Nowadays, marine ecosystems are under severe threat from the simultaneous presence of multiple stressors, including microplastics (MPs) and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (B[a]P). In addition to their presence in various marine compartments, there are increasing concerns on the potential capacity of MPs to sorb, concentrate and transfer these pollutants in the environment. Although their ecotoxicological impacts are currently evident, few works have studied the combined effects of these contaminants. Therefore, the major purpose of this work was to assess the toxicity of environmental relevant concentrations of MPs (<30 μm) and B[a]P, alone and in mixture, in the seaworm Hediste diversicolor by exploring their accumulation and hazardous biological effects for 3 and 7 days. Environmental MPs were able to increase B[a]P in a time-dependent manner. The obtained results showed that individual treatments, as well as co-exposure to contaminants, caused cytotoxicity and genotoxicity in the cœlomic fluid cells, while oxidative stress effects were observed at tissue and gene levels associated with alteration in neurotransmission. Overall, our findings provide additional clues about MPs as organic pollutant vectors in the marine environment, and contribute to a clearer understanding of their toxicological risk to aquatic invertebrates.

Percolation of water through oily sludge during storage and handling of the sludge can cause soil and groundwater contamination. In this study, oily sludge from a refinery was equilibrated with water to obtain the water-soluble fraction (WSF) of oily sludge. The WSF had dissolved organic carbon (DOC) of 166 mg/L. Human cell line-based toxicity assay revealed IC₅₀ of 41 mg/L indicating its toxic nature. The predominant compounds in WSF of oily sludge included isomers of methyl, dimethyl and trimethyl quinolines and naphthalenes along with phenol derivatives and other polynuclear aromatic hydrocarbons (PAHs). Biodegradation of WSF of oily sludge was studied using a consortium of Rhodococcus ruber, Bacillus sp. and Bacillus cereus isolated from the refinery sludge. The consortium of the three strains resulted in 70% degradation over 15 days with a first-order degradation rate of 0.161 day⁻¹. Further analysis of the WSF was performed using the stir-bar sorptive extraction (SBSE) followed by GCxGC-TOF MS employing a PDMS Twister. The GCxGC analysis showed that Bacillus cereus was capable of degrading the quinoline, phenol and naphthalene derivatives in WSF of oily sludge at a faster rate compared to pyridine and benzoquinoline derivatives. Quinoline, phenol, biphenyl, naphthalene, pyridine and benzoquinolines derivatives in the WSF of oily sludge were reduced by 87%, 92%, 88%, 77%, 40% and 62%, respectively with respect to the controls. The WSF of oily sludge contained, n-alkanes, ranging from n-C12 to n-C18 which were removed within 2 days of biodegradation.

Trace elements (TEs) from various natural and anthropogenic activities contaminate the agricultural water and soil environments. The use of nanoparticles (NPs) as nano-fertilizers or nano-pesticides is gaining popularity worldwide. The NPs-mediated fertilizers encourage the balanced availability of essential nutrients to plants compared to traditional fertilizers, especially in the presence of excessive amounts of TEs. Moreover, NPs could reduce and/or restrict the bioavailability of TEs to plants due to their high sorption ability. In this review, we summarize the potential influence of NPs on plant physiological attributes, mineral absorption, and TEs sorption, accumulation, and translocation. It also unveils the NPs-mediated TE scavenging-mechanisms at plant and soil interface. NPs immobilized TEs in soil solution effectively by altering the speciation of TEs and modifying the physiological, biochemical, and biological properties of soil. In plants, NPs inhibit the transfer of TEs from roots to shoots by inducing structural modifications, altering gene transcription, and strengthening antioxidant defense mechanisms. On the other hand, the mechanisms underpinning NPs-mediated TEs absorption and cytotoxicity mitigation differ depending on the NPs type, distribution strategy, duration of NP exposure, and plants (e.g., types, varieties, and growth rate). The review highlights that NPs may bring new possibilities for resolving the issue of TE cytotoxicity in crops, which may also assist in reducing the threats to the human dietary system. Although the potential ability of NPs in decontaminating soils is just beginning to be understood, further research is needed to uncover the sub-cellular-based mechanisms of NPs-induced TE scavenging in soils and absorption in plants.

We investigated the biological response of soluble organic fraction (SOF) and water-soluble fraction (WSF) extracted from particulate matter (PM) emitted by an automotive diesel engine operating in a representative urban driving condition. The engine was fueled with ultra-low sulfur diesel (ULSD), and its binary blends by volume with 13% of butanol (Bu13), and with hydrotreated vegetable oil (HVO) at 13% (HVO13) and 20% (HVO20). Cytotoxicity, genotoxicity, oxidative DNA damage and ecotoxicity tests were carried out, and 16 polycyclic aromatic hydrocarbons (PAH) expressed as tbenzo(a)pyrene total toxicity equivalent (BaP-TEQ) were also analyzed. The Hepatocarcinoma epithelial cell line (HepG2) was exposed to SOF for 24 h and analyzed using comet assay, with the inclusion of formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (Endo III) to recognize oxidized DNA bases. The WSF was evaluated through acute ecotoxicity tests with the aquatic microcrustacean Daphnia pulex (D. Pulex). Results showed that there was no cytotoxic activity for all tested SOF concentrations. Genotoxic responses by all the SOF samples were at same level, except for the HVO13 which was weaker in the absence of the enzymes. The addition of the FPG and Endo III enzymes resulted in a significant increase in the comet tail, indicating that the DNA damage from SOF for all tested fuel blends involves oxidative damage including a higher level of oxidized purines for ULSD and Bu13 in comparison with HVO blends, but the oxidized pyrimidines for HVO blends were slightly higher compared to Bu13. The WSF did not show acute ecotoxicity for any of the fuels. Unlike other samples, Bu13-derived particles significantly increase the BaP-TEQ. The contribution to the genotoxic activity and oxidative DNA from SOF was not correlated to BaP-TEQ, which means that the biological activity of PM might be affected also by other toxic compounds present in particulate phase.

