Brief Report: Adolescent civic engagement: Lessons from Black Lives Matter

In 2020, individuals of all ages engaged in demonstrations condemning police brutality and supporting the Black Lives Matter (BLM) movement. Research that used parent reports and trends commented on in popular media suggested that adolescents under 18 had become increasingly involved in this movement. In the first large-scale quantitative survey of adolescents’ exposure to BLM demonstrations, 4,970 youth (mean_age = 12.88 y) across the United States highlighted that they were highly engaged, particularly with media, and experienced positive emotions when exposed to the BLM movement. In addition to reporting strong engagement and positive emotions related to BLM demonstrations, Black adolescents in particular reported higher negative emotions when engaging with different types of media and more exposure to violence during in-person BLM demonstrations. Appreciating youth civic engagement, while also providing support for processing complex experiences and feelings, is important for the health and welfare of young people and society.     

Schisandrae Fructus ethanol extract attenuates particulate matter 2.5-induced inflammatory and oxidative responses by blocking the activation of the ROS-dependent NF-κB signaling pathway

BACKGROUND/OBJECTIVESSchisandrae Fructus, the fruit of Schisandra chinensis Baill., has traditionally been used as a medicinal herb for the treatment of various diseases, and has proven its various pharmacological effects, including anti-inflammatory and antioxidant activities. In this study, we investigated the inhibitory effect of Schisandrae Fructus ethanol extract (SF) on inflammatory and oxidative stress in particulate matter 2.5 (PM2.5)-treated RAW 264.7 macrophages.MATERIALS/METHODSTo investigate the anti-inflammatory and antioxidant effects of SF in PM2.5-stimulated RAW 264.7 cells, the levels of pro-inflammatory mediator such as nitric oxide (NO) and prostaglandin E₂ (PGE₂), cytokines including interleukin (IL)-6 and IL-1β, and reactive oxygen species (ROS) were measured. To elucidate the mechanism underlying the effect of SF, the expression of genes involved in the generation of inflammatory factors was also investigated. We further evaluated the anti-inflammatory and antioxidant efficacy of SF against PM2.5 in the zebrafish model.RESULTSThe results indicated that SF treatment significantly inhibited the PM2.5-induced release of NO and PGE₂, which was associated with decreased inducible NO synthase and cyclooxygenase-2 expression. SF also attenuated the PM2.5-induced expression of IL-6 and IL-1β, reducing their extracellular secretion. Moreover, SF suppressed the PM2.5-mediated translocation of nuclear factor-kappa B (NF-κB) from the cytosol into nuclei and the degradation of inhibitor IκB-α, indicating that SF exhibited anti-inflammatory effects by inhibiting the NF-κB signaling pathway. In addition, SF abolished PM2.5-induced generation of ROS, similar to the pretreatment of a ROS scavenger, but not by an inhibitor of NF-κB activity. Furthermore, SF showed strong protective effects against NO and ROS production in PM2.5-treated zebrafish larvae.CONCLUSIONSOur findings suggest that SF exerts anti-inflammatory and antioxidant effects against PM2.5 through ROS-dependent down-regulating the NF-κB signaling pathway, and that SF can be a potential functional substance to prevent PM2.5-mediated inflammatory and oxidative damage.     

Air Pollution modifies the association between successful and pathological aging throughout the frailty condition

The rapid growth in the number of older adults has many implications for public health, including the need to better understand the risks posed by environmental exposures. Aging leads to a decline and deterioration of functional properties at the cellular, tissue and organ level. This loss of functional properties yields to a loss of homeostasis and decreased adaptability to internal and external stress. Frailty is a geriatric syndrome characterized by weakness, weight loss, and low activity that is associated with adverse health outcomes. Frailty manifests as an age-related, biological vulnerability to stressors and decreased physiological reserves. Ambient air pollution exposure affects human health, and elderly people appear to be particularly susceptible to its adverse effects.The aim of this paper is to discuss the role of air pollution in the modulation of several biological mechanisms involved in aging. Evidence is presented on how air pollution can modify the bidirectional association between successful and pathological aging throughout the frailty conditions.     

不同粒径室外大气颗粒物与儿童哮喘相关性的研究进展

室外大气颗粒物严重影响人体健康,而儿童由于生长发育的特点对颗粒物较为敏感.大气颗粒物按空气动力学粒径可分为总悬浮颗粒物、可吸入颗粒物、细颗粒物和超细颗粒物等.为探讨颗粒物对儿童哮喘急性发作的影响,该文对不同粒径颗粒物的来源、组成、理化性质、作用机制及其与儿童哮喘相关性的流行病学研究进行综述,为深入研究不同粒径颗粒物对儿童哮喘的影响提供依据.     

