The effects of sieving and spatial variability of estuarine sediment toxicity samples on sediment chemistry.

In 1998, we conducted a field-validation study of the chronic 28-day whole-sediment toxicity test with Leptocheirus plumulosus in Baltimore Harbor, MD, an area where this amphipod is indigenous. This study included an evaluation of the effect of sieving on sediment chemical concentrations and the use of field replicates, or separate grabs from the same site, which provided an estimation of within-site chemical and toxicologic variability. Six stations in Baltimore Harbor, MD, were included in this evaluation. Chemical analysis of two separate unsieved field replicates from the six sites indicated that, overall, the chemical concentrations of replicates within each site were similar, especially for metals. Organic contaminants particularly total PCBs, had the highest variability between replicates. Chemical variability did not appear to be related to differences in organic carbon content or grain size or to variability in toxicologic end points. Results supported the use of composite samples in sediment toxicity tests. In addition, in most cases, sieving had little effect on sediment chemistry. For the metals and trace elements, only selenium showed a substantial change after sieving, with some samples increasing after sieving and others decreasing. Concentrations of acid-volatile sulfide (AVS) increased 194.6% at one station after sieving, although in most other cases, AVS and simultaneously extracted metals remained relatively unchanged. As expected, concentrations of organics generally decreased after sieving, but in the majority of cases this decrease was small (i.e., coefficient of variation < or = 25%). Total benzene hexachloride and total chlordanes had the greatest changes, whereas polychlorinated biphenyl concentrations decreased at only two stations after sieving. Concentrations of polyaromatic hydrocarbons showed little change after sieving. These changes in sediment chemistry due to sieving must be viewed in the larger context of the potentially confounding effects that indigenous organisms may have on the interpretation of test results from whole-sediment toxicity tests.

Effectiveness of the sulfur(IV) compound, sodium bisulfite, in reducing chlorine, chlorine dioxide, and chlorite toxicity to Daphnia magna in well water and pond water.

Flow-through toxicity tests were conducted with Daphnia magna to determine the residual toxicity of chlorine, chlorine dioxide, and chlorite after treatment with the sulfur(IV) compound sodium bisulfite. Daphnids were exposed separately to 0.5-mg/L concentrations of each of the three compounds without the addition of sodium bisulfite, with a low stoichiometric dose of sodium bisulfite, and with a high stoichiometric dose of sodium bisulfite. Tests were performed in well water with a low total organic carbon (TOC) content and pond water with a high TOC content. Analysis of results indicated that sodium bisulfite did not eliminate the toxicity of chlorine dioxide or chlorite to D. magna. Total residual oxidant (TRO) concentrations were reduced and survival times were extended, but acute toxicity persisted even with a S(IV) concentration 10.0 times the stoichiometric ratio of oxidant. Mortality occurred in chlorine dioxide treatments in which no TRO was detected, indicating that standard analytical (amperometric) techniques may be inadequate to detect toxicity. Sodium bisulfite did succeed in eliminating chlorine toxicity except in pond water receiving a low (3.0x) sodium bisulfite dose. Oxidant reactions with organic substrates may have produced chlorinated residuals that were resistant to S(IV) dechlorination.

Pathology of fathead minnows (Pimephales promelas) exposed to chlorine dioxide and chlorite.

Fathead minnows (Pimephales promelas) were exposed to the biocide chlorine dioxide (0.13 and 0.19 mg l-1) for up to 12 h and to its primary decomposition product, chlorite (177 and 304 mg l-1), for up to 96 h followed by recovery periods of up to 14 days. Chlorine dioxide exposure produced dose-dependent gill pathology including epithelial lifting, hypertrophy, hyperplasia, lamellar fusion, and necrosis. Complete recovery, even in fish with severe hypertrophy and lamellar fusion, was achieved within 4 days. Chlorite did not produce gill pathology even at a lethal exposure level (304 mg l-1 for 96 h) but did elicit a chronic inflammatory response with a marked increase in circulating and fixed phagocytes within hematopoietic and vascular tissues. This study indicates that chlorine dioxide is approximately 1000 times more toxic to fathead minnows than chlorite. Further, exposure of fathead minnows to these distinct but related compounds is consistently associated with very different pathologies.