The increasing adoption of intelligent transportation system (ITS) data in smart-city initiatives worldwide has offered unprecedented opportunities for improving transportation air quality management. In this paper, we demonstrate the effective use of ITS and other traffic data to develop a link-level and hourly-based dynamic vehicle emission inventory. Our work takes advantage of the extensive ITS infrastructure deployed in Nanjing, China (6600 km2) that offers high-resolution, multi-source traffic data of the road network. Improved than conventional emission inventories, the ITS data empower the strength of revealing significantly temporal and spatial heterogeneity of traffic dynamics that pronouncedly impacts traffic emission patterns. Four urban districts account for only 4% of the area but approximately 30%–40% of vehicular emissions (e.g., CO2 and air pollutants). Owing to the detailed resolution of road network traffic, two types of emission hotspots are captured by the dynamic emission inventory: those in the urban area dominated by urban passenger traffic, and those along outlying highway corridors reflecting inter-city freight transportation (especially in terms of NOX). Fine-grained quantification of emissions reductions from traffic restriction scenarios is explored. ITS data-driven emission management systems coupled with atmospheric models offer the potential for dynamic air quality management in the future.

Fluoride is capable of inducing neurotoxicity, but its mechanisms remain elusive. This study aimed to explore the roles of endoplasmic reticulum (ER) stress and autophagy in sodium fluoride (NaF)-induced neurotoxicity, focusing on the regulating role of ER stress in autophagy. The in vivo results demonstrated that NaF exposure impaired the learning and memory capabilities of rats, and resulted in histological and ultrastructural abnormalities in rat hippocampus. Moreover, NaF exposure induced excessive ER stress and associated apoptosis, as manifested by elevated IRE1α, GRP78, cleaved caspase-12 and cleaved-caspase-3, as well as defective autophagy, as shown by increased Beclin1, LC3-II and p62 expression in hippocampus. Consistently, the in vitro results further verified the findings of in vivo study that NaF induced excessive ER stress and defective autophagy in SH-SY5Y cells. Notably, inhibition of autophagy in NaF-treated SH-SY5Y cells with Wortmannin or Chloroquine decreased, while induction of autophagy by Rapamycin increased the cell viability. These results were correlated well with the immunofluorescence observations, thus confirming the pivotal role of autophagic flux dysfunction in NaF-induced cell death. Importantly, mitigation of ER stress by 4-phenylbutyrate in NaF-treated SH-SY5Y cells inhibited the expressions of autophagy markers, and decreased cell apoptosis. Taken together, these data suggest that neuronal death resulted from excessive ER stress and autophagic flux dysfunction contributes to fluoride-elicited neurotoxicity. Moreover, the autophagic flux dysfunction was mediated by excessive ER stress, which provided novel insight into a better understanding of fluoride-induced neurotoxicity.

Erythromycin is an antibiotic employed in the treatment of infections caused by Gram positive microorganisms and the increasing use has made it a contaminant of emerging concern in aqueous ecosystems. Cerium oxide nanoparticles (CeO₂ NPs), which are known to have catalytic and antioxidant properties, have also become contaminants of emerging concern. Due to the high reactivity of CeO₂ NPs, they can interact with erythromycin magnifying their effects or on the other hand, considering the redox potential of CeO₂ NPs, it can alleviate the toxicity of erythromycin. The present study was carried out to assess the toxicity of both single compounds as well as mixed on Chlamydomonas reinhardtii and Phaeodactylum tricornutum (freshwater and marine microalgae respectively) employed as target species in ecotoxicological tests. Mechanisms of oxidative damage and those harmful to the photosynthetic apparatus were studied in order to know the toxic mechanisms of erythromycin and the joint effects with CeO₂ NPs. Results showed that erythromycin inhibited the microalgae population growth and effective quantum yield of PSII (E.Q.Y.) in both microalgae. However, the freshwater microalgae Chlamydomonas reinhardtii was more sensitive than the marine diatom Phaeodactylum tricornutum. Responses related to the photosynthetic apparatus such as E.Q.Y. was affected by the exposure to erythromycin of both microalgae, as chloroplasts are target organelle for this antibiotic.Mixed experiments (CeO₂ NPs + erythromycin) showed the protective role of CeO₂ NPs in both microalgae preventing erythromycin toxicity in toxicological responses such as the growth of the microalgae population and E.Q.Y.