Negatively charged 2- and 10-microm particles activate vanilloid receptors,increase cAMP,and induce cytokine release

Exposure to airborne pollutants, such as particulate matter (PM), is associated with increased mortality and morbidity. Indirect evidence suggested that PM-induced responses could be initiated by the activation of proton-gated receptors, including vanilloid receptors (VRs) and acid-sensitive ion channels (e.g. ASICS). We tested this hypothesis by characterizing the effects of 10- and 2-microm polystyrene carboxylate-modified particles (PC(10) and PC(2)) on HEK 293 cells expressing VR1 receptors, rat trigeminal ganglion (TG) neurons, and BEAS-2B airway epithelial cells. Zeta potential measurements revealed that these particles are negatively charged, meaning that when they adhere to a membrane they can lower the surface pH and activate proton-gated receptors. Both types of PCs induced currents and/or elevated intracellular Ca(2+) in cells that were capsaicin sensitive (CS). In about 70% of CS neurons, 10 microM capsazepine (CPZ), a VR antagonist, blocked PC-induced responses. In TG neurons in which VRs were blocked or desensitized, PCs induced an amiloride-inhibitable inward current having the characteristics of ASIC-mediated currents. Incubation of TG neurons with either capsaicin or PCs produced a CPZ-sensitive increase in cyclic AMP and cytokine (IL-6) release. In summary, we provide unequivocal evidence demonstrating that negatively charged PCs could activate VR1 and other proton-gated receptors. These data suggest that pharmacological manipulation of such receptors could prevent the physiological actions of PMs.     

大气细颗粒物水溶成分对大鼠胸主动脉舒缩功能的影响

目的探讨大气细颗粒物(PM2.5,)水溶成分静脉染毒后1、6 h,对大鼠胸主动脉血管环收缩、舒张功能的影响.方法 雄性Wistar大鼠30只,分为空白对照组、1 h对照组、6 h对照组、染毒1 h组、染毒6 h组,每组6只.染毒组以PM2.5水溶成分(1 ml/kg)尾静脉注射1、6 h后,分别以25%乌拉坦腹腔注射(0.4 ml/100 g)麻醉后,迅速开胸取大鼠胸主动脉,制备血管环,置于张力换能器进行实验.1 h,6 h对照组以0.9%氯化钠注射液(1 ml/kg)尾静脉注射,处理同染毒组.结果 空白对照组、1 h对照组、6 h对照组三组间血管环舒缩反应差别无统计学意义.染毒1 h后,胸主动脉血管环对60 mmol/L KCi的收缩反应减弱,6 h后有升高趋势,但仍低于对照组.10-6mol/L去甲肾上腺素(NE)预收缩的血管环:乙酰胆碱(ACh)浓度在10-5moL/L、10-7moL/L水平,染毒后1 h舒张率降低.ACh浓度在10-5～10-7mol/L水平,染毒6 h组舒张率较染毒1 h组升高;硝普钠(SNP)浓度在10-5～10-9mol/L水平,染毒后1 h舒张率降低,在10-6mol/L、10-9mol/L水平,染毒后6 h组舒张率较染毒1 h组升高,在10-5～10-7moL/L水平,染毒6 h组舒张率仍低于对照组.结论 PM2.5水溶成分静脉染毒1 h后引起血管收缩抑制、舒张下降,6 h后该作用减弱.     

Determination of size fractions and concentrations of airborne particulate matter generated from construction and demolition waste processing facilities

Construction and Demolition (C&D) processing and recycling facilities accept waste materials that are generated during construction and demolition activities. The processing facility sorts, processes, and transfers the material to another operation. Active stationary particulate sampling devices were employed to quantify the particle sizes of interest. Results were compared to United States Environmental Protection Agency National Ambient Air Quality Standards (NAAQS) and United States Occupational Safety and Health Administration (OSHA) standards. Airborne particulate levels were found to be higher inside of buildings even when minimal activity is taking place. Interior road type seems to impact airborne particulate levels, and misting activities can significantly reduce the amount of airborne particulate matter exiting a building. The data indicate that C&D processing facilities may exceed current NAAQS at certain locations but do not exceed OSHA standards.     

太原市主要交通路口汽车尾气污染状况

目的了解太原市主要交通路口汽车尾气污染状况,为控制汽车尾气污染提供依据。方法选择太原市交通路口A和B作为监测点,2008年3—4月各自连续采样一周。采用质量法测定细颗粒物(PM2.5)浓度。索氏提取法提取PM2.5无机成分,采用原子荧光仪测定无机成分中砷、汞,采用原子吸收仪测定镍、镉、铬、铅、矾,采用盐酸萘乙二胺分光光度法测定NO_x,采用非色散红外吸收法测定CO。结果A路口空气中PM2.5日均浓度为1.604 mg/m~3,显著高于B路口(0.64 mg/m~3),差异有统计学意义(P<0.05)。A路口空气中镍、铅、汞、镉、铬5种元素的浓度均高于B路口,汞、铅浓度差异有统计学意义(P<0.05)。A路口空气镍浓度最高达0.842μg/m~3。A路口的CO和NO_x浓度分别为5.054、0.106 mg/m~3,显著高于B路口(0、0.063mg/m~3),差异有统计学意义(P<0.01)。结论太原市主要交通路口汽车尾气污染严重,特别是PM2.5、CO和镍。     

