Data on particulate matter of diameter <2.5 μm (PM2.5) in the city of Chongqing were first announced in 2013. We wished to assess the effects of pollutants on asthmatic children in Chongqing, China. Daily numbers of hospital visits because of asthma attacks in children aged 0–18 years in 2013 were collected from the Children's Hospital of Chongqing Medical University. Data on pollutants were accessed from the nine air quality-monitoring stations in Chongqing. A time-stratified case–crossover design was applied and conditional logistic regression was undertaken to analyze the data. We found that short-term exposure to PM10, PM2.5, sodium dioxide, nitrogen and carbon monoxide could trigger hospital visits for asthma in children. Nitrogen dioxide had an important role, whereas ozone had no effect.

The polycyclic aromatic hydrocarbons (PAHs) located on the epidermal tissues showed distinctive toxic effects to root, while the retention and distribution of PAHs on mangrove seedlings poorly understood. Our results confirmed that the partition coefficients (Kf) of the PAHs retained on the epidermal tissue of mangrove roots, such as Kandelia obovata, Avicennia marina and Aegiceras corniculatum, were much higher than the Poaceae plants roots, for example wheat and maize (Wild et al., 2005). Moreover, to the parent and alkyl PAHs, a well negative correlation was observed between the surface polarity of these three species of mangrove root and the Kf values (p < 0.05). To the N/O/S containing PAHs, these relationships were not obviously due to existing of the π-π, n-π interactions and hydrogen bonding between the N/O/S-containing PAHs and epidermal tissues. The PAHs retained on these three species of mangrove root epidermal tissues formed larger clusters than that of on Poaceae plants, such as wheat and maize (Wild et al., 2005) due to the limitation of the suberization of the root exodermis and endodermis. After exposure of 30 d, rhizo- and endophytic bacteria degraded parts of the N/O/S-containing PAHs to medium-lifetime fluorescence substances. To our knowledge, this is the first time to assess the retention of PAHs on the epidermal tissue of mangrove root, which will improve our understanding of the root uptake PAHs process.

Chronic Obstructive Pulmonary Disease (COPD) is associated with T lymphocytes subset (Th1/Th2, Th17/Treg) imbalance. Notch signaling pathway plays a key role in the development of the adaptive immunity. The immune disorder induced by fine particulate matter (PM2.5) is related to COPD. The aim of this study was to investigate the mechanism by which PM2.5 influences the Notch signaling pathway leading to worsening immune disorder and accelerating COPD development. A COPD mouse model was established by cigarette smoke exposure. PM2.5 exposure was performed by aerosol inhalation. γ-secretase inhibitor (GSI) was given using intraperitoneal injection. Splenic T lymphocytes were purified using a density gradient centrifugation method. CD4+ T lymphocyte subsets (Th1/Th2, Th17/Treg) were detected using flow cytometry. mRNA and proteins of Notch1/2/3/4, Hes1/5, and Hey1 were detected using RT-PCR and Western blot. Serum INF-γ, IL-4, IL-17 and IL-10 concentrations were measured using ELISA. The results showed that in COPD mice Th1% and Th17%, Th1/Th2 and Th17/Treg were increased, and the levels of mRNA and protein in Notch1/2/3/4, Hes1/5, and Hey1 and serum INF-γ and IL-17 concentrations were significantly increased, and Th2%, Treg%, and serum IL-4 and IL-10 concentrations were significantly decreased. COPD Mice have Th1- and Th17-mediated immune disorder, and the Notch signaling pathway is in an overactivated state. PM2.5 promotes the overactivation of the Notch signaling pathway and aggravates the immune disorder of COPD. GSI can partially inhibit the activation of the Notch signaling pathway and alleviate the immune disorder under basal state and the immune disorder of COPD caused by PM2.5. This result suggests that PM2.5 is involved in the immune disorder of mice with COPD by affecting the Notch signaling pathway and that PM2.5 aggravates COPD.

Laccase is a widely present extracellular phenoloxidase excreted by fungi, bacteria, and high plants. It is able to catalyze one-electron oxidation of phenolic compounds into radical intermediates that can subsequently couple to each other via covalent bonds. These reactions are believed to play an important role in humification process and the transformation of contaminants containing phenolic functionalities in the environment. In this study, we investigated the kinetics of triclosan transformation catalyzed by laccase. It was found that the rate of triclosan oxidation was first order to the concentrations of both substrate and enzyme. Humic acid (HA) could inhibit the reaction by quenching the radical intermediate of triclosan generated by laccase oxidation. Such inhibition was more significant in the presence of divalent metal cations. This is because that binding to metal ions neutralized the negative charge of HA molecules, thus making them more accessible to laccase molecule that is also negatively charged. Therefore, it has greater chance to quench the radical intermediate that is very unstable and can only diffuse a limited distance after being released from the enzyme catalytic center. Based on these understandings, a reaction model was developed by integration of metal-HA binding equilibriums and kinetic equations. This model precisely predicted the transformation rate of triclosan in the presence of HA and divalent metal ions including Ca2+, Mg2+, Cd2+, Co2+, Mn2+, Ba2+, and Zn2+. Overall, this work reveals important insights into laccase catalyzed oxidative coupling process.

