Passive air sampling was conducted in Toronto and the Greater Toronto Area from 2016 to 2017 for 6 periods, in order to investigate ambient levels of polycyclic aromatic compounds (PACs) associated with different source types. The selected sampling sites (n = 8) cover geographical areas with varying source emissions including background, traffic, urban, industrial and residential sites. Passive air samples were analyzed for PACs which include PAHs, alkylated PAHs (alk-PAHs), dibenzothiophene and alkylated dibenzothiophenes (DBTs) and results for PAHs were used to calculate inhalation cancer risks using different approaches. The samples were also characterized for PAH derivatives including nitrated PAHs (NPAHs) and oxygenated PAHs (OPAHs). Concentrations of Σalk-PAHs and DBTs, which are known to be enriched in fossil fuels, as well as ΣNPAHs, were highest at a traffic site (MECP) located adjacent to the 18-lane Highway 401 that runs across Toronto. Except for an industrial site (HH/BU), PAC compositions were similar across the sampling sites with Σalk-PAHs being the most abundant class of PACs suggesting traffic emission was a major contributor to PACs in the atmosphere of Toronto. The industrial site exhibited a distinct chemical composition with ΣPAHs dominating over Σalk-PAHs and with elevated levels of fluoranthene, 9-nitroanthracene, and 9,10-anthraquinone, which likely reflects emissions from nearby industrial sources. MECP and HH/BU exhibited higher lifetime excess inhalation cancer risks indicating an association with traffic and industrial sources. The importance of the traffic sector as a source of PACs to ambient air is further supported by strong correlations of the ΣPAHs, Σalk-PAHs, DBTs, and ΣOPAHs with NOx. This study highlights the importance of traffic as an emission source of PACs to urban air and the relevance of PAC classes other than just unsubstituted PAHs that are important but currently not included in air quality guidelines or for assessing inhalation cancer risks.

Peroxyacetyl nitrate (PAN) is an important reservoir of atmospheric nitrogen, modulating reactive nitrogen cycle and ozone (O3) formation. To understand the origins of PAN, a field measurement was conducted at Tung Chung site (TC) in suburban Hong Kong from October to November 2016. The average level of PAN was 0.63 ± 0.05 ppbv, with a maximum of 7.30 ppbv. Higher PAN/O3 ratio (0.043–0.058) was captured on episodes, i.e. when hourly maximum O3 exceeded 80 ppbv, than on non-episodes (0.01), since O3 production was less efficient than PAN when there was an elevation of precursors (i.e. volatile organic compounds (VOCs) and nitrogen oxide (NOx)). Model simulations revealed that oxidations of acetaldehyde (65.3 ± 2.3%), methylglyoxal (MGLY, 12.7 ± 1.2%) and other oxygenated VOCs (OVOCs) (8.0 ± 0.6%), and radical cycling (12.2 ± 0.8%) were the major production pathways of peroxyacetyl (PA) radical, while local PAN formation was controlled by both VOCs and nitrogen dioxide (NO2). Among all VOC species, carbonyls made the highest contribution (59%) to PAN formation, followed by aromatics (26%) and biogenic VOCs (BVOCs) (10%) through direct oxidation/decomposition. Besides, active VOCs (i.e. carbonyls, aromatics, BVOCs and alkenes/alkynes) could stimulate hydroxyl (OH) production, thus indirectly facilitating the PAN formation. Apart from primary emissions, carbonyls were also generated from oxidation of first-generation precursors, i.e., hydrocarbons, of which xylenes contributed the most to PAN production. Furthermore, PAN formation suppressed local O3 formation at a rate of 2.84 ppbv/ppbv, when NO2, OH and hydroperoxy (HO2) levels decreased and nitrogen monoxide (NO) value enhanced. Namely, O3 was reduced by 2.84 ppbv per ppbv PAN formation. Net O3 production rate was weakened (∼36%) due to PAN photochemistry, so as each individual production and loss pathway. The findings advanced our knowledge of atmospheric PAN and its impact on O3 production.

