Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.

Previous studies have associated the risk of autism spectrum disorder (ASD) with increased exposures to metals and metalloids such as arsenic. In this study, we used an animal-to-human translational strategy to identify key molecular changes that potentially mediated the effects of arsenic exposures on ASD development. In a previously established rat model, we have induced autistic behaviors in rat pups with gestational arsenic exposures (10 and 45 μg/L As₂O₃ in drinking water). Neuronal apoptosis and the associated epigenetic dysregulations in frontal cortex were assayed to screen potential mediating pathways, which were subsequently validated with qPCR, western blotting, and immunohistochemistry analyses. Furthermore, the identified pathway, along with serum levels of 26 elements including arsenic, were characterized in a case-control study with 21 ASD children and 21 age-matched healthy controls. In animals, we found that arsenic exposures caused difficulties of social interaction and increased stereotypic behaviors in a dose-dependent manner, accompanied by increased neuronal apoptosis and upregulation of Hipk2-p53 pathway in the frontal cortex. In humans, we found that serum levels of Hipk2 and p53 were 24.7 (95%CI: 8.5 to 43.4) % and 23.7 (95%CI: 10.5 to 38.5) % higher in ASD children than in healthy controls. ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53. Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.

Microplastic exposure in one generation of marine organism is believed to impact future generations; the nature of this impact, however, remains unclear, especially across different life stages. We investigated within-generational, latent, and intergenerational effects of various sizes (1.7, 6.8, 10.4, and 19.0 μm) and concentrations (1, 10, 100, and 1000 beads mL⁻¹) of polystyrene microplastics on the planktonic larval and benthic adult life stages of the intertidal barnacle Amphibalanus amphitrite. We exposed parents to microplastics during different developmental stages and examined the life history traits of their offspring. Microplastics had prominent intergenerational—but no within-generational—effects. Parental exposure to 1.7, 6.8, and 10.4 μm microplastics from the larvae to adults significantly increased offspring larval mortality. 1.7 and 6.8 μm microplastics at 1000 beads mL⁻¹ delayed larval development in offspring. Intergenerational effects were observed when microplastics were exposed to parent larvae, suggesting that parental experiences during sensitive early-life stages can have profound impacts across generations. Adverse intergenerational effects of microplastics might drastically reduce larval recruitment and threaten long-term zooplankton sustainability.

Soil salinity is a global threat to the environmental sustainability, in particular to the developing countries due to their limited resources for soil reclamation. In a greenhouse pot experiment, Pennisetum giganteum, was investigated for its tolerance to salt stress and simultaneous phytoremediation capability. 4 weeks post-germination, NaCl (10, 50, 150, 250, 350, 450 and 550 mM) and tap water (control) was applied after every 2 consecutive days for two weeks in a completely randomized design and their effects were established in the growth and physico-chemical aspects of these plants. Our results indicated that P. giganteum withstood high salt stress (with 550 mM NaCl tolerance threshold level). Interestingly, the plants grown under saline conditions had higher biomass yield when compared to the control. Furthermore, the antioxidant activity and proline content of plants under saline conditions were significantly (p < 0.05) higher than those of control plants, indicating their adaptability to high salt stress. Biochemical analysis such as chlorophyll contents, total soluble sugar, total phenol and protein contents revealed considerable differences between plants grown under higher NaCl stress compared to the control conditions. Additionally, significantly different ionic flux along with high K⁺/Na⁺ ratio was observed in plants grown under a range of saline conditions. The results obtained are therefore of value to indicate P. giganteum an eco-friendly alternate source for the phytoremediation of saline soils and may be used as base for future research on this plant. Effective strategies need to be adopted with this plant to reclaim saline-degraded as well as marginal soils.