White rot fungi have been proved to be a promising option for the removal of heavy metals, understanding their toxic response to heavy metals is conducive to developing and popularizing fungi-based remediation technologies so as to lessen the hazard of heavy metals. In this study, Cr(VI)-induced oxidative stress and apoptosis in Pycnoporus sanguineus, a species of white rot fungi were investigated. The results suggested that high level of Cr(VI) promoted the formation of ROS, including H2O2, O2•− and ·OH. With the increment of Cr(VI) concentration, the SOD and CAT activity along with GSH content increased within the first 24 h, but decreased afterwards, companied with a significant enhancement of MDA content. Cr(VI)-induced oxidative damage further caused and aggravated apoptosis in Pycnoporus sanguineus, especially at Cr(VI) concentrations above 20 mg/L. Cr(VI)-induced apoptosis was involved with mitochondrial dysfunction including mitochondrial depolarization, the enhancement of mitochondrial permeability and release of cytochrome c. The early and late apoptosis hallmarks, such as metacaspase activation, phosphatidylserine (PS) externalization, DNA fragmentation and the nuclear condensation and fragmentation were observed. Moreover, we also found disturbances of ion homeostasis, which was featured by K+ effluxes and overload of cytoplasmic and mitochondrial Ca2+.Based on these results, we suggest that Cr(VI) induced oxidative stress and apoptosis in white rot fungi, Pycnoporus sanguineus.

The Mesel gold mine in the Ratatotok Sub-district operated between 1996 and 2004 with tailings disposal via an engineered submarine tailings placement (STP) into Buyat Bay. This operation raised concerns of increased levels of arsenic (As) and mercury (Hg) associated disease in the local communities from consumption of seafood contaminated with anthropogenic As and Hg. This report uses the dietary exposure to As and Hg, from local fishermen and market-purchased Codex “as consumed” and environmental fish results from the pre-mining baseline (1990–1995), the mine operational (1996–2004) and post-closure monitoring (2007–2016) to examine the potential health effects. The Ratatotok Sub-district consumers total As average daily intake from fish was between 152 and 317 μg/day (adults) and 58 and 105 μg/day (infants). The average daily intake of inorganic arsenic (Asi) from the dietary staples fish and rice and drinking water consumption was 77 μg/day (adults) and 35 μg/day (infants) at Buyat Pantai and 39 μg/day (adults) and 19 μg/day (infants) at Ratatotok township. Fish consumption contributed 8.2% (adults) and 6.5% (infants) to total daily Asi intake. Average Hg intake from fish consumption, exceeded the FAO WHO PTWI for methylmercury (MeHg) for all age and gender groups at Buyat Pantai 4.6 μg/kg bw/wk (adults) and 7.3 μg/kg bw/wk (infants) and for the infants at Buyat village and Ratatotok township (2.5 and 2.8 μg/kg bw/wk respectively). The Manado City consumers had average intakes below the MeHg PTWI. The Hg exceedances resulted from the high fish consumption in coastal communities and not elevated levels of Hg in fish. Hg exposure levels from the pre-mining baseline, Mesel STP operation and post-closure monitoring, confirmed that exceedances were unrelated to the tailings deposited into Buyat Bay.

Understanding the sources, occurrence and sinks of perfluoroalkyl and polyfluoroalkyl substances (PFASs) in the urban water cycle is important to protect and utilize local water resources. Concentrations of 22 target PFASs and general water quality parameters were determined monthly for a year in filtered water samples from five tributaries and three sampling stations of an urban water body. Of the 22 target PFASs, 17 PFASs were detected with a frequency >93% including PFCAs: C4-C12 perfluoroalkyl carboxylates, C4, C6, C8, and C10 perfluoroalkane sulfonates, perfluorooctane sulfonamides and perfluorooctane sulfonamide substances (FOSAMs), C10 perfluoroalkyl phosphonic acid (C10 PFPA), 6:2 fluorotelomer sulfonic acid (6:2 FTSA) and C8/C8 perfluoroalkyl phosphinic acid (C8/C8-PFPIA). The most abundant PFASs in water were PFBS (1.4–55 ng/L), PFBA (1.0–23 ng/L), PFOS (1.5–24 ng/L) and PFOA (2.0–21 ng/L). In the tributaries, PFNA concentrations ranged from 1.2 to 87.1 ng/L except in the May 2013 samples of two tributaries, which reached 520 and 260 ng/L. Total PFAS concentrations in the sediment samples ranged from 1.6 to 15 ng/g d.w. with EtFOSAA, PFDoA, PFOS and PFDA being the dominant species. Based on water and sediment data, two types of sources were inferred: one-time or intermittent point sources and continuous non-point sources. FOSAMs and PFOS released continually from non-point sources, C8/C8 PFPIA, PFDoA and PFUnA was released from point sources. The highly water soluble short-chain PFASs including PFBA, PFPeA and PFBS remained predominantly in the water column. The factors governing solution phase concentrations appear to be compound hydrophobicity and sorption to suspended particles. Correlation of the dissolved phase concentrations with precipitation data suggested stormwater was a significant source of PFBA, PFBS, PFUnA and PFDoA. Negative correlations with precipitation indicated sources feeding FOSAA and FOSA directly into the tributaries.

