Per- and polyfluoroalkyl substances (PFAS) have been produced and used in a broad range of products since the 1950s. This class, comprising of thousands of chemicals, have been used in many different products ranging from firefighting foam to personal care products and clothes. Even at relatively low levels of exposure, PFAS have been linked to various health effects in humans such as lower birth weight, increased serum cholesterol levels, and reduced antibody response to vaccination. Human biomonitoring data demonstrates ubiquitous exposure to PFAS across all age groups. This has been attributed to PFAS-contaminated water and dietary intake, as well as inadvertent ingestion of indoor dust for adults and toddlers. In utero exposure and breast milk have been indicated as important exposure pathways for foetuses and nursing infants. More recently, PFAS have been identified in a wide range of products, many of which come in contact with skin (e.g., cosmetics and fabrics). Despite this, few studies have evaluated dermal uptake as a possible route for human exposure and little is known about the dermal absorption potential of different PFAS. This article critically investigates the current state-of-knowledge on human exposure to PFAS, highlighting the lack of dermal exposure data. Additionally, the different approaches for dermal uptake assessment studies are discussed and the available literature on human dermal absorption of PFAS is critically reviewed and compared to other halogenated contaminants, e.g., brominated flame retardants and its implications for dermal exposure to PFAS. Finally, the urgent need for dermal permeation and uptake studies for a wide range of PFAS and their precursors is highlighted and recommendations for future research to advance the current understanding of human dermal exposure to PFAS are discussed.

In recent years, the cardiovascular toxicity of urban fine particulate matter (PM₂.₅) has sparked significant alarm. Mitochondria produce 90% of ATP and make up 30% of the volume of cardiomyocytes. Thus knowledge of myocardial mitochondrial dysfunction due to PM₂.₅ exposure is essential for further cardiotoxic effects. Here, the mechanism of PM₂.₅-induced cardiac hypertrophy through calcium overload and mitochondrial dysfunction was investigated in vivo and in vitro. Male and female BALB/c mice were given 1.28, 5.5, and 11 mg PM₂.₅/kg bodyweight weekly through oropharyngeal inhalation for four weeks and were assigned to low, medium, and high dose groups, respectively. PM₂.₅-induced myocardial edema and cardiac hypertrophy were detected in the high-dose group. Mitochondria were scattered and ruptured with abnormal ultrastructural morphology. In vitro experiments on human cardiomyocyte AC16 showed that exposure to PM₂.₅ for 24 h caused opened mitochondrial permeability transition pore --leading to excessive calcium production, decreased mitochondrial membrane potential, weakened mitochondrial respiratory metabolism capacity, and decreased ATP production. Nevertheless, the administration of calcium chelator ameliorated the mitochondrial damage in the PM₂.₅-treated group. Our in vivo and in vitro results confirmed that calcium overload under PM₂.₅ exposure triggered mTOR/AKT/GSK-3β activation, leading to mitochondrial bioenergetics dysfunction and cardiac hypertrophy.

Microplastics (MPs) are an emerging global concern as they are abundant in the environment and can act as vectors of various contaminants. However, whether and how MPs can be vectors of antibiotic resistance genes (ARGs), especially extracellular ARGs (eARGs), remains far from explicit. This study addresses the adsorption of both intracellular ARGs (iARGs) and eARGs by four types of MPs in municipal wastewater, and then explores the potential horizontal gene transfer of iARGs and eARGs exposed to MPs. Results indicate that though MPs significantly adsorbed both iARGs and eARGs, eARGs were adsorbed with a significantly higher fold enrichment (2.0–5.0 log versus 2.0–3.3 log) and rate (0.0056 min⁻¹ versus 0.0037 min⁻¹) than iARGs. While all four types of MPs adsorbed ARGs, polypropylene MPs showed the highest adsorption capacity for ARGs. Background constituents such as humic acid and antibiotics significantly inhibited adsorption of iARGs, but not eARGs on MPs. The presence of sodium chloride didn't significantly affect adsorption of iARGs or eARGs. The adsorption of ARGs was well explained by the extended Derjaguin–Landau–Verwey–Overbeek (XDLVO) interaction energy profile. Higher eARG adsorption was attributed to a lower energy barrier between MPs and eARGs than that between MPs and iARGs. Exposure to MPs enhanced horizontal gene transfer of both iARGs and eARGs by 1.5 and 2.0 times, respectively. The improved contact potential between donors and recipients, as well as the increased cell permeability of recipients induced the improved horizontal gene transfer by MPs. This study underscores the need to address ARG propagation through adsorption to MPs.