Global burden of disease estimates reveal that people in Nigeria are living shorter lifespan than the regional or global average life expectancy. Ambient air pollution is a top risk factor responsible for the reduced longevity. But, the magnitude of the loss or the gains in longevity accruing from the pollution reductions, which are capable of driving mitigation interventions in Nigeria, remain unknown. Thus, we estimate the loss, and the gains in longevity resulting from ambient PM2.5 pollution reductions at the local sub-national level using life table approach. Surface average PM2.5 concentration datasets covering Nigeria with spatial resolution of ∼1 km were obtained from the global gridded concentration fields, and combined with ∼1 km gridded population of the world (GPWv4), and global administrative unit layers (GAUL) for territorial boundaries classification. We estimate the loss or gains in longevity using population-weighted average pollution level and baseline mortality data for cardiopulmonary disease and lung cancer in adults ≥25 years and for respiratory infection in children under 5. As at 2015, there are six “highly polluted”, thirty “polluted” and one “moderately polluted” States in Nigeria. People residing in these States lose ∼3.8–4.0, 3.0–3.6 and 2.7 years of life expectancy, respectively, due to the pollution exposure. But, assuming interventions achieve global air quality guideline of 10 μg/m3, longevity would increase by 2.6–2.9, 1.9–2.5 and 1.6 years for people in the State-categories, respectively. The longevity gains are indeed high, but to achieve them, mitigation interventions should target emission sources having the highest population exposures.

Obesity and exposure to particular matter (PM) have become two leading global threats to public health. However, the exact mechanisms and tissue-specificity of their health effects are largely unknown. Here we investigate whether a metabolic challenge (early nutritional obesity) synergistically interacts with an environmental challenge (PM exposure) to alter genes representing key response pathways, in a tissue-specific manner. Mice subjected to 7 weeks obesogenic nutrition were exposed every other day during the final week and a half to aqueous extracts of PM collected in the city of London (UK). The expression of 61 selected genes representing key response pathways were investigated in lung, liver, white and brown adipose tissues. Principal component analysis (PCA) revealed distinct patterns of expression changes between the 4 tissues, particularly in the lungs and the liver. Surprisingly, the lung responded to the nutrition challenge. The response of these organs to the PM challenge displayed opposite patterns for some key genes, in particular, those related to the Nrf2 pathway. While the contribution to the variance in gene expression changes in mice exposed to the combined challenge were largely similar among the tissues in PCA1, PCA2 exhibited predominant contribution of inflammatory and oxidative stress responses to the variance in the lungs, and a greater contribution of autophagy genes and MAP kinases in adipose tissues. Possible involvement of alterations in DNA methylation was demonstrated by cell-type-specific responses to a methylation inhibitor. Correspondingly, the DNA methyltransferase Dnmt3a2 increased in the lungs but decreased in the liver, demonstrating potential tissue-differential synergism between nutritional and PM exposure. The results suggest that urban PM, containing dissolved metals, interacts with obesogenic nutrition to regulate diverse response pathways including inflammation and oxidative stress, in a tissue-specific manner. Tissue-differential effects on DNA methylation may underlie tissue-specific responses to key stress-response genes such as catalase and Nrf2.