Genotoxic potential of Polycyclic Aromatic Hydrocarbons-coated onto airborne Particulate Matter (PM 2.5) in human lung epithelial A549 cells

To improve the knowledge of the underlying mechanisms of action involved in air pollution Particulate Matter (PM)-induced toxicity in human lungs, with a particular interest of the crucial role played by coated-organic chemicals, we were interested in the metabolic activation of Polycyclic Aromatic Hydrocarbons (PAH)-coated onto air pollution PM, and, thereafter, the formation of PAH-DNA adducts in a human lung epithelial cell model (A549 cell line). Cells were exposed to Dunkerque city's PM(2.5) at its Lethal Concentrations at 10% and 50% (i.e. LC(10)=23.72 microg/mL or 6.33 microg/cm2, and LC(50)=118.60 microg/mL or 31.63 microg/cm2), and the study of Cytochrome P450 (CYP) 1A1 gene expression (i.e. RT-PCR) and protein activity (i.e. EROD activity), and the formation of PAH-DNA adducts (i.e. 32P-postlabeling), were investigated after 24, 48, and/or 72 h. PAH, PolyChlorinated Dibenzo-p-Dioxins and -Furans (PCDD/F), Dioxin-Like PolyChlorinated Biphenyls (DLPCB), and PolyChlorinated Biphenyls (PCB)-coated onto collected PM were determined (i.e. GC/MS and HRGC/HRMS, respectively), Negative (i.e. TiO2 or desorbed PM, dPM; EqLC10=19.42 microg/mL or 5.18 microg/cm2, and EqLC50=97.13 microg/mL or 25.90 microg/cm2), and positive (i.e. benzo(a)pyrene; 1 microM) controls were included in the experimental design. Statistically significant increases of CYP1A1 gene expression and protein activity were observed in A549 cells, 24, 48 and 72 h after their exposure to dPM, suggesting thereby that the employed outgassing method was not efficient enough to remove total PAH. Both the CYP1A1 gene expression and EROD activity were highly induced 24, 48 and 72 h after cell exposure to PM. However, only very low levels of PAH-DNA adducts, also not reliably quantifiable, were reported 72 h after cell exposure to dPM, and, particularly, PM. The relatively low levels of PAH together with the presence of PCDD/F, DLPCB, and PCB-coated onto Dunkerque City's PM 2.5 could notably contribute to explain the borderline detection of PAH-DNA adducts in dPM and/or PM-exposed A549 cells. Hence, remaining very low doses of PAH in dPM or relatively low doses of PAH-coated onto PM were involved in enzymatic induction, a key feature in PAH-toxicity, but failed to show a clear genotoxicity in this in vitro study. We also concluded that, in the human lung epithelial cell model we used, and in the experimental conditions we chose, bulky-DNA adduct formation was apparently not a major factor involved in the Dunkerque City's PM 2.5-induced toxicity.     

Calcium dependent and independent cytokine synthesis by air pollution particle-exposed human bronchial epithelial cells

Exposure to ambient air pollution particles with a diameter of <10 microm (PM(10)) has been associated with increased cardiopulmonary morbidity and mortality. We have shown that human bronchial epithelial cells (HBECs) exposed to PM(10) produce pro-inflammatory mediators that contribute to a local and systemic inflammatory response. Changes in intracellular calcium concentrations ([Ca(2+)](i)) have been demonstrated to regulate several functions of the airway epithelium including the production of pro-inflammatory mediators. The aim of the present study was to determine the nature and mechanism of calcium responses induced by PM(10) in HBECs and its relationship to cytokine synthesis. METHODS: Primary HBECs were exposed to urban air pollution particles (EHC-93) and [Ca(2+)](i) responses were measured using the fluoroprobe (Fura-2). Cytokine levels were measured at mRNA and protein levels using real-time PCR and ELISA. RESULTS: PM(10) increased [Ca(2+)](i) in a dose-dependent manner. This calcium response was reduced by blocking the influx of calcium into cells (i.e. calcium-free medium, NiCl(2), LaCl(3)). PM(10) also decreased the activity of calcium pumps. PM(10) increased the production of IL-1beta, IL-8, GM-CSF and LIF. Preincubation with intracellular calcium chelator (BAPTA-AM) attenuated IL-1beta and IL-8 production, but not GM-CSF and LIF production. CONCLUSION: We conclude that exposure to PM(10) induces an increase in cytosolic calcium and cytokine production in bronchial epithelial cells. Our results also suggest that PM(10) induces the production of pro-inflammatory mediators via either intracellular calcium-dependent (IL-1beta, IL-8) or -independent (GM-CSF, LIF) pathways.