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.

Aquatic natural colloids are closely related to the environmental behavior of pollutants, which may affect their bioavailability in aquatic organisms. This study explored the potential mechanisms of the natural colloids at environmentally relevant concentrations affecting the bioaccumulation process of benzophenone-3 (BP3) in zebrafish (Danio rerio). The results of kinetic model fitting showed that the natural colloids decreased the uptake and loss rate of BP3 by zebrafish but prolonged the time to reach the cumulative equilibrium, eventually resulting in a higher cumulative concentration in zebrafish. According to the tissue concentration at equilibrium and the results of toxicokinetic analysis, the presence of high molecular colloids could enhance the bioaccumulation of freely dissolved BP3 due to its high desorption rate with BP3 in the intestines of fish, increasing the freely dissolved BP3 concentrations to which zebrafish were exposed. Both natural colloids and BP3 could enhance the cell permeability of zebrafish, which allowed colloid-bound BP3 to directly enter the fish and accumulate in its muscle. Besides, although both natural colloids and BP3 could cause the metabolic disorders in adult zebrafish, they affected the physiological and biochemical activities of zebrafish through different pathways. The disturbance of glutathione metabolism in zebrafish induced by natural colloids may be the reason for the diminished ability of zebrafish to clear and transform BP3 in the mixture system. The carrier effect of natural colloids and reduced clearance ability of zebrafish eventually increased the bioaccumulation of BP3 in zebrafish. This study highlights the significance of natural colloids at environmentally relevant concentrations on the biological effects of emerging contaminants in actual waters, however, natural colloids are always ignored in most field investigation of pollutants, which would ultimately lead to an underestimation of the true ecological risk of pollutants.

The current study provides an information on the combined effect of pollution with potentially toxic elements (PTEs) and polycyclic aromatic hydrocarbons (PAHs) in hydromorphic soils on the accumulation, growth, functional and morphological-anatomical changes of macrophyte plant, i.e., Phragmites australis Cav., as well as information about their bioindication status on the example of small rivers of the Azov basin. The territory of the lower reaches of the Kagalnik River is one of the small rivers of the Eastern Azov region was examined with different levels of PTEs contamination in soils, where the excess of the lithosphere clarkes and maximum permissible concentrations (MPC) for Mn, Cr, Zn, Pb, Cu, and Cd were found. The features of the 16 priority PAHs quantitative and qualitative composition in hydromorphic soils and P. australis were revealed. The influence of soil pollution on accumulation in P. australis, as well as changes in the morphological parameters were shown. It has been observed that morphometric changes in P. australis at sites experiencing the сontamination and salinity are reflected with the changes in the ultrastructure of plastids, mitochondria, and EPR elements of plant cells. PTEs accumulated in inactive organs and damaged cell structures. At the same time, PAHs penetrated through the biomembranes and violated their integrity, increased permeability, resulted cell disorganization, meristem, and conductive tissues of roots. The nature and extent of the structural alterations found are dependent on the type and extent of pollution in the examined regions and can be utilized as bioindicators for evaluating the degree of soil phytotoxicity characterized by the accumulation of PTE and PAHs.

Microplastics (MPs) have been shown to act as sorbent phases and thus carriers of organic chemicals in the aquatic environment. Therefore, concerns exist that MP ingestion increases the uptake and accumulation of organic chemicals by aquatic organisms. However, it is unclear if this pathway is relevant compared to other exposure pathways. Here we compared the bioconcentration capacity of two hydrophobic organic chemicals (i.e., chlorpyrifos and hexachlorobenzene) in a freshwater fish (Danio rerio) when exposed to chemicals through water only and in combination with contaminated polyethylene MPs. Additionally, a suite of biomarker analyses (acetylcholine esterase, glutathione S-transferase, alkaline phosphatase, catalase) was carried out to test whether MPs can enhance the toxic stress caused by chemicals. Two 14-day semi-static experiments (one for each chemical) were carried out with adult fish. Each experiment consisted of (1) a control treatment (no chemicals, no MPs); (2) a treatment in which fish were exposed to chlorpyrifos or hexachlorobenzene only through water; (3) a treatment in which fish were exposed to the chemicals through water and contaminated polyethylene MPs (100 mg MP/L). Two additional treatments were included for the biomarker analysis. These contained MPs at two different concentrations (5 and 100 mg MP/L) but no chemicals. The presence of contaminated MPs in contaminated water did not enhance but rather decreased the bioconcentration of both chemicals in fish compared to the treatment that contained contaminated water in absence of MPs. This was more pronounced for hexachlorobenzene, which is more hydrophobic than chlorpyrifos. Enzyme activity levels in fish were only significantly altered in the presence of MPs for alkaline phosphatase. This study indicates that MP presence in freshwater ecosystems is not expected to increase the risks associated with chemical bioconcentration in aquatic organisms and that other exposure pathways (i.e., uptake via respiration, skin permeability) may be of higher importance.

