Several environmental pollutants, including pesticides, herbicides and persistent organic pollutants play an important role in the development of chronic diseases. However, most studies have examined environmental pollutants toxicity in target organisms or using a specific toxicological test, losing the real effect throughout the ecosystem. In this sense an integrative environmental risk of pollutants assessment, using different model organisms is necessary to predict the real impact in the ecosystem and implications for target and non-target organisms.The objective of this study was to use alachlor, a chloroacetanilide herbicide responsible for chronic toxicity, to understand its impact in target and non-target organisms and at different levels of biological organization by using several model organisms, including membranes of dipalmitoylphosphatidylcholine (DPPC), rat liver mitochondria, bacterial (Bacillus stearothermophilus), plant (Lemna gibba) and mammalian cell lines (HeLa and neuro2a).Our results demonstrated that alachlor strongly interacted with membranes of DPPC and interfered with mitochondrial bioenergetics by reducing the respiratory control ratio and the transmembrane potential. Moreover, alachlor also decreased the growth of B. stearothermophilus and its respiratory activity, as well as decreased the viability of both mammalian cell lines. The values of TC₅₀ increased in the following order: Lemna gibba < neuro2a < HeLa cells < Bacillus stearothermophilus. Together, the results suggest that biological membranes constitute a putative target for the toxic action of this lipophilic herbicide and point out the risks of its dissemination on environment, compromising ecosystem equilibrium and human health.

and perfluorinated alkyl substances (PFASs) are ubiquitously detected all around the world. Herein, for the first time, concentrations of 16 selected legacy and emerging PFASs are reported for sediment and edible fish collected from the Saudi Arabian Red Sea. Mean concentrations varied from 0.57 to 2.6 μg kg⁻¹ dry weight (dw) in sediment, 3.89–7.63 μg kg⁻¹ dw in fish muscle, and 17.9–58.5 μg kg⁻¹ dw in fish liver. Wastewater treatment plant effluents represented the main source of these compounds and contributed to the exposure of PFAS to biota. Perfluorooctane sulfonate (PFOS) was the most abundant compound in sediment and fish tissues analysed, comprising between 42 and 99% of the ∑₁₆PFAS. The short chain perfluorobutanoate (PFBA) was the second most dominant compound in sediment and was detected at a maximum concentration of 0.64 μg kg⁻¹ dw. PFAS levels and patterns differed between tissues of investigated fish species. Across all fish species, ∑₁₆PFAS concentrations in liver were significantly higher than in muscle by a factor ranging from 3 to 7 depending on fish species and size. The PFOS replacements fluorotelomer sulfonate (6:2 FTS) and perfluorobutane sulfonate (PFBS) exhibited a bioaccumulation potential in several fish species and 6:2 FTS, was detected at a maximum concentration of 7.1 ± 3.3 μg kg⁻¹ dw in a doublespotted queenfish (Scomberoides lysan) liver. PFBS was detected at a maximum concentration of 2.65 μg kg⁻¹ dw in strong spine silver-biddy (Gerres longirostris) liver. The calculated dietary intake of PFOS, perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA) and perfluorohexane sulfonic acid (PFHxS) exceeded the safety threshold established by the European Food Safety Authority (EFSA) in 2020 in doublespotted queenfish muscle, indicating a potential health risk to humans consuming this fish in Jeddah, Saudi Arabia.

PM₂.₅ has a major impact on the gastrointestinal system, but the specific mechanism behind this action is not fully understood. Current studies have focused on the relationship between PM₂.₅ and intestinal flora disorder, while ignoring the important influence of diet on gut microbes. In this study, SD rats were fed either a normal, high-fat, or high-carbohydrate diet for two months and exposed to PM₂.₅ (7 mg/kg b.w.) by intratracheal instillation. The results showed that the body and kidney weights of the rats in the high-fat diet group were significantly increased relative to those with a normal diet, and changes in the intestinal microbes and metabolites induced by PM₂.₅ were observed. Rats in the high-carbohydrate diet group had a significant response, and the diversity and richness indices of the flora were reduced (p < 0.05); additionally, intestinal Biffidobacterium and Lactobacillus were enriched, while many endogenous metabolites were found. Some amino acids derivatives and long-chain fatty acids were increased (p < 0.05). Both diet structure and PM₂.₅ exposure can affect the composition of gut microbiota, and intestinal metabolites may be associated with cell membrane damage when a high-carbohydrate diet interacts with PM₂.₅. This study considers multiple dietary factors to further supplement the evidence of intestinal damage via PM₂.₅.

