Little is known about the impacts of maternal exposure to acute episodes of outdoor air pollution, such as that resulting from wildfires, on obstetric and neonatal outcomes. This systematic review aims to synthesise the existing literature exploring the relationship between maternal exposure to short-to medium-term changes in outdoor air quality and obstetric and neonatal outcomes.A systematic search of peer-reviewed articles using PubMed, Cochrane Library, EMBASE, ScienceDirect, Web of Science, ProQuest, GreenFILE and Scopus was conducted in January 2018 using selected search terms. Quality of included studies were assessed using the Newcastle Ottawa Scale.Eleven studies were included; eight assessed the impact of maternal exposure to air pollution exacerbation events, such as wildfires, oil well fires and volcanic eruptions, and three assessed the impact of improvement events, such as the 2018 Beijing Olympics and closure of industrial activities, on obstetric and neonatal outcomes. Studies were highly heterogenous in methodology. Six studies found a significant association between acute changes in air quality and markers of fetal growth restriction, while two did not. Three studies found an adverse association between acute changes in air quality and markers of gestational maturity, and one did not.Overall, there is some evidence that maternal exposure to acute changes in air quality of short-to medium-term duration increases the risk of fetal growth restriction and preterm birth. The relationship for other adverse obstetric or neonatal outcomes is less clear.

Polycyclic aromatic hydrocarbons (PAHs) in urban soils are a risk to the health of residents. To predict those risks, the distribution and the factors influencing the concentration of PAHs were studied by collecting 1120 records of soil PAHs published during 2006–2017 from 26 cities. The mean concentrations of 16 PAHs (∑PAHs) in soil varied from 123 μg/kg to 5568 μg/kg, with a mean value of 1083 μg/kg, suggesting that a few cities were polluted. The distribution of ∑PAHs in the cities followed two gradients, namely from northern China through eastern China to southern China and from industrial cities through developed cities to cities that are main tourist attractions. The concentrations were significantly correlated to annual temperature, the efficiency of energy use, and to such measures of air quality as PM₁₀ and NO₂ concentrations. A regression equation developed to predict the concentration of ∑PAHs in soil and the corresponding health risks to residents of 35 major Chinese cities of China showed that the risks to adults and children were slight in most cities but those in a few industrial cities were of concern, and field investigations are recommended to assess the risk in greater detail. The method offers a useful tool for predicting such risks in other cities even when data on soils PAHs are not available.

Per- and polyfluoroalkyl Substances (PFAS) are ubiquitous in the environmental matrix, and their eco-toxicity on wide life and health risks on humans arising concerns. Due to the information gap, current risk assessments of PFAS ignore the indoor exposure pathway such as indoor dust and the different sources of drinking water. We collected and analyzed 168 indoor dust and 27 drinking water samples (including tap water, filtered water and bottled water). The mean concentrations of six typical PFAS measured in indoor dust and drinking water are in the range of 15.13–491.07 ng g⁻¹ and 0.31–4.14 ng L⁻¹, respectively. For drinking water, PFOA and PFOS were the dominant compounds, while PFHxS was the most abundant in indoor dust. Short-chain PFAS concentrations were higher than long-chain PFAS in both drinking water and indoor dust. Higher concentration of PFAS was observed in tap water and filtered water than bottled water. The total daily intake (TDI) of six PFAS are 20.67–52.97 ng kg⁻¹ d⁻¹ for infants, children, teenagers, and adults. As to children, teenagers, and adults, perfluorooctanoate (PFOA) is the major compound, accounting for 72.9–74.7% of the total daily intake. And PFOA (38.7%) and perfluorooctane sulfonate (PFOS, 42.2%) are the dominant PFAS for infants. The quantitative proportions of exposure sources are firstly revealed in this study, which in the order of foodstuff > indoor dust > drinking water > indoor air. Although the contribution to the PFAS intake of drinking water and indoor dust was not predominant (<9%), the health risks caused by long-term exposure need our attention. The hazard quotient (HQ) values of total PFAS were in the range of 0.154–0.498, which suggesting the relatively lower exposure risk in Chinese population. This study provides important reference to understand PFAS exposure status other than foodstuff.