The impact of ambient air pollution on pregnant women is a concern in China. However, little is known about the association between air pollution and preeclampsia and the potential modifying effects of meteorological conditions have not been assessed. This study aimed to assess the effects of prenatal exposure to air pollution on preeclampsia, and to explore whether temperature and humidity modify the effects. We performed a retrospective cohort study based on 1.21 million singleton births from the birth registration system in Shenzhen, China, between 2005 and 2012. Daily average measurements of particulate matter <10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), air temperature (T), and dew point (Td) were collected. Logistic regression models were performed to estimate associations between air pollution and preeclampsia during the first and second trimesters, and during the entire pregnancy. In each time window, we observed a positive gradient of increasing preeclampsia risk with increasing quartiles of PM10 and SO2 exposure. When stratified by T and Td in three categories (<5th, 5th −95th, and >95th percentile), we found a significant interaction between PM10 and Td on preeclampsia; the adverse effects of PM10 increased with Td. During the entire pregnancy, there was a null association between PM10 and preeclampsia under Td < 5th percentile. Preeclampsia risk increased by 23% (95% CI: 19–26%) when 5th < Td < 95th percentile, and by 34% (16–55%) when Td > 95th percentile. We also found that air pollution effects on preeclampsia in autumn/winter seasons were stronger than those in the spring/summer. This is the first study to address modifying effects of meteorological factors on the association between air pollution and preeclampsia. Findings indicate that prenatal exposure to PM10 and SO2 increase preeclampsia risk in Shenzhen, China, and the effects could be modified by humidity. Pregnant women should limit air pollution exposure, particularly during humid periods.

The aim of this study was to determine the effect of biochar aging on the content of polycyclic aromatic hydrocarbons (PAHs) (the total content – Ctot, and the freely dissolved – Cfree) in biochar and its ecotoxicity. Two biochars (BCS and BCM) with varying properties were aged for 420 days at different temperatures (−20 °C, 4 °C, 20 °C, 70 °C), at a variable temperature (−20/20 °C), in the presence of nutrients, and in the presence of inoculum and nutrients. After the aging process, Ctot and Cfree PAHs were determined in samples obtained and an ecotoxicological analysis was performed, which involved tests with bacteria (Vibrio fischeri), invertebrates (Folsomia candida) and plants (Lepidium sativum). Aging significantly affected all the parameters tested. The range of changes in the studied parameters depended on the type of biochar and ageing conditions. In the case of most of the aging methods, PAH content (Ctot, Cfree) and toxicity were found to decrease. Aging in the presence of microorganisms and nutrients and in the presence of nutrients alone caused the greatest reduction in Ctot PAH content (a reduction from 30 to 100% relative to non-aged biochar), Cfree PAH content (a reduction from 12 to 100%), root growth inhibition (a reduction from 73 to 90%), and luminescence inhibition (a reduction from 24 to 100%). In the case of Cfree PAHs and toxicity to F. candida, some aging methods caused their increase. The study also found a significant relationship between the changes in Ctot PAH content during aging and inhibition of root growth (BCS, BCM) and inhibition of V. fischerii luminescence (BCM). In no case was a significant correlation (P ≥ 0.05) between Cfree PAHs and the investigated toxicity parameters found.

Following the recent progress in magnetic nanotechnology, concern over the optimal benefits and potential risks of iron oxide nanoparticles (Fe NPs), has increased. Hence, to minimize the negative impacts of inorganic Fe NPs, we report the phyco-synthesis and characterization of superparamagnetic Fe3O4 NPs via reduction of ferric/ferrous chloride solution (2:1 M ratio; 88 °C) with green macroalga, Ulva flexuosa (wulfen) J.Agardh aqueous extract. The biogenic process is clean, eco-friendly, rapid, and facile to handle. These green fabricated magnetite NPs are characterized by Fourier transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), transmission electron microscopy (TEM), field emission scanning electron microscopy (FESEM), thermogravimetric analysis (TGA), particle size analysers (PSA), zeta potential (ZP) measurement, and vibrating sample magnetometry (VSM) techniques. The results confirmed that the cubo-spherical, polydisperse of biosynthesized Fe3O4 NPs with an average diameter of 12.3 nm was formed. The antagonistic effects of algal extract, chemo-route and U. flexuosa-derived Fe3O4 MgNPs on selective human pathogenic microbes (i.e. n = 11) resulted in strong antibacterial and moderate antifungal activity. The comparative toxic and reproductive effects of the chemo- and bio-routes of Fe3O4-MgNPs against rotifer B. rotundiformis exhibited low acute toxicity with a lower inducing effect of biogenic nano-magnetite on reduction rotifer reproductive rate than its chemogenic counterpart. In view of the nanoecotoxicity, though the current study covered a wide range of exposure concentrations (10-500 mg/L) of organic and inorganic nano sizes of Fe3O4 in brackish water rotifer, a biotoxicity assay at higher dosage or a comprehensive risk assessment in different aqua-organisms is recommended.

