We investigated the associations between exposure to polycyclic aromatic hydrocarbons (PAHs) and selected respiratory physiologic measures in cycles 2 and 3 of the Canadian Health Measures Survey, a nationally representative population sample. Using generalized linear mixed models, we tested the association between selected PAH metabolites and 1-second forced expiratory volume (FEV1), forced vital capacity (FVC), and the ratio between the two (FEV1/FVC) in 3531 people from 6 to 79 years of age. An interquartile change in urinary PAH metabolite was associated with significant decrements in FEV1 and FVC for eight PAHs, 2-hydroxynapthalene, 1-, and 2-hydroxyphenanthrene, 2-, 3-, and 9-hydroxyfluorene and 3- and 4-hydroxyphenanthrene. Exposure to PAH may negatively affect lung function in the Canadian population.

We assessed mercury (Hg) pollution in China's coastal waters, including the Bohai Sea, the Yellow Sea, the East China Sea and the South China Sea, based on a nationwide dataset from 301 sampling sites. A methylmercury (MeHg) intake model for humans based on the marine food chain and human fish consumption was established to determine the linkage between water pollutants and the pollutant intake by humans. The predicted MeHg concentration in fish from the Bohai Sea was the highest among the four seas included in the study. The MeHg intake through dietary ingestion was dominant for the fish and was considerably higher than the MeHg intake through water respiration. The predicted MeHg concentrations in human blood in the coastal regions of China ranged from 1.37 to 2.77 μg/L for pregnant woman and from 0.43 to 1.00 μg/L for infants, respectively, based on different diet sources. The carnivorous fish consumption advisory for pregnant women was estimated to be 288–654 g per week to maintain MeHg concentrations in human blood at levels below the threshold level (4.4 μg/L established by the US Environmental Protection Agency). With a 50% increase in Hg concentrations in water in the Bohai Sea, the bioaccumulated MeHg concentration (4.5 μg/L) in the fish consumers will be higher than the threshold level. This study demonstrates the importance in controlling Hg pollution in China's coastal waters. An official recommendation guideline for the fish consumption rate and its sources will be necessary for vulnerable populations in China.

The presence of organic pollutants in the aquatic environment, usually found at trace concentrations (i.e., between ng L−1 and μg L−1 or even lower, known as micropollutants), has been highlighted in recent decades as a worldwide environmental concern due to their difficult elimination by conventional water and wastewater treatment processes. The relevant information on constructed wetlands (CWs) and their application for the removal of a specific group of pollutants, 41 organic priority substances/classes of substances (PSs) and 8 certain other substances with environmental quality standards (EQS) listed in Directive 2013/39/EU as well as 17 contaminants of emerging concern (CECs) of the Watch List of Decision 2015/495/EU, is herein reviewed. Studies were found for 24 PSs and 2 other substances with EQS: octylphenol, nonylphenol, perfluorooctane sulfonic acid, di(2-ethylhexyl)phthalate, trichloromethane, dichloromethane, 1,2-dichloroethane, pentachlorobenzene, benzene, polychlorinated dibenzo-p-dioxins, naphthalene, fluoranthene, trifluralin, alachlor, isoproturon, diuron, tributyltin compounds, simazine, atrazine, chlorpyrifos (chlorpyrifos-ethyl), chlorfenvinphos, hexachlorobenzene, pentachlorophenol, endosulfan, dichlorodiphenyltrichloroethane (or DDT) and dieldrin. A few reports were also published for 8 CECs: imidacloprid, erythromycin, clarithromycin, azithromycin, diclofenac, estrone, 17-beta-estradiol and 17-alpha-ethinylestradiol. No references were found for the other 17 PSs, 6 certain other substances with EQS and 9 CECs listed in EU legislation.

Vehicle emissions have become one of the key factors affecting the urban air quality and climate change in the Pearl River Delta (PRD) region, so it is important to design policies of emission reduction based on quantitative Co-benefits for air pollutants and greenhouse gas (GHG). Emissions of air pollutants and GHG by 2020 was predicted firstly based on the no-control scenario, and five vehicle emissions reduction scenarios were designed in view of the economy, technology and policy, whose emissions reduction were calculated. Then Co-benefits between air pollutants and GHG were quantitatively analyzed by the methods of coordinate system and cross-elasticity. Results show that the emissions reduction effects and the Co-benefits of different measures vary greatly in 2015–2020. If no control scheme was applied, most air pollutants and GHG would increase substantially by 20–64% by 2020, with the exception of CO, VOC and PM2.5. Different control measures had different reduction effects for single air pollutant and GHG. The worst reduction measure was Eliminating Motorcycles with average reducing rate 0.09% for air pollutants and GHG, while the rate from Updated Emission Standard was 41.74%. Eliminating Yellow-label Vehicle scenario had an obvious reduction effect for every single pollutant in the earlier years, but Co-benefits would descent to zero in later by 2020. From the perspective of emission reductions and co-control effect, Updated Emission Standard scenario was best for reducing air pollutants and GHG substantially (tanα=1.43 and Els=1.77).

