Trophic transfer of Cd from larval chironomids (Chironomus riparius) exposed via sediment or waterborne routes, to zebrafish (Danio rerio): tissue-specific and subcellular comparisons.

Zebrafish were fed chironomid larvae (8% wet weight daily ration) for 7 days, followed by 3 days of gut clearance in a static-renewal system. Regardless of whether the chironomids had been loaded with Cd via a waterborne exposure or sediment exposure, they had similar subcellular distributions of Cd, with the largest areas of storage being metal rich granules (MRG)>organelles (ORG)>enzymes (ENZ) except that sediment-exposed chironomids had significantly more Cd in the metallothionein-like protein (MTLP) fraction, and significantly less Cd in the cellular debris (CD) fraction. When zebrafish fed sediment-exposed chironomids (153+/-11 microg Cd/g dry weight) were compared directly to zebrafish fed waterborne exposed chironomids (288+/-12microg Cd/g dry weight), identical whole-body Cd levels were observed, despite the difference in the concentration in the food source. Thus trophic transfer efficiency (TTE) of Cd was significantly greater from sediment-exposed chironomids (2.0+/-0.5%) than from waterborne-exposed chironomids (0.7+/-0.2%). Subsequent tests with waterborne exposed chironomids loaded to comparable Cd concentrations, as well as with Cd-spiked manufactured pellets, demonstrated that TTEs were concentration-independent. In all treatments, zebrafish exhibited similar subcellular storage of Cd, with the greatest uptake occurring in the ORG fraction followed by the ENZ fraction. However, neither trophically available metal (TAM) nor metabolically available fractions (MAF) were good predictors for the TTEs found in this study. Tissue Cd concentrations were highest in the kidney and gut tissue, then liver, but lower in the gill, and carcass. Overall, the gut and carcass contributed >/=71% to total body burdens on a mass-weighted basis. This study presents evidence that Cd may be acquired by fish from natural diets at levels of environmental relevance for contaminated sites, and that the exposure route of the prey influences the TTE.

Acute toxicity of waterborne Cd, Cu, Pb, Ni, and Zn to first-instar Chironomus riparius larvae.

The acute toxicities of waterborne Cd, Cu, Pb, Ni, and Zn were determined in the first-instar larvae (generally considered to be the most sensitive) of Chironomus riparius, under standardized conditions. Toxicity tests were conducted in soft water (hardness, 8 mg/L as CaCO(3) equivalents) in the absence of food and were limited to 24 h to avoid control mortality associated with food deprivation. For each metal, a logarithmic range of concentrations was tested between 0 and 25 mg/L. First-instar C. riparius are most sensitive to Pb, with a 24-h LC50 of 0.61 mg/L (CI of 0.26-1.15 mg/L), and to Cu, with a 24-h LC50 of 2.09 mg/L (CI of 1.57-2.96 mg/L). The LC50 for Cd was 9.38 mg/L, while the LC50s for Zn and Ni were both higher than the highest tested concentration of 25 mg metal/L. Our results found that even first-instar chironomid larvae are well protected by both the current CCME Canadian water quality guidelines for the protection of aquatic life and the USEPA Water Quality Criteria, as LC50s were at least 25 times higher than the guideline concentrations.

The pathology of transfusion-related acute lung injury.

Transfusion-related acute lung injury is an uncommon condition characterized by the rapid onset of respiratory distress soon after transfusion. Our understanding of its pathophysiology is based on animal models of complement (C5a) and antibody-induced lung injury and a limited number of autopsies. These models suggest that transfusion-related acute lung injury is induced by granulocytes that aggregate in the pulmonary microvasculature after activation by transfusion-derived antibodies or biologically active lipids. The published autopsy reports provide little support for this model, as they are invariably confounded by underlying pulmonary infection, preexisting disease, and resuscitation injury. We report the case of a previously well 58-year-old man who died of transfusion-related acute lung injury within 2 hours of the onset of pulmonary distress; autopsy showed evidence of massive pulmonary edema with granulocyte aggregation within the pulmonary microvasculature and extravasation into alveoli. Electron microscopy revealed capillary endothelial damage with activated granulocytes in contact with the alveolar basement membranes. These findings provide direct support for the proposed model of transfusion-related acute lung injury pathogenesis.