Review on DDT and metabolites in birds and mammals of aquatic ecosystems

Numerical sediment quality guidelines (SQGs) for freshwater ecosystems have previously been developed using a variety of approaches. Each approach has certain advantages and limitations which influence their application in the sediment quality assessment process. In an effort to focus on the agreement among these various published SQGs, consensus-based SQGs were developed for 28 chemicals of concern in freshwater sediments (i.e., metals, polycyclic aromatic hydrocarbons, polychlorinated biphenyls, and pesticides). For each contaminant of concern, two SQGs were developed from the published SQGs, including a threshold effect concentration (TEC) and a probable effect concentration (PEC). The resultant SQGs for each chemical were evaluated for reliability using matching sediment chemistry and toxicity data from field studies conducted throughout the United States. The results of this evaluation indicated that most of the TECs (i.e., 21 of 28) provide an accurate basis for predicting the absence of sediment toxicity. Similarly, most of the PECs (i.e., 16 of 28) provide an accurate basis for predicting sediment toxicity. Mean PEC quotients were calculated to evaluate the combined effects of multiple contaminants in sediment. Results of the evaluation indicate that the incidence of toxicity is highly correlated to the mean PEC quotient (R(2) = 0.98 for 347 samples). It was concluded that the consensus-based SQGs provide a reliable basis for assessing sediment quality conditions in freshwater ecosystems.

Malaria parasite transmission depends on the successful transition of Plasmodium through discrete developmental stages in the lumen of the mosquito midgut. Like the human intestinal tract, the mosquito midgut contains a diverse microbial flora, which may compromise the ability of Plasmodium to establish infection. We have identified an Enterobacter bacterium isolated from wild mosquito populations in Zambia that renders the mosquito resistant to infection with the human malaria parasite Plasmodium falciparum by interfering with parasite development before invasion of the midgut epithelium. Phenotypic analyses showed that the anti-Plasmodium mechanism requires small populations of replicating bacteria and is mediated through a mosquito-independent interaction with the malaria parasite. We show that this anti-Plasmodium effect is largely caused by bacterial generation of reactive oxygen species.