Measuring black carbon (BC) is critical to understand the impact of combustion aerosols on air quality and climate change. In this study, BC was measured in 2014 at a unique community formed with rapid economic development and urbanization in an urban-rural fringe area of Beijing. Hourly BC concentrations were 0.1–33.5 μg/m3 with the annual average of 4.4 ± 3.7 μg/m3. BC concentrations had clear diurnal, weekly, and seasonal variations, and were closely related with atmospheric visibility. The absorption coefficient of aerosols increased while its contribution to extinction coefficient decreased with the enhancement of PM2.5 concentration. The high mass absorption efficiency (MAE) of EC was attributed to a combination of coal combustion, vehicular emission and rapidly coating by water-soluble ions and organic carbon (OC). BC concentrations followed a typical lognormal pattern, with over 88% samples in 0.1–10.0 μg/m3. Low BC levels were mostly bounded up with winds from north and northwest. Coal combustion and biomass burning were closely associated with severe haze pollution events. Firework discharge had significant UV absorption contribution. During the Asia-Pacific Economic Cooperation (APEC) forum in November 2014, air quality obviously improved due to various control strategies.

Perfluorooctane sulfonate (PFOS), a hepatic toxicant and a potential hepatocarcinogen, is commonly used in industrial products. The widespread contamination of PFOS in human maternal and cord blood has raised concerns about its potential risks to the fetus. It is believed that adverse environmental exposure during the critical period of embryo development can have long-lasting consequences in later life. In this report, we used transcriptome sequencing, followed by bioinformatics analysis, to elucidate the potential hepatotoxic and hepatocarcinogenic effects of prenatal PFOS exposure in the fetus. Our results demonstrated that prenatal PFOS exposure could activate the synthesis and metabolism of fatty acids and lipids, leading to liver damage and interference with liver development in the fetus. In addition, a number of cancer-promoting signaling pathways, including Wnt/β-catenin, Rac, and TGF-β, were found to be activated in the fetal liver. More importantly, hepatic transaminase activity, including aspartate aminotransferase and alanine transaminase activity, was induced in the liver of mice offspring after prenatal PFOS exposure. For the first time, our results demonstrate that the hepatotoxic effects of prenatal exposure to PFOS may predispose to a long-term liver disorder in the offspring.

Although organophosphate esters (OPEs) have been detected with growing frequency in water ecosystems, the underlying accumulation mechanisms of these compounds in fish are still unknown. Here, we investigated the tissue-specific accumulation and depuration of seven OPEs in adult zebrafish at three levels (0, 1/150 LC50 (environmentally relevant level), and 1/30 LC50 per OPE congener) in laboratory after 19 days exposure and 3 days depuration. The bioaccumulation of OPEs varied among tissues. Muscle contained the lowest level of OPEs and liver had the highest level of two (TPP and TCEP) of the seven OPEs at steady state. The high levels and slow depuration rates of TDCIPP, TPHP, and TCP observed in roe indicated that the accumulated OPEs were potentially stored in roe and transferred to the next generation. After examination of the major metabolites (organophosphate diesters) in selected tissues, a physiologically based toxicokinetic (PBTK) model used in fish was adopted to explore the key factors affecting the bioaccumulation of OPEs in zebrafish. Biotransformation of OPEs with polychlorinated alkyl moieties (i.e. TDCIPP) and aryl moieties (i.e. TPHP and TCP) has more significant impacts on the accumulation than those of OPEs with alkyl or short chain chlorinated alkyl moieties. Furthermore, the partition process between tissues and blood was also investigated, and was demonstrated to be the dominant process for OPEs accumulation in zebrafish. This study provides critical information on the bioaccumulation, tissue distribution, and metabolization of OPEs in relation with OPE structures in fish, as well as the underlying bioaccumulation mechanisms/pathways of OPEs in aquatic life.

