline water than in acidic medium.(2)Based on the measurement of Cd toxicity to P.phosphoreum at varying water quality parameters,a model was developed to predict cadmium induced bioluminescence inhibition.The effects of water quality factors including Ca2+(as CaCl2),Mg2+(as MgSO4),K+(as KCl),pH,the complexant EDTA and DOM(a commercial DOM and three homemade DOMs)on Cd toxicity to P.phosphoreum were evaluated in standardized 15 min acute toxicity tests.Increases in Ca2+ and Mg2+concentration resulted in higher EC50 values,whereas increasing K+ in test solutions decreased the EC50 values.The toxicity alleviation by H+ was observed over the tested pH range of 5.0-9.0.Additions of EDTA and DOM into the exposure water reduced Cd bioavailability via complexation of Cd2+.The influence of these toxicity modifying factors was finally incorporated into a model by the statistical method.After validation with laboratory and natural waters,the model can be used to predict acute cadmium toxicity toward P.phosphoreum for a relatively broad range of water quality characteristics.(3)Experiments were conducted to investigate the effect of four different CNTs on Cd toxicity(24h-EC50)to D.magna.The four CNTs including single-walled carbon nanotubes(SWCNTs),multi-walled carbon nanotubes(MWCNTs),hydroxylated multi-walled carbon nanotubes(OH-MWCNTs)and carboxylated multi-walled carbon nanotubes(COOH-MWCNTs)were detailedly characterized and used in toxicity tests.At a CNT concentration of 10 mg/L,the EC50 value of Cd was decreased by SWCNTs,MWCNTs,OH-MWCNTs and COOH-MWCNTs,indicating that all CNTs could enhance the toxicity of Cd to D.magna.The filtrate toxicity,purified CNTs toxicity,adsorption/desorption and accumulation/depuration tests were conducted to explore the underlying mechanisms for the enhanced toxicity.The results showed that the toxicity-increasing effect of the two non-functionalized CNTs(SWCNTs and MWCNTs)in the overall system was mainly caused by metal catalysts impurities in the pristine CNTs,whereas the two functionalized CNTs(OH-MWCNTs and COOH-MWCNTs)have a greater adsorption capacity for Cd,leading to enhanced Cd accumulation and subsequent toxicity.(4)The effects of Cd and OH-MWCNTs co-exposure on Cd accumulation and hepatic antioxidant defenses were studied using the goldfish Carassius auratus as the test organism.The fish were exposed to 0.1 mg/L Cd,0.5 mg/L OH-MWCNTs,or 0.1 mg/L Cd + 0.5 mg/L OH-MWCNTs for 3 and 12 days.Then,the Cd concentration was determined in the gill,liver and muscle.Moreover,hepatic antioxidant enzyme(SOD,CAT and GPx)activity,GSH level and MDA content were also measured.A continuous accumulation of Cd was observed throughout the experimental period.Cd accumulation in tissues occurred in the following order:gill>liver>muscle at 3 days and liver>gill>muscle at 12 days.The concentrations of Cd in the livers of fish exposed to the combination of Cd + OH-MWCNTs were significantly higher than those in fish exposed to either single chemical after 12 d of exposure.Meanwhile,the mixture evoked severe oxidative stress in the exposed fish,as indicated by significant inhibition of SOD,CAT and GPx activity,a remarkable decrease in GSH level and simultaneous elevation of MDA content.Enhanced cadmium bioavailability resulting from the great adsorption of Cd onto OH-MWCNTs may explain the toxicity increase in the co-exposure group.(5)The aquatic oligocheate L.hoffmeisteri was chosen as the test organism to investigate the acute toxicity,bioaccumulation and oxidative stress status caused by co-exposure to Cd and PFOS under different pH levels.The effect of PFOS on acute Cd toxicity(48h-LC50)was determined at three pH values(pH 6.2,7.0 and 8.0),and we observed that Cd toxicity was increased with pH increasing from 6.2 to 8.0,and the presence of PFOS could enhance the overall toxicity of the combined system.After exposure to Cd(0.02 and 0.1 mg/L),PFOS(0.2 ? 2.0 mg/L)and Cd + PFOS(0.02 + 0.2 mg/L and 0.1 + 2.0 mg/L)at the three pH for 2 and 8 days,the accumulation of Cd and PFOS in the organism and the oxidative stress status was evaluated.When the worms were exposed to Cd or PFOS alone,the accumulated Cd and PFOS content increased with increasing pollutant concentration and prolonged exposure time.Due to the possible complexation of Cd and PFOS,the co-exposure simultaneously decreased internal Cd and PFOS concentration.Single Cd and PFOS exposure caused minimal damage to the antioxidant system at pH 6.2 and pH 8.0,respectively;whereas the low and high concentration mixture was the least toxicat pH 8.0 and pH 6.2,respectively.In the studied pH range,the combined effects of the Cd+ PFOS binary mixture on oxidative stress were mostly antagonism,consistent with the bioaccumulation of the two chemicals in the co-exposure group.