Triphenyl phosphate (TPHP) is a frequently used flame retardant and indoor semi-volatile pollutant exposing humans with endocrinal disrupting effects. However, its respiratory tract toxicity remains unclear. Herein, we mainly focused on exploring the cytotoxicity of TPHP to the cells from five different parts of the human respiratory tract (from top to bottom): human nasal epithelial (HNEpC) cells, human bronchial epithelial (16HBE) cells, normal nasopharyngeal epithelial (NP69) cells, human lung epithelial cells (Beas-2B) cells, and human lung fibrocells (HFL1 cells) cells. The cell viability, micronucleus induction, endoplasmic reticulum stress gene, intracellular Ca²⁺ concentration, mitochondrial membrane potential (MMP) were investigated in short-term as well as extended exposure of TPHP. HFL1 and HNEpC cells were found to be irreversible damage, while other three type cells achieved homeostasis through self-rescue. Moreover, expression of downstream genes of Nrf2 signaling pathway were upregulated for 1.3–7.0 times and glutathione detoxification enzyme activity changed for 2–10 (U/mg protein) in HNEpC cells. Furthermore, the vascular endothelial growth factor (VEGF), a disease-related factor, increased 1.0–3.5-fold in HNEpC cells. RNA-sequencing results suggested that protein linkage recombination, molecular function regulation and metabolic processes signal pathway were all affected by TPHP exposure in HNEpC. This is a first report to compare respiratory cytotoxicity in whole human respiratory tract under OPFR exposure and found HNEpC cells were the most sensitive target of TPHP. Molecular biological mechanisms uncovered that TPHP exposure in HNEpC can induce the activation of MAPK signal pathway and demonstrate potential respiratory growth differentiation and stress disorder in human nasal cells upon TPHP exposure.

Systemic studies on the bioremediation of co-contaminated PAHs and heavy metals are lacking, and this paper provides an in-depth review on the topic. The released sources and transport of co-contaminated PAHs and heavy metals, including their co-occurrence through formation of cation-π interactions and their adsorption in soil are examined. Moreover, it is investigated that co-contamination of PAHs and heavy metals can drive a synergistic positive influence on bioremediation through enhanced secretion of extracellular polymeric substances (EPSs), production of biosynthetic genes, organic acid and enzymatic proliferation. However, PAHs molecular structure, PAHs-heavy metals bioavailability and their interactive cytotoxic effects on microorganisms can exert a challenging influence on the bioremediation under co-contaminated conditions. The fluctuations in bioavailability for microorganisms are associated with soil properties, chemical coordinative interactions, and biological activities under the co-contaminated PAHs-heavy metals conditions. The interactive cytotoxicity caused by the emergence of co-contaminants includes microbial cell disruption, denaturation of DNA and protein structure, and deregulation of antioxidant biological molecules. Finally, this paper presents the emerging strategies to overcome the bioavailability problems and recommends the use of biostimulation and bioaugmentation along with the microbial immobilization for enhanced bioremediation of PAHs-heavy metals co-contaminated sites. Better knowledge of the bioremediation potential is imperative to improve the use of these approaches for the sustainable and cost-effective remediation of PAHs and heavy metals co-contamination in the near future.

Cellular transport of metal nanoparticles (NPs) is critical in determining their potential toxicity, but the transformation of metal ions released from the internalized NPs is largely unknown. Cu-based NPs are the only metallic-based NPs that are reported to induce higher toxicity compared with their corresponding ions, likely due to their unique cellular turnover. In the present study, we developed a novel gold core to differentiate the particulate and ionic Cu in the Cu₂O microparticles (MPs), and the kinetics of bioaccumulation, exocytosis, and cytotoxicity of Au@Cu₂O MPs to zebrafish embryonic cells were subsequently studied. We demonstrated that the internalized MPs were rapidly dissolved to Cu ions, which then undergo lysosome-mediated exocytosis. The uptake rate of smaller MPs (130 nm) was lower than that of larger ones (200 nm), but smaller MPs were dissolved much quickly in cells and therefore activated the exocytosis more quickly. The rapid release of Cu ions resulted in an immediate toxic action of Cu₂O MPs, while the cell deaths mainly occurred by necrosis. During this process, the buffering ability of glutathione greatly alleviated the Cu toxicity. Therefore, although the turnover of intracellular Cu at a sublethal exposure level was hundred times faster than the basal values, labile Cu(I) concentration increased by only 2 times at most. Overall, this work provided new insights into the toxicity of copper NPs, suggesting that tolerance to Cu-based NPs depended on their ability to discharge the released Cu ions.

