Study on the correlation of bisphenol A exposure, pro-inflammatory gene expression, and C-reactive protein with potential cardiovascular disease symptoms in young adults.

Bisphenol A (BPA) is a plasticizer used in the manufacture of polycarbonate and epoxy resins. It was found that higher urinary BPA levels are more likely to be associated with coronary artery disease (CVD). In recent years, the increasing incidence of CVD among young people is observed, which may be related with inflammation rather than the traditional triple-H risk factors. BPA is an endocrine-disrupting chemical, and can induce oxidative stress and chronic inflammation since its estrogenic effect. Inflammatory responses could come from the stimulation of IκB kinases (IKKs) by estrogen receptors (ERs). Therefore, this study investigated the association of BPA exposure with the gene expression of pro-inflammatory response (ERs and IKKs), an inflammation biomarker of CVD (C-reactive protein, CRP), and physiologic index potency of CVD development symptoms in young adults. This study divided BPA exposure levels into high and low groups based on the median plasma BPA level (4.34 ng/mL), and found that the high BPA group obviously had higher BMI, blood pressure, plasma CRP levels, and gene expression of ERß and IKKß. BMI and gene expression of IKKß were also positively correlated with plasma CRP secretion. Furthermore, the study subjects with potential CVD development symptoms had the increased levels of BPA (OR 2.10, 95% CI 0.83-5.39), CRP (OR 2.61, 95% CI 1.03-10.6) and IKKß (OR 4.29, 95% CI 1.51-15.6). These results indicated that exposure to BPA is potentially associated with expression of pro-inflammatory genes related to CRP secretion, which may promote the risk of CVD development symptoms in young adults. This study highlighted the possible connection between BPA exposure and CVD development but the mechanism between them needs to be further explored.

A simple approach for the ultrasensitive detection of paraquat residue in adzuki beans by surface-enhanced Raman scattering.

Paraquat (PQ), a broad-spectrum contact herbicide, has been used in many countries for controlling weed growth in agriculture because of its quick-acting and nonselective contact with green plant tissue. PQ is also toxic to humans, and even contributes to the development of neurodegenerative diseases. However, PQ is generally excluded from pesticide residue monitoring programs due to the lack of suitable determination methods. Thus, this study developed a detection method combined with simple extraction and surface-enhanced Raman spectroscopy (SERS) to rapidly determine and quantify the PQ residue on legumes without destructive procedures and high-cost instruments. Following the extraction procedure of the QuPPe-method, however, we took whole adzuki beans (Vigna angularis) extracted via a mixture of methanol and 1% formic acid at room temperature and followed by a 1 min cleanup by SPE. The PQ values for adzuki beans determined by LC/MSMS showed that regardless of whether extraction was followed by the QuPPe-method or the method we proposed, a consistent and low relative standard deviation (RSD) below <22% was found. In this study, we proposed to extract PQ on the surface of the beans by shaking briefly with solvent, and then the PQ molecules were detected and quantified by depositing Ag nanoparticles (AgNPs) and performing SERS within 10 min. Using a coating of deposited Ag nanoparticles, SERS can achieve a limit of detection (LOD) for PQ on the order of 1 µg L-1 (∼4 × 10-9 M) and a method detection limit (MDL) for adzuki beans of 0.8 µg kg-1 (∼3.3 × 10-9 M). This sensitivity at the ppb level absolutely met the maximum residue limit (MRL) for PQ in dried beans as declared by most countries, including the US (0.3 mg kg-1), Australia (1.0 mg kg-1) and Taiwan (0.2 mg kg-1). Taiwan will ban the use of PQ as a defoliating agent for harvest in adzuki bean fields in 2019; therefore, developing a method for detecting PQ residues in the field or in import markets is necessary for consumer health and for authorities. This study provided an opportunity to utilize SERS in the field of on-site pesticide residue screening.

From the Cover: Comparative Proteomics Reveals Silver Nanoparticles Alter Fatty Acid Metabolism and Amyloid Beta Clearance for Neuronal Apoptosis in a Triple Cell Coculture Model of the Blood-Brain Barrier.

Silver nanoparticles (AgNPs) enter the central nervous system through the blood-brain barrier (BBB). AgNP exposure can increase amyloid beta (Aß) deposition in neuronal cells to potentially induce Alzheimer's disease (AD) progression. However, the mechanism through which AgNPs alter BBB permeability in endothelial cells and subsequently lead to AD progression remains unclear. This study investigated whether AgNPs disrupt the tight junction proteins of brain endothelial cells, and alter the proteomic metabolism of neuronal cells underlying AD progression in a triple cell coculture model constructed using mouse brain endothelial (bEnd.3) cells, mouse brain astrocytes (ALT), and mouse neuroblastoma neuro-2a (N2a) cells. The results showed that AgNPs accumulated in ALT and N2a cells because of the disruption of tight junction proteins, claudin-5 and ZO-1, in bEnd.3 cells. The proteomic profiling of N2a cells after AgNP exposure identified 298 differentially expressed proteins related to fatty acid metabolism. Particularly, AgNP-induced palmitic acid production was observed in N2a cells, which might promote Aß generation. Moreover, AgNP exposure increased the protein expression of amyloid precursor protein (APP) and Aß generation-related secretases, PSEN1, PSEN2, and ß-site APP cleaving enzyme for APP cleavage in ALT and N2a cells, stimulated Aß40 and Aß42 secretion in the culture medium, and attenuated the gene expression of Aß clearance-related receptors, P-gp and LRP-1, in bEnd.3 cells. Increased Aß might further aggregate on the neuronal cell surface to enhance the secretion of inflammatory cytokines, MCP-1 and IL-6, thus inducing apoptosis in N2a cells. This study suggested that AgNP exposure might cause Aß deposition and inflammation for subsequent neuronal cell apoptosis to potentially induce AD progression.

Ambient PM2.5 in the residential area near industrial complexes: Spatiotemporal variation, source apportionment, and health impact.

This study systemically investigated the ambient PM2.5 (n=108) with comprehensive analyses of the chemical composition, identification of the potential contributors, and estimation of the resultant respiratory physician visits in the residential regions near energy-consuming and high-polluting industries in central Taiwan. The positive matrix fraction (PMF) model with chemical profiles of trace metals, water-soluble ions, and organic/elemental carbons (OC/EC) was applied to quantify the potential sources of PM2.5. The influences of local sources were also explored using the conditional probability function (CPF). Associations between the daily PM2.5 concentration and the risk of respiratory physician visits for the elderly (≥65years of age) were estimated using time-series analysis. A seasonal variation, with higher concentrations of PM2.5, metals (As, Cd, Sb, and Pb), OC/EC and ions (i.e., NO3-, SO42- and NH4+) in the winter than in the spring and summer, was observed. Overall, an increase of 10µgm-3 in the same-day PM2.5 was associated with an ~2% (95% CI: 1.5%-2.5%) increase in respiratory physician visits. Considering the health benefits of an effective reduction, we suggest that the emission from coal combustion (23.5%), iron ore and steel industry (17.1%), and non-ferrous metallurgy (14.4%), accounting for ~70% of the primary PM2.5 in the winter are prioritized to control.