Thiocyanate (SCN⁻)-based autotrophic denitrification (AD) has recently been demonstrated as a promising technology that could be integrated with anaerobic ammonium oxidation (Anammox) to achieve simultaneous removal of nitrogen and SCN⁻. However, there is still a lack of a complete SCN⁻-based AD model, and the potential microbial competition/synergy between AD bacteria and Anammox bacteria under different operating conditions remains unknown, which significantly hinders the possible application of coupling SCN⁻-based AD with Anammox. To this end, a complete SCN⁻-based AD model was firstly developed and reliably calibrated/validated using experimental datasets. The obtained SCN⁻-based AD model was then integrated with the well-established Anammox model and satisfactorily verified with experimental data from a system coupling AD with Anammox. The integrated model was lastly applied to investigate the impacts of influent NH₄⁺-N/NO₂⁻-N ratio and SCN⁻ concentration on the steady-state microbial composition as well as the removal of nitrogen and SCN⁻. The results showed that the NH₄⁺-N/NO₂⁻-N ratio in the presence of a certain SCN⁻ level should be controlled at a proper value so that the maximum synergy between AD bacteria and Anammox bacteria could be achieved while their competition for NO₂⁻ would be minimized. For the simultaneous maximum removal (>95%) of nitrogen and SCN⁻, there existed a negative relationship between the influent SCN⁻ concentration and the optimal NH₄⁺-N/NO₂⁻-N ratio needed.

In this study, data collected from an urban air quality monitoring network are being used for the purpose of evaluating various methodologies used for spatial interpolation in the context of proposing an effective yet simple to apply scheme for PM spatial point estimations. The examined methods are the Inverse Distance Weighting, two linear regression models, the Multiple Linear Regression and the Linear Mixed Model, along with a Feed Forward Neural Network (FFNN) model. These schemes utilize daily PM₁₀ and PM₂.₅ concentrations collected from five and three air quality monitoring sites respectively. In order to obtain the resulted estimations, the leave-one-out cross-validation methodology is used for all methods. The evaluation of their predictive ability is performed by using a combination of difference and correlation statistical measures, scatter plots and statistical tests. The results indicate the usefulness of FFNNs as they are found to be statistically significantly superior for modelling the particulate matter spatial variability. The model performance statistics show that in most cases the error values are considerably lower for the FFNN model. Additionally, the rank and Wilcoxon rank tests reveal that the null hypothesis for equal predictive accuracy is rejected for the majority of monitoring sites and schemes (values lower than the critical t-value). According to the comparison results, the FFNN model is selected for forecasting air quality limit exceedances set by the European Union and World Health Organization air quality standards. For two monitoring sites in which the largest number of exceedances occurred, the probability of detection is high while the probability of false detection is very low, further establishing the neural networks’ predictive ability.

Black carbon (BC) can combine with organic matter and form secondary pollutants known as aged BC. BC and aged BC can cause respiratory system inflammation and induce lesions at relevant sites, but the underlying mechanism has remained unknown. To gain insight into the potential mechanisms, we focused on macrophages and transforming growth factor β-activated kinase 1 (TAK1) which are a crucial factor in inflammation. Our research aims to determine the role of TAK1 in macrophages in pulmonary inflammation induced by particulate matter. In this study, BC and 1,4-naphthoquinone were mixed to model aged BC (1,4NQ-BC) in atmosphere. BC induced mice lung inflammation model, lung macrophage knock-down TAK1 animal model and primary macrophage knock-down TAK1 model were used to explore whether TAK1 in macrophage is a critical role in the process of inflammation. The results showed that the expressions of inflammatory cytokines (IL-1β, IL-6, IL-33) mRNA were significantly increased and the phosphorylation of MAPK and NF-κB signaling pathway related proteins were enhanced in RAW 264.7 cell lines. In vivo studies revealed that the indicators of pulmonary inflammation (pathology, inflammatory cell numbers) and related cytokines (IL-1β, IL-6, IL-33) mRNA expressions in CD11c-Map3k7⁻/⁻ animals were significantly lower than wild-type animals after mice were instilled particles. In mice primary macrophages, the expressions of IL-6, IL-33 mRNA were inhibited after TAK1 gene was knock-down. These results unequivocally demonstrated that TAK1 plays a crucial role in BC induced lung inflammation in mice, and we can infer that BC and 1,4NQ-BC cause these inflammatory responses by stimulating pulmonary macrophages.

