Developmental exposures to estrogenic chemicals possibly cause structural and functional abnormalities of reproductive organs in vertebrates. Bisphenol AF (BPAF), a bisphenol A (BPA) analogue, has been shown to have higher estrogenic activity than BPA, but little is known about the effects of BPAF on gonadal development, particularly gonadal differentiation. We aimed to determine whether low concentrations of BPAF could disrupt gonadal differentiation and subsequent development using Xenopus laevis, a model species for studying feminizing effects of estrogenic chemicals. X. laevis tadpoles were exposed to BPAF (1, 10, 100 nM) or 17β-estradiol (E2, positive control) from stages 45/46 to 53 and 66 in a semi-static exposure system, with a prolonged treatment with the highest concentration to the eighth week post-metamorphosis (WPM8). Gonadal morphology and histology as well as sexually dimorphic gene expression were examined to evaluate the effects of BPAF. All concentrations of BPAF caused changes in testicular morphology at different developmental stages compared with controls. Specifically, at stage 53, BPAF like E2 resulted in decreases in both the size and the number of gonadal metameres (gonomeres) in testes, looking like ovaries. Some of BPAF-treated testes remained segmented and even became discontinuous and fragmented at subsequent stages. Histological abnormalities were also observed in BPAF-treated testes, such as ovarian cavity at stages 53 and 66 and poorly developed seminiferous tubules on WPM8. At the molecular level, BPAF inhibited expression of male highly expressed genes in testes at stage 53. Correspondingly, BPAF, like E2, inhibited cell proliferation in testes at stage 50. All results show that low concentrations of BPAF inhibited testicular differentiation and subsequent development in X. laevis, along with feminizing effects to some degree. Our finding implies a risk of BPAF to the male reproductive system of vertebrates including humans.

Microplastics are ubiquitous in marine environments. Sediments and marine organisms are recognized as the carriers and final destinations of microplastics. However, research on the concentration and abundance of microplastics in deep-sea sediments and organisms is limited. In this study, samples of sediments and organisms were collected from deep-sea locations of the western Pacific Ocean, with the depth ranging from 4601 m to 5732 m. Microplastics were extracted from the samples and analyzed by micro-Fourier-transform infrared spectroscopy. The average abundance of microplastics in the sediments was 240 items per kg dry weight of sediment. The microplastics were predominantly fibrous in shape (52.5%), blue in color (45.0%), and less than 1 mm in size (90.0%). The most commonly detected polymers were poly(propylene-ethylene) copolymer (40.0%) and polyethylene terephthalate (27.5%). The concentrations of polychlorinated biphenyls (PCBs), which are representatives of persistent organic pollutants, in the pore water of sediment samples were also investigated. A significant correlation between the distribution of microplastics and the PCB concentrations in sediments was found (P = 0.016). Microplastics were also detected in deep-sea organisms (i.e., Crinoidea, Pheronematidae, Ophiuroidea, and Gammaridea) in the sampling region, with an abundance of 0–3 items per individual biological sample. This assessment of microplastics in deep-sea sediments and benthic organisms of the western Pacific Ocean confirms that microplastic pollution exists in the deep-sea ecosystems of this region.

Whether toxicity of silver nanoparticles (AgNPs) to organisms originates from the nanoparticles themselves or from the dissolved Ag-ions is still debated, with the majority of studies claiming that extracellular release of Ag-ions is the main cause of toxicity. The objective of this study was to determine the contributions of both particles and dissolved ions to toxic responses, and to better understand the underlying mechanisms of toxicity. In addition, the pathways of AgNPs exposure to plants might play an important role and therefore are explicitly studied as well. We systematically assessed the phytotoxicity, internalization, biodistribution, and antioxidant responses in lettuce (Lactuca sativa) following root or foliar exposure to AgNPs and ionic Ag at various concentrations. For each endpoint the relative contribution of the particle-specific versus the ionic form was quantified. The results reveal particle-specific toxicity and uptake of AgNPs in lettuce as the relative contribution of particulate Ag accounted for more than 65% to the overall toxicity and the Ag accumulation in whole plant tissues. In addition, particle toxicity is shown to originate from the accumulation of Ag in plants by blocking nutrient transport, while ion toxicity is likely due to the induction of excess ROS production. Root exposure induced higher toxicity than foliar exposure at comparable exposure levels. Ag was found to be taken up and subsequently translocated from the exposed parts of plants to other portions regardless of the exposure pathway. These findings suggest particle related toxicity, and demonstrate that the accumulation and translocation of silver nanoparticles need to be considered in assessment of environmental risks and of food safety following consumption of plants exposed to AgNPs by humans.