The association between polycyclic aromatic hydrocarbons (PAHs) and male reproductive dysfunction has attracted increasing attention. The purpose of this study was to compare the male reproductive toxicity of multiple PAHs and to investigate the underlying molecular mechanisms. TM4 cells (mouse testicular Sertoli cells, SCs) were treated with benzo(a)pyrene (BaP), pyrene (Py), fluoranthene (Fl) and phenanthrene (Phe) (0, 0.1, 1, 10, 50, or 100 μM) for varying time points (4, 12, 24, or 48 h), and male C57BL/6 mice were administered BaP and Py (0, 10, 50, or 100 mg/kg body weight) for 14 days based on the cell experimental results. Histopathological examination, western blotting, ELISA, biochemical assays, RT–PCR, flow cytometry, JC-1 staining and trans-epithelium electrical resistance (TEER) measurements were used to assess apoptosis, blood-testis barrier (BTB) integrity, intracellular calcium ([Ca²⁺]ᵢ) concentrations and oxidative stress (OS). The results revealed that the mRNA levels and enzymatic activities of CYP450 and GST family members; levels of ROS, MDA, cleaved caspase 3 (c-caspase 3), caspase 9, Bax, and cytochrome C (CytC); and numbers of TUNEL-positive cells were significantly increased by BaP and Py, while levels of AhR, GSH, SOD, CAT, Bcl-2 and ΔΨm were decreased. Additionally, BaP and Py notably interfered with tight junctions (TJs) and adherens junctions (AJs) in the BTB. Intriguingly, BaP, but not Py, induced [Ca²⁺]ᵢ overload and gap junction (GJ) destruction. There was no dramatic effect of Fl and/or Phe on any of the above parameters except that slight cytotoxicity was observed with higher doses of Fl. Collectively, these findings showed that BaP and Py elicited SC apoptosis and BTB disruption involving mitochondrial dysfunction and OS, but [Ca²⁺]ᵢ fluctuation and GJ injury were only observed with BaP-induced reproductive toxicity. The male reproductive toxicity of the selected PAHs was ranked in the order of BaP > Py > Fl > Phe.

Although the hazards of microplastics (MPs) have been quite well explored, the aberrant metabolism and the involvement of the autophagy pathway as an adverse response to environmental MPs in benthic organisms are still unclear. The present work aims to assess the impact of different environmental MPs collected from the south coast of the Mediterranean Sea, composed by polyethylene (PE), polyethylene vinyl acetate (PEVA), low-density polyethylene (LDPE), high-density polyethylene (HDPE), polypropylene (PP) and polyamide (PA) on the metabolome and proteome of the marine polychaete Hediste diversicolor. As a result, all the microplastic types were detected with Raman microspectroscopy in polychaetes tissues, causing cytoskeleton damage and induced autophagy pathway manifested by immunohistochemical labeling of specific targeted proteins, through Tubulin (Tub), Microtubule-associated protein light chain 3 (LC3), and p62 (also named Sequestosome 1). Metabolomics was conducted to further investigate the metabolic alterations induced by the environmental MPs-mixture in polychaetes. A total of 28 metabolites were differentially expressed between control and MPs-treated polychaetes, which showed elevated levels of amino acids, glucose, ATP/ADP, osmolytes, glutathione, choline and phosphocholine, and reduced concentration of aspartate. These novel findings extend our understanding given the toxicity of environmental microplastics and unravel their underlying mechanisms.

Iron particles present in drinking water distribution systems (DWDSs) could cause discoloration, while organic pollutants in DWDSs, such as perfluorooctanoic acid (PFOA), could be enriched by iron particles. However, little is known about the enhanced effects of PFOA and iron particles in DWDSs. To fill in these knowledge gaps, herein, iron-PFOA (FEP) particles were generated using residual chlorine as an oxidant in drinking water conditions and then separated into different sizes (ranging from small to large: FEP-S, FEP-M ，and FEP-L). FEP-S harbored the greatest cytotoxicity among the sizes. Interestingly, our data revealed that the PFOA released from FEP particles transformed into PFOS (perfluorooctane sulfonate) upon digestion in the gastrointestinal environment (GI), and FEP-L bored the strongest transformation, showing a toxicity profile that was distinct from that of FEP-S. Furthermore, mechanistic studies revealed that FEP per se should be accountable for the conversion of PFOA to PFOS dependent on the generation of hydroxyl radicals (·OH) in GI, and that FEP-L revealed the greatest production of ·OH. Collectively, these results showed how iron particles and PFOA could result in enhanced toxicity effects in drinking water: (i) PFOA could increase the toxicity of iron particles by reducing particle size and inducing higher generation of ·OH; (ii) iron particles could induce the transformation of PFOA into more toxic PFOS through digestion.