Crude oil and its constituents can have adverse effects on ecological and human health when released into the environment. The Canadian Council of Ministers of the Environment (CCME) has developed remedial guidelines and a risk assessment framework for both ecological and human exposure to PHC. One of the assumptions used in the derivation of these guidelines is that plants are unable to take up PHC from contaminated soil and therefore subsequent exposure at higher trophic levels is not a concern. However, various studies suggest that plants are indeed able to take up PHC into their tissues. Consumption of plants is a potential exposure pathway in both ecological (e.g., herbivorous and omnivorous birds, and mammals) and human health risk assessments. If plants can uptake PHC, then the current approach for risk assessment of PHC may underestimate exposures to ecological and human receptors. The present review aims to assess whether or not plants are capable of PHC uptake and accumulation. Twenty-one articles were deemed relevant to the study objective and form the basis of this review. Of the 21 primary research articles, 19 reported detectable PHC and/or its constituents in plant tissues. All but five of the 21 articles were published after the publication of the CCME Canada-Wide Standards. Overall, the present literature review provides some evidence of uptake of PHC and its constituents into plant tissues. Various plant species, including some edible plants, were shown to take up PHC from contaminated soil and aqueous media in both laboratory and field studies. Based on the findings of this review, it is recommended that the soil-plant-wildlife/human pathway should be considered in risk assessments to avoid underestimating exposure and subsequent toxicological risks to humans and wildlife.

Nearshore environments are a critical transitional zone that connects the marine and terrestrial/freshwater ecosystems. The release of anthropogenic chemicals into nearshore ecosystems pose a human and environmental health risk. We investigated the microbial diversity, abundance and function in metal-contaminated sediments collected from the Rongjiang, Hanjiang and Lianjiang River estuaries and adjacent coastal areas using high throughput sequencing. The concentration of nutrients (NO3-N, NO2-N, NH4-N, PO4-P) and metal (Cu, Zn, Cd, Pb, As, Hg) contaminants were higher at the mouth of the rivers compared to the coastal lines, and this was confirmed using cluster analysis. Estimates obtained using geoaccumulation index showed that about 38.9% of the sites were contaminated with Pb and the pollution load index showed that sediment from the mouth of Hanjiang River Estuary was moderately polluted with metals. In the nearshore sediment samples collected, Proteobacteria, Bacteroidetes, Planctomycetes, Chloroflexi, Acidobacteria were the dominant phylum with relative abundances of 46.6%, 8.05%, 6.47%, 5.26%, and 4.59%, respectively. There was no significant correlation between environmental variables and microbial abundance and diversity except for total organic carbon (TOC) (diversity; r = 0.569, p < 0.05) and Cr (diversity; r = 0.581, p < 0.05). At phyla level, Nitrospirae had a significant negative correlation with all metals except Cr, while OD1 had a significant positive correlation with all the metals. Overall, changes in nearshore sediment microbial communities by environmental factors were observed, and these may affect biogeochemical cycling.

