Combined Toxicity Of Cadmium Research Articles

NMR technique revealed the metabolic interference mechanism of the combined exposure to cadmium and tributyltin in grass carp larvae.

Widespread human activity has resulted in the presence of different pollutants in the aquatic environment that does not exist in isolation. The study of the effects of contamination of aquatic organisms is of great significance. To assess the individual and combined toxicity of cadmium (Cd) and tributyltin (TBT) to aquatic organisms, juvenile grass carp (Ctenopharyngodon idella) were exposed to Cd (2.97mg/L), TBT (7.5μg/L), and their mixture MIX. The biological response was evaluated by nuclear magnetic resonance (NMR) analysis of plasma metabolites. Plasma samples at 1, 2, 4, 8, 16, 32, and 48days post-exposure were analyzed using detection by NMR technique. The typical correlation analysis (CCA) analysis revealed that TBT had the greatest effect on plasma metabolism, followed by MIX and Cd. The interference pathway to grass carp was similar to that of TBT and MIX. Both Cd and TBT exposure alone or in combination can lead to metabolic abnormalities in TCA cycle-related pathways and interfere with energy metabolism. These results provide more detailed information for the metabolic study of pollutants and data for assessing the health risks of Cd, TBT, and MIX at the metabolic level.

Combined toxicity of cadmium and lead on early life stages of the Pacific oyster, Crassostrea gigas

Trace metals cause toxic effect on the early development period of marine animals, however only few studies address the toxic interactions of trace metals on bivalves. In the present study, the individual and combined toxicities of dissolved cadmium (Cd) and lead (Pb) on early life stages of the Pacific oyster Crassostrea gigas have been investigated. Embryotoxicity, larvae mortality and genotoxicity were measured under single and combined exposure of the two tested metals. For embryotoxicity, the median effective concentration (EC50) values for individual Cd, Pb and their mixture were of 272.2 μg/L, 660.3 μg/L and 373.1 μg/L, respectively. The median lethal concentrations (LC50) for 96 h larval mortality were determined to be 353.3 μg/L, 699.5 μg/L and 205.5 μg/L for individual Cd, Pb and their mixture, respectively. Moreover, the Marking-Dawson additive toxicity indices were 0.10 for embryogenesis and 1.40 for larval mortality indicating, respectively, an additive effect and a trend to synergism for the Cd and Pb combination. Furthermore, DNA strand breaks were observed in oyster embryos after individual Cd, Pb and their mixture exposure, and a significant positive correlation was demonstrated between embryotoxicity and genotoxicty. The current study suggests the toxicity of Cd is higher than that of Pb, and the Cd-Pb mixture is slightly more toxic than individual Cd or Pb to the Pacific oyster. These data will be helpful to predict the toxicity of metal mixtures, and provide biological criteria for the implementation of marine water quality standards to protect these marine organisms.

Combined toxicity of cadmium and copper in Avicennia marina seedlings and the regulation of exogenous jasmonic acid

Seedlings of Avicennia marina were exposed to single and combined metal treatments of cadmium (Cd) and copper (Cu) in a factorial design, and the combined toxicity of Cu and Cd was tested. The effects of the exogenous jasmonic acid (JA) on chlorophyll concentration, lipid peroxidation, Cd and Cu uptake, antioxidative capacity, endogenous JA concentration, and type-2 metallothionein gene (AmMT2) expression in seedlings of A. marina exposed to combined metal treatments were also investigated. A binary mixture of low-dose Cd (9µmolL−1) and high-dose Cu (900µmolL−1) showed toxicity to the seedlings, indicated by the significant augmentation in leaf malondialdehyde (MDA) and reduction in leaf chlorophylls. The toxicity of the combined metals was significantly alleviated by the addition of exogenous JA at 1µmolL−1, and the chlorophyll and MDA contents were found to be restored to levels comparable to those of the control. Compare to treatment with Cd and Cu only, 1 and 10µmolL−1 JA significantly enhanced the ascorbate peroxidase activity, and 10µmolL−1 JA significantly decreased the uptake of Cd in A. marina leaves. The relative expression of leaf AmMT2 gene was also significantly enhanced by 1 and 10µmolL−1 JA, which helped reduce Cd toxicity in A. marina seedlings.

Further Study of the Association Between Icipient Renal Damage and Urine Levels of Cadmium and Lead in Preschool Children

P-443 Introduction: Results of the pilot study reported to the ISEE 17 Conference suggested that a sub-clinical renal damage in 89 children dwellers of industrialized urban areas could be associated with the combined toxicity of cadmium and lead. The aim of the present study was to try and find this association in a bigger group of children living in other towns of the same region. Methods: We examined children aged 3–7 years in two neighboring towns in the Middle Urals polluted with emissions of a big copper smelter. We collected morning urine samples from 184 children in apparent good health who had no history or symptoms of renal or urological disease. Concentrations of cadmium and lead, both well established renal toxins, and beta-2-microglobulin (B2u), a physiological marker for renal damage, were measured, along with usual clinical laboratory indices. Results: The B2u levels in the cohort ranged from 10 to 1200 ug/L. Only twelve children had levels >300 ug/L. To facilitate evaluation of the association between sub-clinical renal damage and body burdens (in particular, impacts on kidneys) of lead and cadmium the cohort was divided into two halves: those above the median B2u level of 120 ug/L (“cases”), and those at or below the median (“controls”). The cases had the following mean concentrations (in ug/L): 241.5±19.7 B2u, 6.5±0.7 cadmium, and 62.1±2.7 lead. The control group had mean concentrations (in ug/L) of: 82.1±3.0 B2u, 4.9±0.6 cadmium, and 41.9±2.01 lead. The t scores for B2u, cadmium, and lead were 8.0, 1.90, and 5.5, respectively. (All the values are higher than they were in the previous study due to higher levels of the environmental pollution.) Within the control group, there was an increase in both metals’ mean concentration in the 2nd quartile of the B2u data distribution as compared with the 1st quartile. Odds ratios (OR) obtained through one-metal regression models that incorporated adjustments only for gender and area were (per 1 ug/L of a metal)1.13 (95% CI 1.05–1.22) for cadmium and 1.03 (1.02–1.05) for lead, with P<0.005 and <0.001, respectively. Additional adjustment for frequent respiratory infections (the only IRF proved significant in the univariate modeling) has not changed these ORs. Dwelling in the town located closer to the copper smelter proved a significant risk factor for both metals, especially for cadmium. When we made the same adjustment in a two-metals regression model, a statistically significant OR ≠ 1.0 was found only for lead: 1.04 (1.02–1.05), P<0.001. It can be explained by the fact that, unlike previous study, cadmium and lead urine concentrations were significantly correlated (r=0.49. P<0.001) due to the common source of environmental pollution with them. Conclusion: Taken as a whole, the results obtained in both studies demonstrate that in children even moderate body burdens of cadmium and lead increase probability of an incipient renal damage.