Organophosphate Ester Flame Retardants and Plasticizers in ocean sediments from the North Pacific to the Arctic Ocean

The occurence of organophosphate ester (OPE) flame retardants and plasticizers in surface sediment from the North Pacific to Arctic Ocean was observed for the first time during the fourth National Arctic Research Expedition of China in the summer of 2010. The samples were analyzed for three halogenated OPEs [tris(2-chloroethyl) phosphate (TCEP), tris(1-chloro-2-propyl) phosphate (TCPP), and tris(dichloroisopropyl) phosphate], three alkylated OPEs [triisobutyl phosphate (TiBP), tri-n-butyl phosphate, and tripentyl phosphate], and triphenyl phosphate. Σ7OPEs (total concentration of the observed OPEs) was in the range of 159–4658 pg/g of dry weight. Halogenated OPEs were generally more abundant than the nonhalogenated OPEs; TCEP and TiBP dominated the overall concentrations. Except for that of the Bering Sea, Σ7OPEs values increased with increasing latitudes from Bering Strait to the Central Arctic Ocean, while the contributions of halogenated OPEs (typically TCEP and TCPP) to the total OPE profile also increased from the Bering Strait to the Central Arctic Ocean, indicating they are more likely to be transported to the remote Arctic. The median budget of 52 (range of 17–292) tons for Σ7OPEs in sediment from the Central Arctic Ocean represents only a very small amount of their total production volume, yet the amount of OPEs in Arctic Ocean sediment was significantly larger than the sum of polybrominated diphenyl ethers (PBDEs) in the sediment, indicating they are equally prone to long-range transport away from source regions. Given the increasing level of production and usage of OPEs as substitutes of PBDEs, OPEs will continue to accumulate in the remote Arctic

Organophosphate ester pollution in the oceans

The large-scale use of organophosphate esters (OPEs) as flame retardants and plasticizers has led to their prevalence in the environment, with still unknown broader impacts. This Review describes the transport and occurrence of OPEs in marine systems and summarizes emerging evidence of their biogeochemical and ecosystem impacts. Long-range environmental transport via the atmosphere and ocean currents distributes OPEs from industrialized regions to the open ocean. OPEs are most prevalent in coastal regions, but notable concentrations are also found in the Arctic and regions far from shore. Air–water interactions are important for the transport of OPEs to remote oceans and polar regions. Processes such as degradation and sinking of particle-bound compounds modulate the properties and fate of OPEs in the water column, where they are potentially a non-accounted source of anthropogenic organic phosphorus for microbial communities. Some OPEs have toxic effects in marine species and are found in measurable quantities in fish and other aquatic organisms. However, there is conflicting evidence on the potential for bioaccumulation and biomagnification of OPEs. Future work must constrain the large-scale impact of OPEs on marine biota and biogeochemistry to support more effective regulation and mitigation

Polycyclic aromatic hydrocarbons in ocean sediments from the North Pacific to the Arctic Ocean

Abstract Eighteen polycyclic aromatic hydrocarbons (PAHs) were measured in surficial sediments along a marine transect from the North Pacific into the Arctic Ocean. The highest average Σ18PAHs concentrations were observed along the continental slope of the Canada Basin in the Arctic (68.3 ± 8.5 ng g−1 dw), followed by sediments in the Chukchi Sea shelf (49.7 ± 21.2 ng g−1 dw) and Bering Sea (39.5 ± 11.3 ng g−1 dw), while the Bering Strait (16.8 ± 7.1 ng g−1 dw) and Central Arctic Ocean sediments (13.1 ± 9.6 ng g−1 dw) had relatively lower average concentrations. The use of principal components analysis with multiple linear regression (PCA/MLR) indicated that on average oil related or petrogenic sources contributed ∼42% of the measured PAHs in the sediments and marked by higher concentrations of two methylnaphthalenes over the non-alkylated parent PAH, naphthalene. Wood and coal combustion contributed ∼32%, and high temperature pyrogenic sources contributing ∼26%. Petrogenic sources, such as oil seeps, allochthonous coal and coastally eroded material such as terrigenous sediments particularly affected the Chukchi Sea shelf and slope of the Canada Basin, while biomass and coal combustion sources appeared to have greater influence in the central Arctic Ocean, possibly due to the effects of episodic summertime forest fires

Occurrences and distribution characteristics of organophosphate ester flame retardants and plasticizers in the sediments of the Bohai and Yellow Seas, China

