Ambient fine particulate matter (PM₂.₅) can change the expression profile of microRNAs (miRs), which may play important roles in mediating inflammatory responses. The present study attempts to investigate the roles of miR-146a-5p in regulating cytokine expression in a human monocytic leukemia cell line (THP-1). Four types of PM₂.₅ extracts obtained from Beijing, China, were subjected to cytotoxic tests in THP-1 cells. These four PM₂.₅ extracts included two water extracts collected from non-heating and heating season (WN and WH), and two organic extracts from non-heating and heating season (DN and DH). Firstly, the four PM₂.₅ extracts caused cytotoxicity, oxidative stress responses, cytokine gene expressions and interleukin 8 (IL-8) release in THP-1 cells, with WH showing the highest cytotoxicity, WN showing the highest oxidative stress and inflammatory responses. Additionally, we observed expression of miR-146a-5p was significantly increased, with the maximal response of six folds in WN group. Cellular autophagy was initiated by PM₂.₅ indicated by related protein and gene expressions. Both RNA interference and autophagy inhibitor were applied to interrupt autophagy process in THP-1 cells. Autophagy dysfunction could alleviate IL-8 expression, suggesting autophagy process regulated cytokine expression and inflammatory response caused by PM₂.₅. A chemical inhibitor was applied to inhibit the function of miR-146a-5p, and then the expressions of IL-8 and autophagic genes were significantly aggravated. Meanwhile, two target genes of miR-146a-5p, interleukin-1 associated-kinase-1 (IRAK1) and tumor-necrosis factor receptor-associated factor-6 (TRAF6) were increased dramatically, which also played important roles in regulation of autophagy. These data suggested miR-146a-5p negatively modulated cytokine expression caused by PM₂.₅ via autophagy process through the target genes of IRAK1 and TRAF6. Our findings raised the concerns of the changes of miR expression profile and following responses caused by PM₂.₅.

In this study, we analyzed 30 legacy and emerging poly- and perfluoroalkyl substances (PFASs) in paired atmospheric particulate and bark samples collected around a Chinese fluorochemical manufacturing park (FMP), with the aim to explore the sources of PFASs in tree bark. The results showed that PFASs in atmospheric particulate and tree bark samples were consistently dominated by perfluorooctanoate (mean 73 ng/g; 44 pg/m³), perfluorohexanoate (47 ng/g; 36 pg/m³), perfluorononanoate (9.1 ng/g; 8.8 pg/m³), and 10:2 fluorotelomer alcohol (10:2 FTOH; 5.6 ng/g; 12 pg/m³). Spatially, concentrations of C₈–C₁₂ perfluoroalkyl carboxylates (PFCAs) and 10:2 FTOH all showed a similar and exponentially decreased trend in both bark and atmospheric particulate samples with the increasing distance from the FMP. For the first time, we observed strongly significant (Spearman’s correlation coefficient = 0.53–0.79, p < 0.01) correlations between bark and atmospheric particulate concentrations for C₈–C₁₂ PFCAs and 10:2 FTOH over 1–2 orders of magnitude, suggesting that the continues trapping of atmospheric particulates resulted in the accumulation of these compounds in bark. Overall, this study provides the first evidence that atmospheric particulate is an obvious source of C₈–C₁₂ PFCAs and 10:2 FTOH in tree bark. This result may further contribute to the application of tree bark as an indicator of certain PFASs in atmospheric particulate.

Organochlorine pesticides (OCPs) are well known synthetic pesticides widely used in agricultural practices and public health program. Higher toxicity, slow degradation, and bioaccumulation are the significant challenges of OCPs. Due to its uses in agricultural and public health, contamination of drinking water and water table also increases day by day. Contaminated drinking water has become a significant issue and alarming signal for public health globally. The purpose of this study was to assess the recent trend of organochlorine pesticides (OCPs) level in drinking water and blood samples of the North Indian population and also to find out its association with glucose intolerance, lipid metabolism, and insulin resistance, which are known risk factors of type 2 diabetes mellitus (T2DM). A case-control study was conducted on 130 Non-Glucose intolerance (NGT), 130 pre-diabetes and 130 recently diagnosed T2DM subjects of the age group of 30–70 years. Patients consuming drinking water from the same source for at least ten years were included in this study for blood and water samples collection. Significantly higher levels of α-HCH, β-HCH, γ-HCH, p,p’-DDE, and o,p’-DDT were found in groundwater samples. However, in tap water samples, the level of α-HCH was found to be slightly higher than the permissible limit of 0.001. Among all recruited subjects consuming contaminated groundwater, 42% had T2DM, 38% pre-diabetes, and the remaining 20% were found normal. We also observed that OCP contamination in groundwater is higher than tap and filter water. The levels of β-HCH, p,p’-DDE, and o,p’-DDT were higher in the pre-diabetes and T2DM group than the NGT group. With an increase of OCPs level in groundwater, the blood OCPs level tends to increase T2DM risk. It depicts that the elevated OCPs level in consumed groundwater may contribute to increased risk for the development of T2DM after a certain period of exposure.

