Characteristics and fate of plastic pollution in urban stormwater ponds.

Stormwater runoff is often assumed to be an important pathway for microplastics from the terrestrial to the marine environment, although few studies have attempted to quantify the significance of this pathway or the interactions between stormwater infrastructure and plastic pollution. The objective of this study was to determine what factors influence the concentrations and behaviors of microplastics in stormwater ponds. Samples were taken from the water and bottom sediments of six stormwater ponds in Tampa (Florida, USA) using a neuston net and a sediment dredger. They were processed using a combination of density separations, visual sorting, and Raman spectroscopy. Concentrations ranged by several orders of magnitude between sites and rounds of sampling (0.0-55.5 items/m3 in water, 2.5-203.0 items/kg dry weight in sediment) but were comparable to other studies. The sediments of fenced and residential sites had significantly lower plastic count concentrations, compared to unfenced sites with mixed land uses. The ratio of impervious drainage area to pond surface area was found to be positively correlated with sediment concentrations. Particle shapes in water were more variable than those found in sediments, suggesting that regular-shaped plastics tend to settle first. Circularity was identified as an important parameter in determining settling behaviors. Shape characteristics were similar to those observed in a downstream river, suggesting that degradation leading to the observed shapes occurred prior to entering the ponds. This study highlights the importance of stormwater infrastructure in understanding plastic transport and how plastic shape characteristics can impact their behavior in the environment.

Nod2 protects mice from inflammation and obesity-dependent liver cancer.

Nod2 is a pattern recognition receptor that modulates host innate immune responses and protects from inflammation, steatosis, and obesity. Obesity and inflammation are risk factors for hepatocellular carcinoma, however, the role of Nod2 in obesity-dependent hepatic tumorigenesis is not known. Here we tested the hypothesis that Nod2 protects from high fat diet (HFD)-dependent hepatic cancer. We used an obesity-dependent hepatic tumor model. WT and Nod2-/- mice were treated with the carcinogen dimethylbenz[a]anthracene (DMBA) and maintained on HFD. Nod2-/- mice treated with DMBA and maintained on HFD gain significantly more weight and develop more liver tumors than similarly treated WT mice. Livers of Nod2-/- tumorigenic mice had increased expression of genes involved in cell proliferation, immune responses, and cholesterol biosynthesis, increased infiltration of neutrophils, inflammatory monocytes, and T cells, and increased activation of STAT3 and ERK during the later stages of tumorigenesis. Bioinformatic analyses of genes with differential expression predicted an increase in cancer, immune, and cholesterol biosynthesis pathways. In summary, we have identified a novel role for Nod2 and demonstrate that Nod2 protects from HFD-dependent liver malignancy and this protection is accompanied by decreased cell proliferation, inflammation, steroid biosynthesis, neutrophils and macrophages infiltration, and STAT3 and MAPK signaling in the liver.