Soil contamination in urban environment by trace metals is of public concerns. For better risk assessment, it is important to determine their background concentrations in urban soils. For this study, we determined the background concentrations of 9 trace metals including As, Ba, Cd, Co, Cu, Ni, Pb, Se, and Zn in 214 urban soils in Florida from two large cities (Orlando and Tampa) and 4 small cities (Clay County, Ocala, Pensacola and West Palm Beach). The objectives were to determine: 1) total concentrations of trace metals in urban soils in cities of different size; 2) compare background concentrations to Florida Soil Cleanup Target Levels (FSCTLs); and 3) determine their distribution and variability in urban soils via multivariate statistical analysis. Elemental concentrations in urban soils were variable, with Pb being the highest in 5 cities (165–552 mg kg⁻¹) and Zn being the highest concentration in Tampa (1,000 mg kg⁻¹). Besides, the As and Pb concentrations in some soils exceeded the FSCTL for residential sites at 2.1 mg kg⁻¹ As and 400 mg kg⁻¹ Pb. Among the cities, Clay County and Orlando had the lowest concentrations for most elements, with Cd, Co, and As being the lowest while Ba, Pb and Zn being the highest. Among all values, geometric means were the lowest while 95th percentile was the highest for all metals. Most 95th percentile values were 2–3 folds higher than the GM data, with Pb presenting the greatest difference, being 4 times greater than GM value (58.9 vs. 13.6 mg kg⁻¹). Still they were lower than FSCTL, with As exceeding FSCTL for residential sites at 2.1 mg kg⁻¹. In addition, the linear discriminate analysis showed distinct separation among the cities: Ocala (Ba & Ni) and Pensacola (As & Pb) were distinctly different from each other and from other cities with higher metal concentrations. The large variations among elemental concentrations showed the importance to establish proper background concentrations of trace metals in urban soils.

Both air pollution and dyslipidemias contributed to large number of deaths and disability-adjusted life lost years. Long-term air pollution exposure was related to changed blood lipids and risk of dyslipidemias. This study was designed to evaluate relationships between air pollutants, blood lipids and prevalence of dyslipidemias in a Chinese rural population exposed to high-level air pollution based on baseline data of The Henan Rural Cohort study. An amount of 39,057 participants from rural areas in China were included. The 3-year average exposure of air pollutants (PM2.5, PM10, NO2) was estimated by a spatiotemporal model. Logistic and linear regression models were employed to explore relationships between air pollutants, blood lipids (TC, TG, HDL-C and LDL-C) and prevalence of dyslipidemias. The three-year concentration of PM2.5, PM10 and NO2 was 72.8 ± 2.3 μg/m3, 131.5 ± 5.7 μg/m3and 39.1 ± 3.1 μg/m3, respectively. Overall, increased air pollution exposure was related to increased TC and LDL-C, while decreased TG and HDL-C. Each 1-μg/m3 increment of PM2.5 was related to 0.10% (0.07%–0.19%) increase in TC, 0.63% (0.50%–0.77%) increase in LDL-C, 2.93% (2.70%–3.16%) decrease in TG, 0.49% (0.38%–0.60%) decrease in HDL-C; and 5.7% (95%CI: 3.7%–7.6%), 4.0% (95%CI: 2.1%–6.0%) and 3.8% (95%CI: 2.5%–5.1%) increase in odds for hypercholesterolemia, hyperbetalipoproteinemia and hypoalphalipoproteinemia, respectively. Stronger associations were found in male and older participants. Findings suggest that air pollutants were associated with changed blood lipid levels and higher risk of dyslipidemias among rural population. Male and elder people should pay more attention to personal safety protection.

In this study, a weather-based multicomponent model was developed based on the unique biostructures and metabolic processes of mushrooms to evaluate their uptake of pesticides from soils, and the effects of temperature and relative humidity on the bioaccumulation of pesticides in mushrooms was comprehensively quantified. Additionally, a new pseudo-partition coefficient between mushrooms and soils was introduced to assess the impacts of different physiochemical properties on the pesticide uptake process. The results indicate that, in general, the pseudo-partition coefficient increases as the relative humidity increases for both the air and soil according to Fick’s law of gas diffusion and the spatial competition of molecules, respectively. Meanwhile, the effect of temperature on the pesticide bioaccumulation process is more complex. For most pesticides (e.g., atrazine), the pseudo-partition coefficient that was computed from the transpiration component had a maximum value at a specific temperature due to the temperature dependency of the transpiration and biodegradation processes. For some pesticides (e.g., ethoprophos), the pseudo-partition coefficient of the air-deposition component had a maximum value at a certain temperature that was caused by the ratio of the soil–air internal transfer energy and degradation activation energy of the pesticide. It was also concluded that for relatively low-volatility pesticides, transpiration dominated the bioaccumulation process; this was mainly determined from the pesticide water solubility. For nonbiodegradable pesticides (e.g., lindane), the computed coefficient values were relatively low due to their insolubility in water, which inhibits bioaccumulation in mushrooms and is one of the main reasons for their long-term persistence in soils.