The effects of voltage intensity on the nutrient removal performance and microbial community in the iron electrolysis-integrated aerobic granular sludge (AGS) system were investigated over a period of 15 weeks. Results revealed that the application outcomes of iron electrolysis for AGS systems relied on voltage intensity. When a constant voltage of 1.5 V was applied, the sludge granulation was most obviously accelerated with a specific growth rate of the sludge diameter of 0.078 day⁻¹, and the removal efficiencies of total nitrogen (TN) and total phosphorus (TP) increased by 14.1% and 20.2%, respectively, compared to the control reactor (without the iron electrolysis-integration). Moreover, the AGS developed at different voltages included different microbial communities, whose shifts were driven by the Fe content and the average diameter of AGS. Both heterotrophic nitrifiers and mixotrophic denitrifiers were significantly enriched in the AGS developed at 1.5 V, which effectively enhanced TN removal. Together with the response of the functional genes involved in Fe, N, and P metabolism, the electrolytic iron-driven nutrient degradation pathway was further elaborated. Overall, this study clarified the optimum voltage condition when iron electrolysis was integrated into the AGS system, and revealed the enhancement mechanism of this coupling technology on nutrient removal during the treatment of low-strength municipal wastewater.

The objective of this study was to validate the hypothesis that increased serum concentrations of perfluoroalkyl substances (PFASs) cause kidney damage. A causal interpretative study was designed using the US 2003–2018 National Health and Nutrition Examination Survey (NHANES) datasets.Three statistical models, including multivariable linear regression, generalized additive model, and regression discontinuity model (RDM), were applied to the US 2003–2018 NHANES datasets to evaluate the causal relationship between the four PFAS agents and estimated glomerular filtration rate (eGFR). Directed acyclic graphs were plotted for a more valid causal inference.In the RDM, when the natural logarithm of each PFAS agent increases by 1 ng/mL after each cut-off value, eGFR decreased 4.63 mL/min/1.73 m² for perfluorooctanoic acid, 3.42 mL/min/1.73 m² for perfluorooctane sulfonic acid, 2.37 mL/min/1.73 m² for perfluorohexane sulfonic acid, and 2.87 mL/min/1.73 m² for perfluorononanoic acid. The possibility of reverse causation that increased serum PFAS concentration is the consequence of reduced eGFR, not the cause, was low, and an additional adjustment of potential confounders was not needed.This study contributes to the understanding of PFAS-induced kidney damage. Further longitudinal epidemiological and toxicological studies are recommended.

Organic ultraviolet filters (OUVFs) are used in a wide range of manufactured products including personal care (e.g. sunscreens) and plastic items. This review summarizes the available data regarding the toxic effects of OUVFs on marine and freshwater organisms and generates the predicted no-effect concentration (PNEC) values necessary for assessing ecological risk. Through a systematic search of the literature, 89 studies were identified and ecotoxicological data extracted. Collectively, these studies described toxicity testing with 39 OUVF from 10 structural classes, with derivatives of benzophenones (49%) and camphors (16%) most studied. There was a bias towards selecting freshwater species (61%), and evaluating single OUVF effects (87%) rather than OUVF mixtures. Short-term (acute) experimentation (58%) was marginally more common than long-term (chronic) testing (42%). Reproductive, developmental, genetic, and neurological toxicity were the most commonly identified effects in aquatic organism, and were associated with molecular interactions with steroid receptors, DNA, or the production of reactive oxygen species. Species sensitivity distribution and/or assessment factors were used to calculate PNECs for 22 OUVFs and the risk quotients for 12 OUVFs. When using maximum concentrations, high risk was observed for six OUVFs in marine environments (4-methylbenzylidene-camphor, octocrylene, padimate-O, benzophenone-1, and oxybenzone, ethylhexyl-4-methoxycinnamate), and for four OUVFs in freshwater environments (ethylhexyl-4-methoxycinnamate, octocrylene, avobenzone and oxybenzone). When using median concentrations, a risk to marine environments was observed for oxybenzone. The results of this review underline that there is limited knowledge of the pathological effects of OUVFs and their metabolites in aquatic environments, and this inhibits the development of informed water-quality guidelines.

The two forage species used in New Zealand pastoral agricultural systems, chicory (Cichorium intybus) and plantain (Plantago lanceolata) show differential ability to absorb and translocate cadmium (Cd) from roots to shoots. Chicory can accumulate Cd from even low Cd soils to levels that might exceed regulatory guidelines for Cd in fodder crops and food. Chicory and plantain were grown in soil-filled rhizocolumns under increasing Cd levels (0 (Control), 0.4, 0.8 and 1.6 mg Cd/kg soil) for 60 days and showed variable secretion of oxalic, fumaric, malic and acetic acids as a function of Cd treatment. Plant roots secrete such Low Molecular Weight Organic Acids into the rhizosphere soil, which can influence Cd uptake. Chicory showed significantly (P < 0.05) lower secretion of fumaric acid, and higher secretion of acetic acid than plantain at all Cd treatments. We propose that the significant secretion differences between the two species can explain the significantly (P < 0.05) higher shoot Cd concentration in chicory for all Cd treatments. Understanding the mechanism for increased uptake in chicory may lead to breeding or genetic modification which yield low Cd uptake cultivars needed to mitigate the risk of Cd accumulation in pastoral agricultural food chains from this increasingly important fodder crop.

Inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) is a type II acute-phase protein; however, the role of pulmonary ITIH4 after exposure to air pollution remains unclear. In this study, we investigated the role of ITIH4 in the lungs in response to air pollution. ITIH4 expression in bronchoalveolar lavage fluid (BAL) of 47 healthy human subjects and of Sprague-Dawley rats whole-body exposed to air pollution was determined, and the underlying antiapoptotic and matrix-stabilizing pathways in alveolar epithelial A549 cells induced by diesel exhaust particles (DEPs) as well as ITIH4-knockdown were investigated. We found that an interquartile range (IQR) increase in PM₂.₅ was associated with a decrease of 2.673 ng/mL in ITIH4, an increase of 1.104 pg/mL of 8-isoprostane, and an increase of 6.918 pg/mL of interleukin (IL)-6 in human BAL. In rats, increases in 8-isoprostane, IL-6, and p53 and a decrease in sirtuin-1 (Sirt1) in the lungs and decreases in ITIH4 in the BAL, lungs, and serum were observed after PM₂.₅ and gaseous exposure. ITIH4 levels in lung lysates were correlated with levels in BAL samples (r = 0.377, p < 0.01), whereas ITIH4 levels in BAL were correlated with IL-6 levels (r = −0.420, p < 0.01). ITIH4 expression was significantly reduced in alveolar epithelial A549 cells by DEP in a dose-dependent manner. A decrease in Sirt1 and increases in phosphorylated extracellular signal-regulated kinase (p-ERK) and caspase-3 were observed after DEP exposure and ITIH4-knockdown. In conclusion, air pollution decreased ITIH4 expression in the lungs, which was associated with alveolar epithelial cell senescence and apoptosis. ITIH4 could be a vital protein in regulating alveolar cell destruction and its inhibition after exposure to air pollution.

Copper (Cu) is a vital micronutrient required for numerous fundamental biological processes, but excessive Cu poses potential detrimental effects on public and ecosystem health. However, the molecular details linking endoplasmic reticulum (ER) stress and apoptosis in duck renal tubular epithelial cells have not been fully elucidated. In this study, duck renal tubular epithelial cells exposed to Cu sulfate (CuSO₄) (0, 100 and 200 μM) and a PERK inhibitor (GSK2606414, GSK, 1 μM) for 12 h were used to investigate the crosstalk between ER stress and apoptosis under Cu exposure. Cell and ER morphological and functional characteristics, intracellular calcium (Ca²⁺) levels, apoptotic rates, ER stress and apoptosis-related mRNA and protein levels were examined. The results showed that excessive Cu could cause ER expansion and swelling, increase the expression levels of ER stress-associated genes (PERK, eIF2α, ATF4 and CHOP) and proteins (p-PERK and CHOP), induce intracellular Ca²⁺ overload, upregulate the expression levels of apoptosis-associated genes (Bax, Bak1, Caspase9 and Caspase3) and the cleaved-Caspase3 protein, downregulate Bcl-xl and Bcl2 mRNA levels and trigger apoptosis. PERK inhibitor treatment could ameliorate the above changed factors caused by Cu. In conclusion, these findings indicate that excessive Cu could trigger ER stress via activation of the PERK/ATF4/CHOP signaling pathway and that ER stress might aggravate Cu-induced apoptosis in duck renal tubular epithelial cells.

Antibiotic resistance is exacerbated by the exchange of antibiotic resistance genes (ARGs) between microbes from diverse habitats. Plasmids are important ARGs mobile elements and are spread by horizontal gene transfer (HGT). In this study, we demonstrated the presence of multi-resistant plasmids from inhalable particulate matter (PM) and its effect on gene horizontal transfer. Three transferable multi-resistant plasmids were identified from PM in a hospital, using conjugative mating assays and nanopore sequencing. pTAir-3 contained 26 horizontal transfer elements and 10 ARGs. Importantly pTAir-5 harbored carbapenem resistance gene (blaOXA) which shows homology to plasmids from human and pig commensal bacteria, thus indicating that PM is a media for antibiotic resistant plasmid spread. In addition, 125 μg/mL PM₂.₅ and PM₁₀ significantly increased the conjugative transfer rate by 110% and 30%, respectively, and augmented reactive oxygen species (ROS) levels. Underlying mechanisms were revealed by identifying the upregulated expressional levels of genes related to ROS, SOS, cell membranes, pilus generation, and transposition via genome-wide RNA sequencing. The study highlights the airborne spread of multi-resistant plasmids and the impact of inhalable PM on the horizontal transfer of antibiotic resistance.