Soil fumigation continues to play an important role in soil disinfection, but tools to significantly reduce emissions while providing environmental benefits (e.g., biochar) are lacking. The objective of this study was to determine the effects of biochar products on fumigant 1,3-dichloropropene (1,3-D) and chloropicrin (CP) emissions, their distribution and persistence in soil, nematode control, and potential toxicity to plants in a field trial. Treatments included three biochar products [two derived from almond shells (ASB) at either 550 or 900 °C pyrolysis temperature and one from coconut shells (CSB) at 550 °C] at 30 and 60 t ha⁻¹, a surface covering with a low permeability film (TIF), and no surface covering (control). A mixture of 1,3-D (∼65%) and CP (∼35%) was injected to ∼60 cm soil depth at a combined rate of 640 kg ha⁻¹. All biochar treatments significantly reduced emissions by 38–100% compared to the control. The ASB (900 °C) at both rates reduced emissions as effectively as the TIF (by 99–100%). Both fumigant emission reduction and residue in surface soil were positively correlated with biochar's adsorption capacity while cucumber germination rate and dry biomass were negatively correlated with residual fumigant concentrations in surface soil. This research demonstrated the potential and benefits of using biochar produced from local orchard feedstocks to control fumigant emissions. Additional research is needed to maximize the benefits of biochar on fumigant emission reductions without impacting plant growth.

Xanthan gels were assessed to control the reductive dechlorination of hexachlorocyclohexanes (HCHs) and trichlorobenzenes (TCBs) in a strong permeability contrast and high velocity sedimentary aquifer. An alkaline degradation was selected because of the low cost of NaOH and Ca(OH)₂. The rheology of alkaline xanthan gels and their ability to deliver alkalinity homogeneously, while maintaining the latter, were studied. Whereas the xanthan gels behaved like non-Newtonian shear-thinning fluids, alkalinity and Ca(OH)₂ microparticles had detrimental effects, yet, the latter decreased with the shear-rate. Breakthrough curves for the NaOH and Ca(OH)₂ in xanthan solutions, carried out in the lowest permeability soil (9.9 μm²), demonstrated the excellent transmission of alkalinity, while moderate pressure gradients were applied. Injection velocities ranging from 1.8 to 3.8 m h⁻¹ are anticipated in the field, given the permeability range from 9.9 to 848.7 μm². Despite a permeability contrast of 8.7 in an anisotropic aquifer model, the NaOH and the Ca(OH)₂ both in xanthan gels spread only 5- and 7-times faster in the higher permeability zone, demonstrating that the delivery was enhanced. Moreover, the alkaline gels which were injected into a high permeability layer under lateral water flow, showed a persistent blocking effect and longevity (timescale of weeks), in contrast to the alkaline solution in absence of xanthan. Kinetics of alkaline dechlorination carried out on the historically contaminated soil, using the Ca(OH)₂ suspension in xanthan solution, showed that HCHs were converted in TCBs by dehydrodechlorination, whereas the latter were then degraded by reductive hydrogenolysis. Degradation kinetics were achieved within 30 h for the major and most reactive fraction of HCHs.

The surface modifications of nanoparticles (NPs), are well-recognized parameters that affect the toxicity, while there has no study on toxicity of Al₂O₃ NPs with different surface modification. Therefore, for the first time, this study pays attention to evaluating the toxicity and potential mechanism of pristine Al₂O₃ NPs (p-Al₂O₃), hydrophilic (w-Al₂O₃) and lipophilic (o-Al₂O₃) modifications of Al₂O₃ NPs both in vitro and in vivo. Applied concentrations of 10, 20, 40, 80,100 and 200 μg/mL for 24 h exposure on Caenorhabditis elegans (C. elegans), while 100 μg/mL of Al₂O₃ NPs significantly decreased the survival rate. Using multiple toxicological endpoints, we found that o-Al₂O₃ NPs (100 μg/mL) could induce more severe toxicity than p-Al₂O₃ and w-Al₂O₃ NPs. After uptake by C. elegans, o-Al₂O₃ NPs increased the intestinal permeability, easily swallow and further destroy the intestinal membrane cells. Besides, cytotoxicity evaluation revealed that o-Al₂O₃ NPs (100 μg/mL) are more toxic than p-Al₂O₃ and w-Al₂O₃. Once inside the cell, o-Al₂O₃ NPs could attack mitochondria and induce the over-production of reactive oxygen species (ROS), which destroy the intracellular redox balance and lead to apoptosis. Furthermore, the transcriptome sequencing and RT-qPCR data also demonstrated that the toxicity of o-Al₂O₃ NPs is highly related to the damage of cell membrane and the imbalance of intracellular redox. Generally, our study has offered a comprehensive sight to the adverse effects of different surface modifications of Al₂O₃ NPs on environmental organisms and the possible underlying mechanisms.