Microplastics exhibit active environmental behavior and unique surface characteristics, and act as carriers for the migration of trivalent arsenic (As(III)) in the environment. Herein, the mechanism by which polytetrafluoroethylene (PTFE) microplastic particles adsorb As(III) is systematically determined. The larger the size of PTFE particles, the smaller the specific surface area, the higher the point of zero charge (PZC), and the more unfavorable adsorption of As(III); the highest adsorption amount can reach 1.05 mg g⁻¹. The adsorption process can be divided into three stages by the intraparticle diffusion model: external mass transfer, intraparticle diffusion, and dynamic equilibrium, of which the external mass transfer stage is the adsorption rate-limiting stage. The Langmuir isotherm model better represented the equilibrium adsorption results. The adsorption of As(III) by PTFE was an exothermic process, and because the increase in temperature broke the hydrogen bond, the amount of adsorption was decreased, which was not conducive to spontaneous adsorption. In the pH range of 3–7, as the pH value increased, the amount of As(III) adsorbed by PTFE gradually decreased, which may be related to the change in PZC for PTFE and the protonation of As(III). The H on the surface hydroxyl group of the PTFE exhibited a very large positive potential (+82.37 kcal mol⁻¹). Thus, it can attract the arsenic oxyanion, and As(III) was subsequently adsorbed on the surface of the PTFE through the hydrogen bond on the hydroxyl group. Electrostatic force and non-covalent interaction were the key mechanisms affecting the PTFE adsorption.

Although plants are often exposed to atmospheric nanoparticles (NPs), the mechanism of NP deposition and their effects on physiology and metabolism, and particularly in combination with other stressors, are not yet understood. Exploring interactions between stressors is particularly important for understanding plant responses in urban environments where elevated temperatures can be associated with air pollution. Accordingly, 3-year-old spruce seedlings were exposed for 2 weeks to aerial cadmium oxide (CdO) NPs of environmentally relevant size (8–62 nm) and concentration (2 × 10⁵ cm⁻³). While half the seedlings were initially acclimated to high temperature (35 °C) and vapour pressure deficit (VPD; 2.81 kPa), the second half of the plants were left under non-stressed conditions (20 °C, 0.58 kPa). Atomic absorption spectrometry was used to determine Cd content in needles, while gas and liquid chromatography was used to determine changes in primary and secondary metabolites. Photosynthesis-related processes were explored with gas-exchange and chlorophyll fluorescence systems. Our work supports the hypothesis that atmospheric CdO NPs penetrate into leaves but high temperature and VPD reduce such penetration due to stomatal closure. The hypothesis that atmospheric CdO NPs influences physiological and metabolic processes in plants was also confirmed. This impact strengthens with increasing time of exposure. Finally, we found evidence that plants acclimated to stress conditions have different sensitivity to CdO NPs compared to plants not so acclimated. These findings have important consequences for understanding impacts of global warming on plants and indicates that although the effects of elevated temperatures can be deleterious, this may limit other forms of plant stress associated with air pollution.

Nitrate (NO₃⁻) is a key component of secondary inorganic aerosols and PM₂.₅. However, the contributions of nitrogen oxides (NOₓ) emission sources to NO₃⁻ in PM₂.₅ remain poorly constrained. This study measured nitrogen (N) isotopes of NO₃⁻ (hereafter as δ¹⁵N-NO₃⁻) in PM₂.₅ collected at Beijing in 2014. We observed that δ¹⁵N-NO₃⁻ values in PM₂.₅ (−2.3‰ − 19.7‰; 7.3 ± 5.4‰ annually) were significantly higher in winter (11.9 ± 4.4‰) than in summer (2.2 ± 2.5‰). The δ¹⁵N differences between source NOₓ and NO₃⁻ in PM₂.₅ (hereafter as Δ values) were estimated by a computation module as 7.8 ± 2.2‰ − 10.4 ± 1.6‰ (8.8 ± 2.4‰). Using the Δ values and δ¹⁵N values of NOₓ from major fossil (coal combustion, vehicle exhausts) and non-fossil sources (biomass burning, microbial N cycle), contributions of major NOₓ sources to NO₃⁻ in PM₂.₅ were further estimated by the SIAR model. We found that seasonal variations of δ¹⁵N-NO₃⁻ values in PM₂.₅ of Beijing were mainly caused by those of NOₓ contributions from coal combustion (38 ± 10% in winter, 20 ± 9% in summer). Annually, NOₓ from coal combustion, vehicle exhausts, biomass burning, and microbial N cycle contributed 28 ± 12%, 29 ± 17%, 27 ± 15%, and 16 ± 7% to NO₃⁻ in PM₂.₅, respectively, showing actually comparable contributions between non-fossil NOₓ (43 ± 16%) and fossil NOₓ (57 ± 21%). These results are useful for planning the reduction of NOₓ emissions in city environments and for elucidating relationships between regional NOₓ emissions and atmospheric NO₃⁻ pollution or deposition.