Rapid development of industrial production has stimulated the growth of consumption of raw and auxiliary materials including organic paints, among which volatile organic compounds (VOCs) are proved harmful to the population who inhale the polluted air based on epidemiologic studies. Therefore, new types of environment-friendly paints were developed to replace solvent-based paints (SBPs). Nevertheless, new types of paints containing VOCs failed to replace SBPs entirely due to certain disadvantages. Hence, five kinds of paints were employed in simulation experiments to assess the health risk of primary receptor including three kinds of water-based paints (WBPs) and two kinds of SBPs. Conclusions showed that mean TVOC concentration in breathing zone of primary receptor ranged from 9.5 to 13.6 mg/m³ and 3.4 × 10³ to 1.4 × 10⁴ mg/m³ for WBPs and SBPs, respectively. Assessments of non-cancer risk concluded that nearly one third quantified compounds exceeded corresponding thresholds for WBPs, and the maximum risk value was 101.33; for SBPs, the maximum risk value reached 50760.20, and twenty-two compounds exceeded the reference limits. The calculation of cancer risk values showed that seventeen compounds were higher than acceptable limit amongst which 1,2-dibromoethane had maximum values of 1.27 × 10⁻² to 3.24 × 10⁻² for WBPs; for SBPs, all quantified compounds exceeded the acceptable limit, and 82.61% VOCs were distributed in a scope larger than 1 × 10⁻³. Additionally, a removal efficiency of 60% was considered for primary receptor with personal protective equipment, and subsequent results confirmed its inability of lowering the risk resulted from hazardous VOCs. The calculated potential health risk could be applied to estimate the total health risk for both primary and secondary receptor based on consumed materials. The finding suggested that WBPs could improve VOCs exposure condition and reduce the direct and potential health risk significantly for primary receptor, although they might dissatisfy acceptable limit.

Several studies have indicated the presence of contaminants in Alpine aquatic ecosystems. Even if measured concentrations are far below those that cause acute effects, continuous exposure to sub-lethal concentrations may have detrimental effects on the aquatic species present in these remote environments. This may lead to a cascade of indirect effects at higher levels of the ecological hierarchy (i.e., the community). To improve the determination of ecologically relevant risk endpoints, behavioural alterations in organisms due to pollutants are increasingly studied in ecotoxicology. In fact, behaviour links physiological function with ecological processes, and can be very sensitive to environmental stimuli and chemical exposure. This is the first study on behavioural alteration in a wild population of an Alpine species. In the present study, a video tracking system was standardized and subsequently used to identify contaminant-induced behavioural alterations in Diamesa zernyi larvae (Diptera, Chironomidae). Diamesa zernyi larvae, collected in an Italian Alpine stream (Rio Presena, Trentino Region), were acclimated for 24 h and successively exposed to several aquatic contaminants (pesticides: chlorpyrifos, metolachlor, boscalid, captan; pharmaceuticals: ibuprofen, furosemide, trimethoprim) at concentrations corresponding to their Lowest Observed Effect Concentration (LOEC). After 24, 48, 72, and 96 h of exposure, changes in the distance moved, the average speed, and the frequency of body bends were taken to reflect contaminant- and time-dependent effects on larval behaviour. In general, metolachlor, captan, and trimethoprim tended to reduce all the endpoints under consideration, whereas chlorpyrifos, boscalid, ibuprofen, and furosemide seemed to increase the distances moved by the larvae. This could be related to the different mechanisms of action of the investigated chemicals. Independently of the contaminant, after 72 h a general slowing down of all the behavioural activities occurred. Finally, we propose a behavioural stress indicator to compare the overall behavioural effects induced by the various contaminants.