Ozone (O₃) is a potent oxidant associated with adverse health effects. Low-cost O₃ sensors, such as metal oxide (MO) sensors, can complement regulatory O₃ measurements and enhance the spatiotemporal resolution of measurements. However, the quality of MO sensor data remains a challenge. The University of Utah has a network of low-cost air quality sensors (called AirU) that primarily measures PM₂.₅ concentrations around the Salt Lake City valley (Utah, U.S.). The AirU package also contains a low-cost MO sensor ($8) that measures oxidizing/reducing species. These MO sensors exhibited excellent laboratory response to O₃ although they exhibited some intra-sensor variability. Field performance was evaluated by placing eight AirUs at two Division of Air Quality (DAQ) monitoring stations with O₃ federal equivalence methods for one year to develop long-term multiple linear regression (MLR) and artificial neural network (ANN) calibration models to predict O₃ concentrations. Six sensors served as train/test sets. The remaining two sensors served as a holdout set to evaluate the applicability of the new calibration models in predicting O₃ concentrations for other sensors of the same type. A rigorous variable selection method was also performed by least absolute shrinkage and selection operator (LASSO), MLR and ANN models. The variable selection indicated that the AirU’s MO oxidizing species and temperature measurements and DAQ’s solar radiation measurements were the most important variables. The MLR calibration model exhibited moderate performance (R² = 0.491), and the ANN exhibited good performance (R² = 0.767) for the holdout set. We also evaluated the performance of the MLR and ANN models in predicting O₃ for five months after the calibration period and the results showed moderate correlations (R²s of 0.427 and 0.567, respectively). These low-cost MO sensors combined with a long-term ANN calibration model can complement reference measurements to understand geospatial and temporal differences in O₃ levels.

Chemical conditioning is an effective strategy for improved river sediment dewatering affecting both the dewatering efficiency and subsequent resource utilization of the dewatered cake. Two types of conditioning agents, polyaluminium chloride (PAC)/cationic polyacrylamide (PAM) (coagulation precipitation conditioning agent, referred to as P–P conditioning) and ferrous activated sodium persulfate (advanced oxidation conditioning agent, referred to as F–S conditioning) were examined. With increasing leach liquid to solid (L/S) ratio the concentration of Cd for the real time leachates from the dewatered cakes decreased, but the leaching ratio of Cd in both P–P and F–S dewatered cakes increased. With the same L/S, the leaching ratio was reduced for both types of conditioning, as compared to no conditioning, with the leaching ratio being least with F–S conditioning. The leaching ratio of Cd in the dewatered cake with L/S of 100 L kg⁻¹ was reduced from 21.3% of the total Cd present for the un-conditioned sediment to 12.5% upon P–P conditioning and 11.6% upon F–S conditioning. Furthermore, the different conditioning methods affected the Cd speciation in the dewatered cakes reducing the easy-to-leach speciation of exchangeable and carbonate-bound Cd species and increasing the potential-to-leach speciation of iron-manganese oxide and organically bound Cd species and also the difficult-to-leach species. Risk assessment indicates that the risk due to Cd leaching from the dewatered cakes at L/S of 100 L kg⁻¹ was reduced from high risk to medium risk after P–P and F–S conditioning with reduced bioavailability.

This work presents the results of a PM2.5 source apportionment study conducted in urban background sites from 16 European and Asian countries. For some Eastern Europe and Central Asia cities this was the first time that quantitative information on pollution source contributions to ambient particulate matter (PM) has been performed. More than 2200 filters were sampled and analyzed by X-Ray Fluorescence (XRF), Particle-Induced X-Ray Emission (PIXE), and Inductively Coupled Plasma Mass Spectrometry (ICP-MS) to measure the concentrations of chemical elements in fine particles. Samples were also analyzed for the contents of black carbon, elemental carbon, organic carbon, and water-soluble ions. The Positive Matrix Factorization receptor model (EPA PMF 5.0) was used to characterize similarities and heterogeneities in PM2.5 sources and respective contributions in the cities that the number of collected samples exceeded 75. At the end source apportionment was performed in 11 out of the 16 participating cities. Nine major sources were identified to have contributed to PM2.5: biomass burning, secondary sulfates, traffic, fuel oil combustion, industry, coal combustion, soil, salt and “other sources”. From the averages of sources contributions, considering 11 cities 16% of PM2.5 was attributed to biomass burning, 15% to secondary sulfates, 13% to traffic, 12% to soil, 8.0% to fuel oil combustion, 5.5% to coal combustion, 1.9% to salt, 0.8% to industry emissions, 5.1% to “other sources” and 23% to unaccounted mass. Characteristic seasonal patterns were identified for each PM2.5 source. Biomass burning in all cities, coal combustion in Krakow/POL, and oil combustion in Belgrade/SRB and Banja Luka/BIH increased in Winter due to the impact of domestic heating, whereas in most cities secondary sulfates reached higher levels in Summer as a consequence of the enhanced photochemical activity. During high pollution days the largest sources of fine particles were biomass burning, traffic and secondary sulfates.