The effect of land application of sewage sludge on soil microbial communities and the possible spread of antibiotic- and metal-resistant strains and resistance determinants were evaluated during a 720-day field experiment. Enzyme activities, the number of oligotrophic bacteria, the total number of bacteria (qPCR), functional diversity (BIOLOG) and genetic diversity (DGGE) were established. Antibiotic and metal resistance genes (ARGs, MRGs) were assessed, and the number of cultivable antibiotic- (ampicillin, tetracycline) and heavy metal- (Cd, Zn, Cu, Ni) resistant bacteria were monitored during the experiment. The application of 10 t ha⁻¹ of sewage sludge to soil did not increase the organic matter content and caused only a temporary increase in the number of bacteria, as well as in the functional and structural biodiversity. In contrast to expectations, a general adverse effect on the tested microbial parameters was observed in the fertilized soil. The field experiment revealed a significant reduction in the activities of alkaline and acid phosphatases, urease and nitrification potential. Although sewage sludge was identified as the source of several ARGs and MRGs, these genes were not detected in the fertilized soil. The obtained results indicate that the effect of fertilization based on the recommended dose of sewage sludge was not achieved.

We investigated the fates of seven neonicotinoids (NNIs) in full-scale drinking water treatment plants and assessed human exposure to NNIs through consuming drinking water. The total NNI concentrations in raw water and treated water samples from the drinking water treatment plants were 20.4–166 ng/L (median 118 ng/L) and 1.11–94.7 ng/L (median 20.4 ng/L), respectively. The dinotefuran (DIN) concentrations in raw water collected in different seasons were different, and the highest DIN concentration was found in summer. The drinking water treatment processes removed >91% of the NNIs except DIN and thiamethoxam (THIAM), for which the mean removal rates were 70% and 74%, respectively. The removal rates for all of the NNIs were higher for the granular activated carbon filtration process (mean 83.5%) than the other drinking water treatment plant processes (coagulation/sedimentation 22.3%, ozonation 29.2%). However, the removal rates in the granular activated carbon process were lower for DIN and THIAM (61.0% and 59.2%, respectively) than the other NNIs. Significant correlations were found between the NNI removal rates and physicochemical properties (solubility in water and log (octanol–water partition coefficient)). The estimated mean human exposure to NNIs in drinking water was 0.528 ng/(kg body weight d).

The methylcytosine dioxygenase Ten-eleven translocation 1 (TET1) is an important regulator for the balance of DNA methylation and hydroxymethylation through various pathways. Increasing evidence has suggested that TET1 probably involved in DNA methylation and demethylation dysregulation during chemical carcinogenesis. However, the role and mechanism of TET1 during lung cancer remains unclear. In this study, we found that TET1 expression was significantly down-regulated and the methylation level was significantly up-regulated in 3-methylcholanthrene (3-MCA) induced cell malignant transformation model, rat chemical carcinogenesis model, and human lung cancer tissues. Demethylation experiment further confirmed that DNA methylation negatively regulated TET1 gene expression. TET1 overexpression inhibited cell proliferation, migration and invasion in vitro and in vivo, while knockdown of TET1 resulted in an opposite phenotype. DNA hydroxymethylation level in the promoter region of base excision repair (BER) pathway key genes XRCC1, OGG1, APEX1 significantly decreased and the degree of methylation gradually increased in malignant transformed cells. After differential expression of TET1, the level of hydroxymethylation, methylation and expression of these genes also changed significantly. Furthermore, TET1 binds to XRCC1, OGG1, and APEX1 to maintain them hydroxymethylated. Blockade of BER pathway key gene alone or in combination significantly diminished the effect of TET1. Our study demonstrated for the first time that TET1 expression is regulated by DNA methylation and TET1-mediated hydroxymethylation regulates BER pathway to inhibit the proliferation, migration and invasion during 3-MCA-induced lung carcinogenesis. These results suggested that TET1 gene can be a potential biomarker and therapy target for lung cancer.

We used real-world exposure scenarios to evaluate the effect of six ambient air pollutant (PM₂.₅, PM₁₀, NO₂, SO₂, CO, and O₃) exposure on renal function among older adults without chronic kidney disease (CKD). We recruited 169 older adults without CKD in Beijing, China, for a longitudinal study from 2016 to 2018. The Modification of Diet in Renal Disease (MDRD) and the Chronic Kidney Disease Epidemiology Collaboration (EPI) equations were employed to derive the estimated glomerular filtration rate (eGFR). A linear mixed-effects model with random intercepts for participants was employed to determine the effects of air pollutants on renal function evaluated on the basis of eGFR and urinary albumin/creatinine ratio at different exposure windows (1-, 2-, 3-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages). An interquartile range (IQR) increase in NO₂ for was associated with significant decreases of in eGFR (MDRD equation) [percentage changes: −4.49 (95% confidence interval: −8.44, −0.37), −5.51 (−10.43, −0.33), −2.26 (−4.38, −0.08), −3.71 (−6.67, −0.65), −5.44 (−9.58, −1.11), −5.50 (−10.24, −0.51), −6.15 (−10.73, −1.33), and −6.34 (−11.17, −1.25) for 1-, 2-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages, respectively] and in eGFR (EPI equation) [percentage changes: −5.04 (−7.09, −2.94), −6.25 (−8.81, −3.62), −5.16 (−7.34, −2.92), −5.10 (−7.85, −2.28), −5.83 (−8.23, −3.36), −6.04 (−8.55, −3.47) for 1-, 2-, 14-, 28-, 45-, and 60-days moving averages, respectively]. In two-pollutant model, only the association of NO₂ exposure with eGFR remained robust after adjustment for any other pollutant. This association was stronger for individuals with hypertension for the EPI equation or BMI <25 kg/m² for the MDRD equation at lags 1 and 1–2. Our findings suggest that NO₂ exposure is associated with eGFR reduction among older adults without CKD for short (1-, 2-days) and medium (14-, 28-, 45-, 60-days) term exposure periods; thus, NO₂ exposure may contribute to renal impairment.