Particulate matter with aerodynamic diameter not larger than 2.5 μm (PM₂.₅) escalated the risk of respiratory diseases. Mitochondrial dysfunction may play a pivotal role in PM₂.₅-induced airway injury. However, the potential effect of PM₂.₅ on mitochondrial permeability transition pore (mPTP)-related airway injury is still unknown. This study aimed to investigate the role of mPTP in PM₂.₅-induced mitochondrial dysfunction in airway epithelial cells in vitro. PM₂.₅ significantly reduced cell viability and caused apoptosis in BEAS-2B cells. We also found PM₂.₅ caused cellular and mitochondrial morphological alterations, evidenced by the disappearance of mitochondrial cristae, mitochondrial swelling, and the rupture of the outer mitochondrial membrane. PM₂.₅ induced mPTP opening via upregulation of voltage-dependent anion-selective channel (VDAC), leading to deprivation of mitochondrial membrane potential, increased mitochondrial reactive oxygen species (ROS) generation and intracellular calcium level. PM₂.₅ suppressed mitochondrial respiratory function by reducing basal and maximal respiration, and ATP production. The mPTP targeting compounds cyclosporin A [CsA; a potent inhibitor of cyclophilin D (CypD)] and VBIT-12 (a selective VDAC1 inhibitor) significantly inhibited PM₂.₅-induced mPTP opening and apoptosis, and preserved mitochondrial function by restoring mitochondrial membrane potential, reducing mitochondrial ROS generation and intracellular calcium content, and maintaining mitochondrial respiration function. Our data further demonstrated that PM₂.₅ caused reduction in nuclear expressions of PPARγ and PGC-1α, which were reversed in the presence of CsA. These findings suggest that mPTP might be a potential therapeutic target in the treatment of PM₂.₅-induced airway injury.

Fine particulate matter (PM2.5) exposure is a significant cause of chronic obstructive pulmonary disease (COPD), but the detailed mechanisms involved in COPD remain unclear. In this study, we established PM2.5-induced COPD rat models and showed that PM2.5 induced pulmonary microvascular injury via accelerating vascular endothelial apoptosis, increasing vascular permeability, and reducing angiogenesis, thereby contributing to COPD development. Moreover, microvascular injury in COPD was validated by measurements of plasma endothelial microparticles (EMPs) and serum VEGF in COPD patients. We then performed m⁶A sequencing, which confirmed that altered N⁶-methyladenosine (m⁶A) modification was induced by PM2.5 exposure. The results of a series of experiments demonstrated that the expression of methyltransferase-like protein 16 (METTL16), an m⁶A regulator, was upregulated in PM2.5-induced COPD rats, while the expression of other regulators did not differ upon PM2.5-induction. To clarify the regulatory effect of METTL16-mediated m⁶A modification induced by PM2.5 on pulmonary microvascular injury, cell apoptosis, permeability, and tube formation, the m⁶A level in METTL16-knockdown pulmonary microvascular endothelial cells (PMVECs) was evaluated, and the target genes of METTL16 were identified from a set of the differentially expressed and m⁶A-methylated genes associated with vascular injury and containing predicted sites of METTL16 methylation. The results showed that Sulfatase 2 (Sulf2) and Cytohesin-1 (Cyth1) containing the predicted METTL16 methylation sites, exhibited higher m⁶A methylation and were downregulated after PM2.5 exposure. Further studies demonstrated that METTL16 may regulate Sulf2 expression via m⁶A modification and thereby contribute to PM2.5-induced microvascular injury. These findings not only provide a better understanding of the role played by m⁶A modification in PM2.5-induced microvascular injury, but also identify a new therapeutic target for COPD.

Whatever the exposure route, chemical, physical and biological pollutants modify the whole organism response, leading to nerve, cardiac, respiratory, reproductive, and skin system pathologies. Skin acts as a barrier for preventing pollutant modifications. This review aims to present the available scientific models, which help investigate the impact of pollution on the skin. The research question was “Which experimental models illustrate the impact of pollution on the skin in humans?” The review covered a period of 10 years following a PECO statement on in vitro, ex vivo, in vivo and in silico models. Of 582 retrieved articles, 118 articles were eligible. In oral and inhalation routes, dermal exposure had an important impact at both local and systemic levels. Healthy skin models included primary cells, cell lines, co-cultures, reconstructed human epidermis, and skin explants. In silico models estimated skin exposure and permeability. All pollutants affected the skin by altering elasticity, thickness, the structure of epidermal barrier strength, and dermal extracellular integrity. Some specific models concerned wound healing or the skin aging process. Underlying mechanisms were an exacerbated inflammatory skin reaction with the modulation of several cytokines and oxidative stress responses, ending with apoptosis. Pathological skin models revealed the consequences of environmental pollutants on psoriasis, atopic dermatitis, and tumour development. Finally, scientific models were used for evaluating the safety and efficacy of potential skin formulations in preventing the skin aging process or skin irritation after repeated contact. The review gives an overview of scientific skin models used to assess the effects of pollutants. Chemical and physical pollutants were mainly represented while biological contaminants were little studied. In future developments, cell hypoxia and microbiota models may be considered as more representative of clinical situations. Models considering humidity and temperature variations may reflect the impact of these changes.