Current practices employed by most wastewater treatment plants (WWTP) are unable to completely remove endocrine disrupting compounds (EDCs) from reclaimed waters, and consistently discharge these substances to receiving systems. Effluent-dominated and dependent surface waters, especially during low instream flows, can increase exposure and risks to aquatic organisms due to adverse biological effects associated with EDCs. Given the ecological implications that may arise from exposure to such compounds, the present a multi-approach study examined spatio-temporal estrogenic potential of wastewater effluent to fish in East Canyon Creek (ECC), Utah, USA, a unique urban river with instream flows seasonally influenced by snowmelt. Juvenile rainbow trout (Oncorhynchus mykiss) were caged at different upstream and downstream sites from an effluent discharge during the summer and fall seasons. In the summer, where approximately 50% of the streamflow was dominated by effluent, fish from the upstream and a downstream site, located 13 miles away from the effluent discharge, presented significantly elevated concentrations of plasma vitellogenin (VTG). Similarly, significantly high 17β-estradiol to 11-ketotestosterone ratios were measured in the summer across all sites and time points, compared to the fall. In the laboratory, juvenile fish and primary hepatocytes were exposed to concentrated effluent and surface water samples. Quantification of VTG, although in significantly lower levels, resembled response patterns observed in fish from the field study. Furthermore, analytical quantification of common EDCs in wastewater revealed the presence of estriol and estrone, though these did not appear to be related to the observed biological responses, as these were more significant in sites were no EDCs were detected. These combined observations suggest potential estrogenicity for fish in ECC under continuous exposures and highlight the advantages of following weight-of-evidence (WoE) approaches for environmental monitoring, as targeted analytically-based assessments may or may not support the identification of causative contaminants for adverse biological effects.

Very little is currently known regarding the effects of estrogenic endocrine disrupting chemicals on embryonic and larval development in molluscs, nor the potential effects of parental (F₀) exposure on resultant F₁ offspring. In this study, we assessed the embryotoxic impacts of exposure to environmentally relevant concentrations of the synthetic estrogen, 17α-ethinylestradiol (EE2), to male and female parents (50 ng/L) and their offspring (5 and 50 ng/L) in the native Australian Sydney rock oyster, Saccostrea glomerata. There were no detectable effects of parental exposure on fertilisation success, proportions of early larval (F₁) morphs and unfertilised eggs. Offspring impacts were evidenced in terms of developmental delays, with decreased percentages of D-veligers retained by 45 μm mesh, along with a reduction of swimming capabilities of larvae at 2 days post-fertilisation (dpf) when both parents had been exposed to 50 ng/L EE2. Although no significant parental effects were found on the survival of F₁ larvae at 9 dpf, retardation of shell growth was observed on F₁ larvae in treatments where both parents had been exposed to 50 ng/L EE2. Subsequent larval exposure from 2 to 9 dpf caused declines in survival and reduction of shell length in F₁ larvae at both 5 and 50 ng/L EE2 across all parental exposure treatments. Collectively, parental EE2 imparts effects on offspring in terms of retardation of larval development, and subsequent offspring exposure to EE2 further exacerbates impacts to development. Future research should aim to understand the potential mechanisms of EE2 induced toxicity and its transmission resulting in altered phenotypes of the F₁ generation.

Low pH and aluminum (Al)-toxicity often coexist in acidic soils. Citrus sinensis seedlings were treated with nutrient solution at a pH of 2.5, 3.0, 3.5 or 4.0 and an Al concentration of 0 or 1 mM for 18 weeks. Thereafter, malate, citrate, isocitrate, acid-metabolizing enzymes, and nonstructural carbohydrates in roots and leaves, and release of malate and citrate from roots were measured. Al concentration in roots and leaves increased under Al-toxicity, but it declined with elevating nutrient solution pH. Al-toxicity increased the levels of glucose, fructose, sucrose and total soluble sugars in leaves and roots at each given pH except for a similar sucrose level at pH 2.5–3.0, but it reduced or did not alter the levels of starch and total nonstructural carbohydrates (TNC) in leaves and roots with the exception that Al improved TNC level in roots at pH 4.0. Levels of nonstructural carbohydrates in roots and leaves rose with reducing pH with a few exceptions with or without Al-toxicity. A potential model for the possible role of root organic acid (OA) metabolism (anions) in C. sinensis Al-tolerance was proposed. With Al-toxicity, the elevated pH upregulated the OA metabolism, and increased the flow of carbon to OA metabolism, and the accumulation of malate and citrate in roots and subsequent release of them, thus reducing root and leaf Al and hence eliminating Al-toxicity. Without Al-toxicity, low pH stimulated the exudation of malate and citrate, an adaptive response of Citrus to low pH. The interactive effects of pH and pH on OA metabolism were different between roots and leaves.