Concentrations and distribution characteristics of organophosphate esters (OPEs) in surface sediment samples were analyzed and discussed for the first time in the open Bohai Sea (BS) and YellowSea (YS). Three halogenated OPEs [ tris-(2-chloroethyl) phosphate (TCEP), tris-(1-chloro-2-propyl) phosphate (TCPP), and tris-(1,3-dichloro2- propyl) phosphate (TDCPP)] and five non-halogenated OPEs [ tri-isobutyl phosphate (TiBP), tri-n-butyl phosphate (TnBP), tripentyl phosphate (TPeP), triphenyl phosphate (TPhP) and tris-(2-ethylhexyl) phosphate (TEHP)] were detected in this region. The concentrations of eight OPEs in total (Sigma 8OPEs) ranged from 83 to 4552 pg g(-1) dry weight (dw). The halogenated OPEs showed higher abundances than the non-halogenated ones did, with TCEP, TCPP, and TEHP the main compounds. Generally, concentrations of OPEs in the BS were higher than those in the YS. Riverine input (mainly the Changjiang DilutedWater (CDW)) and deposition effect in the mud areas might have influenced the spatial distributions of OPEs. Correlation between OPE concentrations and total organic carbon (TOC) indicated TOC was an effective indicator for the distribution of OPEs. Inventory analysis of OPEs implied that sea sediment might not be the major reservoir of these compounds. (C) 2017 Elsevier B.V. All rights reserved.</p

Role of autophagy in diabetes and endoplasmic reticulum stress of pancreatic β-cells

Type 2 diabetes mellitus is characterized by insulin resistance and failure of pancreatic β-cells producing insulin. Autophagy plays a crucial role in cellular homeostasis through degradation and recycling of organelles such as mitochondria or endoplasmic reticulum (ER). Here we discussed the role of β-cell autophagy in development of diabetes, based on our own studies using mice with β-cell-specific deletion of Atg7 (autophagy-related 7), an important autophagy gene, and studies by others. β-cell-specific Atg7-null mice showed reduction in β-cell mass and pancreatic insulin content. Insulin secretory function ex vivo was also impaired, which might be related to organelle dysfunction associated with autophagy deficiency. As a result, β-cell-specific Atg7-null mice showed hypoinsulinemia and hyperglycemia. However, diabetes never developed in those mice. Obesity and/or lipid are physiological ER stresses that can precipitate β-cell dysfunction. Our recent studies showed that β-cell-specific Atg7-null mice, when bred with ob/ob mice, indeed become diabetic. Thus, autophagy deficiency in β-cells could be a precipitating factor in the progression from obesity to diabetes due to inappropriate response to obesity-induced ER stress

Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes

BACKGROUND: Data are lacking on the long-term effect on cardiovascular events of adding sitagliptin, a dipeptidyl peptidase 4 inhibitor, to usual care in patients with type 2 diabetes and cardiovascular disease. METHODS: In this randomized, double-blind study, we assigned 14,671 patients to add either sitagliptin or placebo to their existing therapy. Open-label use of antihyperglycemic therapy was encouraged as required, aimed at reaching individually appropriate glycemic targets in all patients. To determine whether sitagliptin was noninferior to placebo, we used a relative risk of 1.3 as the marginal upper boundary. The primary cardiovascular outcome was a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. RESULTS: During a median follow-up of 3.0 years, there was a small difference in glycated hemoglobin levels (least-squares mean difference for sitagliptin vs. placebo, -0.29 percentage points; 95% confidence interval [CI], -0.32 to -0.27). Overall, the primary outcome occurred in 839 patients in the sitagliptin group (11.4%; 4.06 per 100 person-years) and 851 patients in the placebo group (11.6%; 4.17 per 100 person-years). Sitagliptin was noninferior to placebo for the primary composite cardiovascular outcome (hazard ratio, 0.98; 95% CI, 0.88 to 1.09; P<0.001). Rates of hospitalization for heart failure did not differ between the two groups (hazard ratio, 1.00; 95% CI, 0.83 to 1.20; P = 0.98). There were no significant between-group differences in rates of acute pancreatitis (P = 0.07) or pancreatic cancer (P = 0.32). CONCLUSIONS: Among patients with type 2 diabetes and established cardiovascular disease, adding sitagliptin to usual care did not appear to increase the risk of major adverse cardiovascular events, hospitalization for heart failure, or other adverse events