Transcription factors including pregnane X receptor (Pxr) and nuclear factor-erythroid 2-related factor-2 (Nrf2) are important modulators of Adenosine triphosphate-binding cassette (ABC) transporters in mammalian cells. However, whether such modulation is conserved in zebrafish embryos remains largely unknown. In this manuscript, pxr- and nrf2-deficient models were constructed with CRISPR/Cas9 system, to evaluate the individual function of Pxr and Nrf2 in the regulation of ABC transporters and detoxification of heavy metal ions like Cd²⁺ and Ag⁺. As a result, both Cd²⁺ and Ag⁺ conferred extensive interactions with ABC transporters in wild type (WT) embryos: their accumulation and toxicity were affected by the activity of ABC transporters, and they significantly induced the mRNA expressions of ABC transporters. These induction effects were reduced by the mutation of pxr and nrf2, but elevations in the basal expression of ABC transporters compensated for the loss of their inducibility. This could be an explanation for remaining transporter function in both mutant models as well as the unaltered toxicity of metal ions in pxr-deficient embryos. However, mutation of nrf2 disrupted the production of glutathione (GSH), resulting in the enhanced toxicity of Cd²⁺/Ag⁺ in zebrafish embryos. In addition, elevated expressions of other transcription factors like aryl hydrocarbon receptor (ahr) 1b, peroxisome proliferator-activated receptor (ppar)-β, and nrf2 were found in pxr-deficient models without any treatment, while enhanced induction of ahr1b, ppar-β and pxr could only be seen in nrf2-deficient embryos after the treatment of metal ions, indicating different compensation phenomena for the absence of transcription factors. After all, pxr-deficient and nrf2-deficient zebrafish embryos are useful tools in the functional investigation of Pxr and Nrf2 in the early life stages of aquatic organisms. However, the compensatory mechanisms should be taken into consideration when interpreting the results and need in-depth investigations.

Research using various species of wild and cultured fish has identified negative effects of short-term exposure to microbeads. Although wild animals might be contaminated with microbeads and/or other pharmaceuticals, data regarding the long-term effects remain limited. To clearly elucidate the effects of microbeads, studies of long-term exposure using animal models are necessary. Our aim was to elucidate the effects of microbeads alone on the growth and fecundity of medaka following long-term exposure (12 weeks). In experiment 1, fish groups (except controls) were temporarily exposed to polyethylene microbeads (10–63 μm diameter) a low dose of 0.065 microbeads-mg/L and high dose of 0.65 microbeads-mg/L. In experiment 2, see-through medaka and fluorescent polyethylene microbeads (10–45 μm diameter) were used to estimate the retention time of ingested microbeads in the digestive tract, which was 4–9 days. The low dose of microbeads did not affect growth but did decrease the number of eggs and the hatching rate. The high dose decreased growth, the number of eggs, and hatching rate. Growth differences were recognized for the first time at 7 weeks, and differences in the number of eggs at 12 weeks. Thus, long-term tests using medaka indicated that microbeads per se exhibit growth inhibition and reproductive toxicity. These effects could be associated with nutritional factors resulting from the long retention time of microbeads in the digestive tract. We also determined the dose that affects only fecundity. This suggests that normal growth of medaka in the wild does not mean the environment is free from microbead contamination. We are thus attempting to identify new biological indexes for monitoring the status of microbead contamination using our system.

Short chain chlorinated paraffins (SCCPs) have attracted worldwide attention in recent years, due to their high production volume, persistent, bioaccumulative and toxic properties. In this study, 1-chlorodecane (CD) was selected as a model of SCCPs to explore its photochemical degradation behavior under UV irradiation. The results found that CD could be completely photochemical degradation within 120 min, and the •OH was found to be the main reactive species from both quenching experiments and electron paramagnetic resonance (EPR) results. However, the contribution of triple excited state of CD (³CD*) was still nonnegligible from the results with the absorption peak at 480 nm obtained by laser flash photolysis. Based on the identified intermediates as well as the data from theoretical chemical calculation, the detailed photochemical degradation mechanism of CD was tentatively proposed that CD firstly was excited and photo-ionized under UV irradiation, and the released Cl• in water could result in generating •OH. Then •OH initiates CD degradation mainly through the H-abstraction pathway, leading to the generation of several dehydrogenation radicals, which further generated alcohols or long chain intermediates through radical-radical reactions. The results will provide a comprehensive understanding of the degradation mechanism and environmental fates of SCCPs in water under UV irradiation.