Using Py-GC/MS to fingerprint additives associated with paper mill effluent toxicity episodes.

Understanding the cause of effluent toxicity is an important requirement for its prevention, remediation and return to compliance. One component of the strategy entails identification and fingerprinting of additives or components in additives that may be the cause of the toxicity episodes. A number of additives used in pulp and papermaking are polymeric compounds that are suspect in effluent toxicity. Their analysis and detection is difficult as they are not amenable to analysis by normal techniques applicable to mill effluents such as gas chromatography. Py-GC/MS is a powerful analytical technique that can be used to fingerprint these additives. The presence of the additives is confirmed by fingerprint pyrograms of the additives (or components in the formulations of the additives) in conjunction with mass spectrometry. The technique has been used to fingerprint and quantify polymeric additives associated with mill effluent toxicity episodes.

Implications of aerated stabilization basin dredging on potential effluent toxicity to fish.

Benthal solids accumulated in aerated stabilization basins (ASBs) must be dredged to regain treatment capacity. While dredging restores treatment performance, it has been associated occasionally with the failure to meet regulatory effluent toxicity limits at the time of dredging. A first study of its kind was undertaken to investigate the implications of ASB dredging on potential effluent toxicity to fish. The study showed that benthal solid slurry removed from the quiescent zone of an ASB with a hydraulic dredge was toxic to rainbow trout with a 96-hour median lethal concentration (LC50) of 2.2%. The high ammonia concentration in the sample was the main cause of fish mortality. Hydrogen sulfide and resin and fatty acids also were present in the dredged material at concentrations that could cause fish mortality. These findings have led to best management practices that can be used to mitigate or eliminate fish toxicity issues during dredging operations.

TRIL, a functional component of the TLR4 signaling complex, highly expressed in brain.

TLR4 is the primary sensor of LPS. In this study, we describe for the first time TLR4 interactor with leucine-rich repeats (TRIL), which is a novel component of the TLR4 complex. TRIL is expressed in a number of tissues, most prominently in the brain but also in the spinal cord, lung, kidney, and ovary. TRIL is composed of a signal sequence, 13 leucine-rich repeats, a fibronectin domain, and a single transmembrane spanning region. TRIL is induced by LPS in the human astrocytoma cell line U373, in murine brain following i.p. injection, and in human PBMC. Endogenous TRIL interacts with TLR4 and this interaction is greatly enhanced following LPS stimulation. TRIL also interacts with the TLR4 ligand LPS. Furthermore, U373 cells stably overexpressing TRIL display enhanced cytokine production in response to LPS. Finally, knockdown of TRIL using small interfering RNA attenuates LPS signaling and cytokine production in cell lines, human PBMC, and primary murine mixed glial cells. These results demonstrate that TRIL is a novel component of the TLR4 complex which may have particular relevance for the functional role of TLR4 in the brain.