As a strong reductant and highly active alkali, hydrazine (N2H4) has been widely used in chemical industry, pharmaceutical manufacturing and agricultural production. However, its high acute toxicity poses a threat to ecosystem and human health. In the present study, a ratiometric fluorescent probe for the detection of N2H4 was designed, utilizing dicyanoisophorone as the fluorescent group and 4-bromobutyryl moiety as the recognition site. 4-(2-(3-(dicyanomethylene)-5,5-dimethylcyclohex-1-enyl) phenyl 4-brobutanoate (DDPB) was readily synthesized and could specially sense N2H4 via an intramolecular charge transfer (ICT) pathway. The cyclization cleavage reaction of N2H4 with a 4-bromobutyryl group released phenolic hydroxyl group and reversed the ICT process between hydroxy group and fluorophore, turning on the fluorescence in the DDPB-N2H4 complexes. DDPB exhibits a low cytotoxicity, reasonable cell permeability, a large Stokes shift (186 nm) and a low detection limit (86.3 nM). The quantitative determination of environmental water systems and the visualization fluorescence of DDPB test strips provides a strong evidence for the applications of DDPB. In addition, DDPB is suitable for the fluorescence imaging of exogenous N2H4 in HeLa cells and zebrafish.

Radon is a natural radioactive gas present in the environment, which is considered as the second most important lung cancer cause worldwide. Currently, radon gas is under focus and was classified as contaminant of emerging concern, which is responsible for serious biological/health effects in human. In presented work we propose the numerical model and analysis method for radon diffusion rate measurements and radon transport parameters determination. The experimental setup for radon diffusion was built in a classical, two chamber configuration, in which the radon source and outlet reservoirs are separated by the sample being tested. The main difference with previously known systems is utilization of only one radon detector, what was achieved by a careful characterization of the Rn-222 source and development of a numerical model, which allows for exact determination of radon transport parameters by fitting simulated radon concentration profile in the outlet reservoir to experimental data. For verification of the developed system, several insulation materials commonly used in building industry and civil engineering, as well as, common building materials (gypsum, hardened cement paste, concrete) were tested for radon diffusion rate through these barriers. The results of radon transmittance, permeability and diffusion coefficients for investigated materials are in compliance with values known previously from the literature. The analysis method is fast and efficient, and requires measurement period varying from a dozen or so hours up to 2–3 days depending on material properties. The described method is entirely based on a numerical analysis of the proposed differential equation model using freely available SCILAB software and experimental data obtained during sample measurements.

The adverse health effects of haze and particle-bound contaminants in China have recently caused increasing concern, and particle size plays a significant role in affecting human exposure to haze-correlated pollutants. To this background, size-segregated particulate samples (nine size fractions (<0.4, 0.4–0.7, 0.7–1.1, 1.1–2.1, 2.1–3.3, 3.3–4.7, 4.7–5.8, 5.8–9.0 and > 9.0 μm) were collected in three scale-gradient cities in northern China and analysed for a series of parent, oxygenated and chlorinated polycyclic aromatic hydrocarbons (PAHs, O-PAHs and Cl-PAHs). The total geometric mean concentrations of PAHs and O-PAHs for Beijing, Zhengzhou and Xinxiang were 98.1 and 27.2, 77.9 and 77.5, 41.0 and 30.7 ng m⁻³, respectively, which were 50–200 times higher than those for Cl-PAHs (0.5, 0.7 and 0.4 ng m⁻³). Though unimodal size-distribution patterns were found for all these contaminants for these three cities, PAHs represented distinctly higher concentration levels around the peak fraction (0.7–2.1 μm) than O-PAHs and Cl-PAHs. With 4–6 ring PAHs as dominant components in all samples, the percentage proportion of 2–3 ring PAHs (ranging from 1% to 26%) generally increased with particle size increasing, implying the sources of these compounds varied little among the 9 size fractions in all three cities. The International Commission on Radiological Protection (ICRP) model and permeability coefficient method were synchronously applied to the size-segregated data for inhalation and dermal exposure assessment to intensively estimate the human exposure doses to airborne PAHs. Further, the incremental lifetime cancer risk (ILCR) was calculated and it’s found that ILCR from inhalation was higher than that from dermal uptake for children and adults in Beijing and Zhengzhou, while the ILCR for Xinxiang presented a contrary pattern, revealing dermal uptake to be an equally significant exposure pathway to airborne PAHs compared to inhalation.

Functional state of intestinal barrier plays an important role for environmental animals in being against various toxicants. We investigated GATA transcriptional factor ELT-2-mediated intestinal response to nanopolystyrere in Caenorhabditis elegans. Prolonged exposure to nanopolystyrene (≥1 μg/L) induced an increase in expression of ELT-2, and intestinal RNA interference (RNAi) knockdown of elt-2 caused enhancement in intestinal permeability. Meanwhile, mutation of elt-2 resulted in susceptibility to nanopolystyrene toxicity, and ELT-2 functioned in intestine to regulate the nanopolystyrene toxicity. ERM-1, CLEC-63, and CLEC-85 were identified as targets of ELT-2 in regulating the nanopolystyrene toxicity. ERM-1 was required for maintaining functional state in intestinal barrier, and functioned synergistically with CLEC-63 or CLEC-85 to regulate nanopolystyrene toxicity. Therefore, activation of intestinal ELT-2 by nanopolystyrere could mediate a protective strategy to maintain the functional state of intestinal barrier. During this process, intestinal ELT-2 activated two different molecular signals (ERM-1 signal and CLEC-63/85 signal) for nematodes against the nanopolystyrene toxicity.