Environmental health is increasingly compromised by persistent toxic substances, which may have serious implications in food safety and, thus, in human health. Polybrominated diphenyl ethers (PBDEs) are anthropogenic contaminants with endocrine disruption abilities and are commonly found in seafood, the main route of human exposure. Growing evidence points out that the human gut microbiota interacts with xenobiotics, which may lead to impairment of host homeostasis if functions of microbiota become compromised. The aim of this study was to ascertain if the physiological balance of human gut microbiome is affected by the presence and degree of exposure to PBDEs. Fermentation was performed in a batch closed-system using an inoculum made from fresh human stool. The volatolomic profile was analysed by solid-phase microextraction coupled to gas chromatography-mass spectrometry. Mesophilic, Gram-negative bacteria and coliforms were quantified by classic plating methods. Changes in the gut microbiome were evaluated after DNA extraction followed by deep sequencing of the 16S rDNA region. The exposure to PBDEs resulted in an imbalance in sulfur, short-chain fatty acids and aromatic organic compounds, changing the microbial volatolome in a dose- and time-dependent manner. Slight deviations in the microbial structure of human gut occurred in the presence of PBDEs, especially for high doses of exposure. For the first time, the impact of PBDEs on the microbial homeostasis of human gut microbiota was taken into consideration, revealing noteworthy modifications with serious health implications even at oral exposure doses considered as safe by worldwide regulatory entities.

Cattle-derived biochar (CB), which is derived from industrial pyrolysis of cattle carcasses in harmless treatment plants, is a naturally occurring mineral form of carbonate-bearing hydroxyapatite (CHAP) with a small amount of elemental carbon. CB has 4.02% of carbonate content, which falls under the B-type substitution of CHAP. In this work, the Cd(II) sorption capacity of CB was determined to be 0.82 mmol/g, with 97.6% of the Cd(II) uptake contributing to CHAP and only 2.36% of the Cd(II) uptake contributing to the elemental carbon component. The calculation and linear combination fitting (LCF) of Cd L₃-edge X-ray absorption near-edge structure (XANES) analysis indicated that the contributions of Cd(II) species to CB presented the following order: ion exchange (57.6%–61.0%) > precipitation (24.4%–29.9%) > surface complexation (12.5%–13.4%). The depth dependent X-ray photoelectron spectroscopy (XPS) showed the presence of ion exchange, which is accompanied by intraparticle diffusion. LCF of XANES and Rietveld analysis of X-ray diffraction (XRD) demonstrated that Cd(II) was precipitated in the form of Cd₅H₂(PO₄)₄·4H₂O on the CB surface. Furthermore, the precipitate was directly observed and identified by scanning electron microscopy with energy-dispersive spectroscopy (SEM-EDS). Consequently, we revealed the intricate binding mechanism of Cd(II) to CHAP-rich CB and confirmed the importance of surface precipitation.

2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47) is associated with various adverse human health effects; however, the knowledge of its toxicity is still very limited. Mitochondrial injury has been observed in liver cells exposed to BDE-47 in vitro. Mitophagy impairment causes the accumulation of dysfunctional mitochondria, contributing to the pathological mechanisms of liver injury. The aim of this study was to investigate whether BDE-47 impairs mitophagy to trigger mitochondrial dysfunction-related liver injury and the underlying mechanisms. This study revealed that BDE-47 elicited mitochondrial dysfunction and related oxidative liver injury by impairing mitophagy. Moreover, our results showed that NAD⁺ insufficiency is responsible for BDE-47-mediated mitophagy defect and mitochondrial dysfunction in mouse livers, which was associated with suppression of Sirt3/FoxO3a/PINK1 signaling. Furthermore, our results indicated a potential role of miR-34a-5p in the hepatotoxicity of BDE-47. Mechanistically, BDE-47 dramatically upregulated miR-34a-5p expression in mouse livers. The data from AAV-sponge-mediated miR-34a-5p inhibition suggested that miR-34a-5p diminished NAD⁺ level by directly targeting NAMPT expression in BDE-47-treated mouse livers, which was confirmed by luciferase reporter assay. Consequently, miR-34a-5p markedly abated Sirt3/FoxO3a/PINK1 signaling-mediated mitophagy to promote mitochondrial dysfunction in BDE-47-treated mouse livers. The present study provided in vivo evidence to reveal a potential mechanism for BDE-47-induced mitochondrial dysfunction and related liver injury and indicated that miR-34a-5p-mediated mitophagy impairment might be a therapeutic target for BDE-47 toxicity.