In polluted environments organisms are commonly exposed to a combination of chemicals with different modes of action, and their effects can be additionally modified by natural abiotic conditions. One possible mechanism for interactions in mixtures is via toxicokinetics, as chemicals may alter the uptake, distribution, biotransformation and/or elimination of each other, and all these processes can be affected by temperature. In this study, the effect of temperature (T) on the toxicokinetics of copper (Cu) and chlorpyriphos (CHP), applied either singly or in binary mixtures, was studied in the earthworm Eisenia fetida. The experiments were conducted at 10 or 20 °C and the earthworms were exposed to environmentally realistic concentrations of Cu and/or CHP for 16 d, followed by a depuration period of 4 d in uncontaminated soil. The earthworms were sampled for body Cu and/or CHP concentrations and acetylcholinesterase (AChE) activity measurements. The CHP degradation rate in the soil was substantially higher at 20 °C and in soil treated with Cu. The significant (p < 0.05) inhibition of AChE activity in the earthworms exposed to CHP was found. The effect of Cu was significant only at p < 0.1. No synergistic effect of the parallel CHP and Cu exposure was found. Four days after transferring the earthworms to uncontaminated soil, the AChE activity recovered to the level observed in control animals. The temperature effect on the toxicokinetic parameters was more pronounced for CHP than for Cu. In the case of CHP, the assimilation rate constant (kA) was significantly higher at 20 °C than at 10 °C, both in CHP-only and CHP + Cu treatments. A similar trend was found for the elimination rate constant (kE), but the difference was statistically significant only for non-Cu treatments. In the case of Cu, the general trend of higher kA and kE at 20 °C and in the absence of CHP was observed.

This study investigated the factors that regulated the degradation of perfluorooctanoic acid (PFOA) in laccase-catalyzed oxidative humification reactions with 1-hydroxybenzotriazole (HBT) as a mediator. The reaction rates were examined under conditions with key factors varied, including initial PFOA concentrations, laccase and HBT dosages, and the ionic contents of the reaction solutions. The PFOA degradation followed pseudo-first order kinetics, and the rate constants (k) were similar for the high (100 μmol L⁻¹) and low (1.00 μmol L⁻¹) initial PFOA concentrations, respectively at 0.0040 day⁻¹ (r² = 0.98) and 0.0042 day⁻¹ (r² = 0.86) under an optimum reaction condition tested in this study. The metal ions contained in the reaction solution appeared to have a strong impact on PFOA degradation. Differential UV-Vis spectrometry revealed that Cu²⁺ can complex with PFOA, which plays an essential role to enable PFOA degradation, probably by bridging the negatively charged PFOA and laccase, so that the free radicals of HBT that are released from laccase can reach and react with PFOA. It was also found that Fe³⁺ plays a similar role as Cu²⁺ to enable PFOA degradation in the laccase-HBT reaction system. In contrast, Mg²⁺ and Mn²⁺ cannot complex with PFOA under the investigated conditions, and do not enable PFOA degradation in the laccase-HBT system. Fluoride and partially fluorinated compounds were detected as PFOA degradation products using ion chromatography and high resolution mass spectrometry. The structures of the products suggest the reaction pathways involving free-radical initiated decarboxylation, rearrangement, and cross-coupling.

Pesticides are implicated in the decline of honey bee populations. Many insecticides are neurotoxic acting by different modes of actions. Although a link between insecticide exposure and changed behaviour has been made, molecular effects underlying these effects are poorly understood. Here we elucidated molecular effects at environmental realistic concentrations of two organophosphates, chlorpyrifos, malathion, the pyrethroid cypermethrin, and the ryanodine receptor activator, chlorantraniliprole. We assessed transcriptional alterations of selected genes at three exposure times (24 h, 48 h, 72 h) in caged honey bees exposed to different concentrations of these compounds. Our targeted gene expression concept focused of several transcripts, including nicotinic acetylcholine receptor α 1 and α 2 (nAChRα1, nAChRα2) subunits, the multifunctional gene vitellogenin, immune system related genes of three immune system pathways, genes belonging to the detoxification system and ER stress genes. Our data indicate a dynamic pattern of expressional changes at different exposure times. All four insecticides induced strong alterations in the expression of immune system related genes suggesting negative implications for honey bee health, as well as cytochrome P450 enzyme transcripts suggesting an interference with metabolism. Exposure to neurotoxic chlorpyrifos, malathion and cypermethrin resulted in up-regulation of nAChRα1 and nAChRα2. Moreover, alterations in the expression of vitellogenin occurred, which suggests implications on foraging activity. Chlorantraniliprole induced ER stress which may be related to toxicity. The comparison of all transcriptional changes indicated that the expression pattern is rather compound-specific and related to its mode of action, but clusters of common transcriptional changes between different compounds occurred. As transcriptional alterations occurred at environmental concentrations our data provide a molecular basis for observed adverse effects of these insecticides to bees.