Adenosine triphosphate-binding cassette (ABC) transporters, including P-glycoprotein (Pgp) and multi-resistance associated proteins (Mrps), have been considered important participants in the self-protection of zebrafish embryos against environmental pollutants, but their possible involvement in the efflux and detoxification of quantum dots (QDs), as well as their regulation mechanism are currently unclear. In this work, gene expression alterations of ABC transporters, nuclear receptors, and oxidative stress signaling in zebrafish embryos after the treatment of mercaptopropionic acid (MPA)CdTe QDs and MPA-CdSCdTe QDs were investigated. It was observed that both QDs caused concentration-dependent delayed hatching effects and the subsequent induction of transporters like mrp1&2 in zebrafish embryos, indicating the protective role of corresponding proteins against CdTe QDs. Accompanying these alterations, expressions of nuclear receptors including the pregnane X receptor (pxr), aryl hydrocarbon receptor (ahr) 1b, and peroxisome proliferator-activated receptor (ppar)-β were induced by QDs in a concentration- and time-dependent manner. Moreover, elevated oxidative stress, reflected by the reduction of glutathione (GSH) level and superoxide dismutase (SOD) activities, as well as the dramatic induction of nuclear factor E2 related factor (nrf) 2, was also found. More importantly, alterations of pxr and nrf2 were more pronounced than that of mrps, and these receptors exhibited an excellent correlation with delayed hatching rate in the same embryos (R² > 0.8). Results from this analysis demonstrated that the induction of mrp1 and mrp2 could be important components for the detoxification of QDs in zebrafish embryos. These transporters could be modulated by nuclear receptors and oxidative stress signaling. In addition, up-regulation of pxr and nrf2 could be developed as toxic biomarkers of CdTe QDs.

Fluoride is a well-known compound for its usefulness in healing dental caries. Similarly, fluoride is also known for its toxicity to various tissues in animals and humans. It causes skeletal fluorosis leading to osteoporosis of the bones. We hypothesized that when bones are affected by fluoride, the skeletal muscles are also likely to be affected by underlying molecular events involving myogenic differentiation. Murine myoblasts C2C12 were cultured in differentiation media with or without NaF (1 ppm-5 ppm) for four days. The effects of NaF on myoblasts and myotubes when exposed to low (1.5 ppm) and high concentration (5 ppm) were assessed based on the proliferation, alteration in gene expression, ROS production, and production of inflammatory cytokines. Changes based on morphology, multinucleated myotube formation, expression of MyHC1 and signaling pathways were also investigated. Concentrations of NaF tested had no effects on cell viability. NaF at low concentration (1.5 ppm) caused myoblast proliferation and when subjected to myogenic differentiation it induced hypertrophy of the myotubes by activating the IGF-1/AKT pathway. NaF at higher concentration (5 ppm), significantly inhibited myotube formation, increased skeletal muscle catabolism, generated reactive oxygen species (ROS) and inflammatory cytokines (TNF-α and IL-6) in C2C12 cells. NaF also enhanced the production of muscle atrophy-related genes, myostatin, and atrogin-1. The data suggest that NaF at low concentration can be used as muscle enhancing factor (hypertrophy), and at higher concentration, it accelerates skeletal muscle atrophy by activating the ubiquitin-proteosome pathway.

This study investigated the chemical components of fine urban road dust from seven sampling sites, based on which we could predict potential human health effects. The elemental compositions, including the contents of metals and volatile or semivolatile organic compounds, were determined to establish comprehensive chemical profiles of solid road dust. The chemical profiles, consisting of C: H ratio, metal contents, and relative abundances of organic compounds, provided a chemical signature for road dust. To overall cytotoxicity values ranging between 7 and 58%, water extracts contributed less than 15%, and cell death mainly occurred via direct contact with solid-phase components, which possibly indicates that the selected chemical profile of solid-phase road dust components could serve as a strong predictor for BJ and WI-38 cytotoxicity. Pure metal oxides (Cr₂O₃, CuO, Fe₂O₃, MnO₂, NiO, or ZnO) exhibited a positive dose-response, and the corresponding metal contents in solid road dust were well correlated with cell viability. The principal component analysis (PCA) results suggested that the metal contents were stronger predictors of cytotoxicity than the benzene derivative or hydrocarbon contents. The chemical profiles established in this study could be further utilized to identify candidate health hazard factors in road dust.