Advanced oxidation processes (AOPs) based on peroxymonosulfate (PMS) activation have attracted increasing attention in recent years for organic pollutants removal. Herein, we put forward a facile method to form cobalt phosphide/carbon composite for PMS activation. Combining impregnation approach with pyrolysis treatment enabled the formation of Co₂P/biochar composites using baker’s yeast and Co²⁺ as precursors. The as-synthesized products exhibited excellent catalytic activity for sulfamethoxazole (SMX) degradation over the pH range 3.0–9.0 b y activating PMS. For example, 100% of SMX (20 mg L⁻¹) removal was achieved in 20 min with catalyst dosage of 0.4 g L⁻¹ and PMS loading of 0.4 g L⁻¹. Near zero Co²⁺ leaching was observed during catalytic reaction, which remarkably lowered the toxic risk of transition metal ion in water. Meanwhile, the reusability of catalyst could be attained by thermal treatment. SMX degradation intermediates were identified by liquid chromatography-mass spectrometry (LC-MS), which facilitated the proposal of possible SMX degradation pathways. Ecological Structure Activity Relationships (ECOSAR) analysis indicated that SMX degradation intermediates may not pose ecological toxicity to the environment. Further investigation verified that Co₂P/biochar composites could set off PMS activation not only for the degradation of SMX but also for other sulfonamides. In this study, we not only developed a facile method of utilizing environmental-benign biomass for transition metal phosphide/carbon composite formation, but also achieved highly efficient antibiotic elimination by PMS-based AOP.

To identify the role of gut microbiota in human health risk assessment, the bioaccessibility of heavy metals in 14 soil samples were determined in simulated gastrointestinal fluids. Compared to the small intestinal phase, the bioaccessibility values of the colon phase varied, either increased by 3.5-fold for As, by 2.2-fold for Cr, and by 1.6-fold for Ni, or reduced by 4.4-fold for Cu, respectively. The colon incubation with adult gut microbiota yielded higher bioaccessibility value of As (1.3 times) and Fe (3.4 times) than that of the child in most soil samples. Colon bioaccessibility was about 60% greater of Cd for the adult and 30% higher of Cr for the child. Congruent data on the bioaccessibility of Cu and Ni was observed. In addition, correlation analysis indicated that in vitro bioaccessibility was primarily related to total concentrations of heavy metals in soils, followed by soil pH and active Fe/Mn oxide. Significantly, risk assessment calculated based on colon bioaccessibility indicated that the target hazard quotient (THQ > 1) of As was presented in 3 soil samples for the adult (1.05–3.35) and in 9 soil samples for the child (1.06–26.93). The hazard index (HI) of the child was 4.00 on average, greater than that of the adult (0.62), primarily due to the contribution of As and Cd. It suggested non-carcinogenic risks are likely to occur in children through typical hand-to-mouth behavior. The adjustment of colon bioaccessibility will result in more accurate risk assessment of human exposure to heavy metals from oral ingestion of contaminated soils.

The continuous influx of opioid compounds into aquatic environments has become an increasing and persistent concern, due to their extensive use. This is especially alarming as wastewater treatment plants (WWTPs) are unable to completely remove them. Despite the reported health concerns, the occurrence of opioid compounds in the environment has not received much attention. The present study investigates the occurrence of 19 opioids in four WWTPs and their respective receiving water bodies. All wastewater samples revealed opioids at concentration ranging from ng/L to μg/L with most influents having higher concentrations than effluents. WWTPs appeared to perform poorly (p > 0.05 between influents and effluents), and were unable to remove some opioids including Methadone (−27.3%) from the Leeuwkuil WWTP, Codeine (−21.7%) and Thebaine (−3.77%) from the Sandspruit WWTP, and Hydrocodone (−1.06%) from the Meyerton WWTP, respectively. Samples collected from the Leeuwkuil WWTP were the most contaminated, with eighteen out of nineteen opioid analogues exceeding 1 μg/L. Upstream surface water contained less opioids (most < LOQ) than downstream (p < 0.05), with Hydrocodone, Oxycodone, Hydromorphone, Fentanyl, Ketamine and Dihydrocodeine not detected. The occurrence of high concentrations of opioid analogues in downstream surface water (298 ng/L −10.8 μg/L for Klip River, 4.49 ng/L −13.1 μg/L for Vaal River, 70.5 ng/L −10.0 μg/L for Soutspruit River and 8.0 ng/L – 2.43 μg/L for Sun Spruit River) was directly linked to their mass loads in the respective wastewater effluent samples.