Invertebrate-mediated leaf litter decomposition is frequently used to assess stress-related implications in stream ecosystem integrity. In situ measures such as the mass loss from leaf bags or the feeding of caged invertebrates deployed for days or weeks may, however, fail to detect transient effects due to recovery or compensatory mechanisms. We assessed the relevance of transient effects using the peak exposure towards an insecticide (i.e., etofenprox) as a model scenario at three levels of complexity. These were 1) the assessment of the decomposition realised by invertebrate communities in stream mesocosms over 21 days via leaf bags, 2) 7-days lasting in situ bioassays quantifying the leaf consumption of Gammarus fossarum, and 3) a laboratory experiment determining the daily feeding rate of the same species over 7 days. Etofenprox did not trigger a significantly altered decomposition by invertebrate communities during the leaf bag assay, while in situ bioassays detected a significant reduction in gammarids’ feeding rate at the highest tested concentration. The laboratory bioassay suggests that observed mismatches might be explained by recovery and post-exposure compensation. As leaf-shredding invertebrates are likely in a vulnerable state following transient effects, biomonitoring for implications of peak exposures and other pulsed stress events must happen at an adequate temporal resolution.

Recently, portable monitors have been increasingly used to quantify air pollutant concentrations at high spatiotemporal resolution. A sampling campaign was conducted to measure the fine particulate matter (PM2.5) and carbon monoxide (CO) exposure concentrations in transport microenvironments (TMEs) in Hong Kong in January and June 2015 using TSI DustTrak and Q-Trak portable monitors. The objectives were to: (1) calibrate DustTrak and Q-Trak; (2) evaluate variability between seasons and microenvironments; (3) estimate indoor/outdoor relationships; and (4) determine minimum sample size. Calibration equations, obtained through side-by-side measurement against stationary reference methods in winter and summer, were applied to correct the measured PM2.5 data set. In general, PM2.5 concentrations in all TMEs were significantly higher in winter than in summer. The mean PM2.5 concentration in winter was lower for underground sections of the Mass Transit Railway (MTR) metro system (31 μg/m3) than for other TMEs, whereas in summer TMEs had mean PM2.5 concentrations in the range of 10–15 μg/m3, with above-ground MTR train as an exception, at 23 μg/m3. PM2.5 concentrations measured in TMEs were strongly correlated with nearby air quality monitoring stations (AQMSs) measurements in winter, but in summer there was little correlation. The minimum sample size estimates varied more among TMEs in summer versus winter because of the differences in PM2.5 concentration distributions related to changes in ambient PM2.5 concentrations and ventilation practices. This study provides a feasible protocol on the calibration and application of portable monitors in TME air quality measurement and develops a method for estimating minimum sample size.

Transport of coal by train through residential neighborhoods in Metro Vancouver, British Columbia, Canada may increase the possibility of exposure to particulate matter at different size ranges, with concomitant potential negative health impacts. This pilot study identifies and quantifies train impacts on particulate matter (PM) concentrations at a single location. Field work was conducted during August and September 2014, with the attributes of a subset of passing trains confirmed visually, and the majority of passages identified with audio data. In addition to fixed ground based monitors at distances 15 and 50 m from the train tracks, an horizontally pointing mini-micropulse lidar system was deployed on three days to make backscatter and depolarization measurements in an attempt to identify the zone of influence, and sources, of train-generated PM. Ancillary wind and dust fall data were also utilized. Trains carrying coal are associated with a 5.3 (54%), 4.1 (33%), and 2.6 (17%) μgm−3 average increase in concentration over a 14 min period compared to the average concentrations over the 10 min prior to and after a train passage (“control” or “background” conditions), for PM3, PM10, and PM20, respectively. In addition, for PM10 and PM20, concentrations during train passages of non-coal-carrying trains were not found to be significantly different from PM concentrations during control conditions. Presence of coal dust particles at the site was confirmed by dust fall measurements. Although enhancements of PM concentrations during 14 min train passages were generally modest, passing coal trains occasionally enhanced concentrations at 50 m from the tracks by ∼100 μgm-3. Results showed that not every train passage increased PM concentrations, and the effect appears to be highly dependent on wind direction, local meteorology and load related factors. LiDAR imagery suggests that re-mobilization of track-side PM by train-induced turbulence may be a significant contributor to coarse particle enhancements.