Assessing the Impact of PM2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability.

Inhalation of fine particulate matter PM2.5-bound arsenic (PM2.5-As) may cause significant cardiovascular damage, due to its high concentration, long transmission range, and good absorption efficiency in organisms. However, both the contribution and the effect of the arsenic exposure pathway, with PM2.5 as the medium, on cardiovascular system damage in nonferrous smelting sites remain to be studied. In this work, a one-year site sample collection and analysis work showed that the annual concentration of PM2.5-As reached 0.74 µg/m3, which was 120 times the national standard. The predominant species in the PM2.5 samples were As (V) and As (III). A panel study among workers revealed that PM2.5-As exposure dominantly contributed to human absorption of As. After exposure of mice to PM2.5-As for 8 weeks, the accumulation of As in the high exposure group reached equilibrium, and its bioavailability was 24.5%. A series of animal experiments revealed that PM2.5-As exposure induced cardiac injury and dysfunction at the environmental relevant concentration and speciation. By integrating environmental and animal exposure assessments, more accurate health risk assessment models exposed to PM2.5-As were established for metal smelting areas. Therefore, our research provides an important scientific basis for relevant departments to formulate industry supervision, prevention and control policies.

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM2.5 components.

Fine particulate matter (PM2.5) is globally recognized for its adverse implications on human health. Yet, remain limited the individual contribution of particular PM2.5 components to its toxicity, especially considering regional disparities. Moreover, prevention solutions for PM2.5-associated health effects are scarce. In the present study, we comprehensively characterized and compared the primary PM2.5 constituents and their altered metabolites from two locations: Taiyuan and Guangzhou. Analysis of year-long PM2.5 samples revealed 84 major components, encompassing organic carbon, elemental carbon, ions, metals, and organic chemicals. PM2.5 from Taiyuan exhibited higher contamination, associated health risks, dithiothreitol activity, and cytotoxicities than Guangzhou's counterpart. Applying metabolomics, BEAS-2B lung cells exposed to PM2.5 from both cities were screened for significant alterations. A correlation analysis revealed the metabolites altered by PM2.5 and the critical toxic PM2.5 components in both regions. Among the PM2.5-down-regulated metabolites, phosphocholine emerged as a promising intervention for PM2.5 cytotoxicities. Its supplementation effectively attenuated PM2.5-induced energy metabolism disorder and cell death via activating fatty acid oxidation and inhibiting Phospho1 expression. The highlighted toxic chemicals displayed combined toxicities, potentially counteracted by phosphocholine. Our study offered a promising functional metabolite to alleviate PM2.5-induced cellular disorder and provided insights into the geo-based variability in toxic PM2.5 components.

A large-scale survey of urinary parabens and triclocarban in the Chinese population as well as the influencing factors and health risks.

Parabens and triclocarban are widely applied as antimicrobial preservatives in foodstuffs, pharmaceuticals, cosmetics, and personal care products. However, few studies have been conducted on large-scale biomonitoring of parabens and triclocarban in the Chinese general population. In the present study, there were 1157 urine samples collected from 26 Chinese provincial capitals for parabens and triclocarban measurement to evaluate the exposure levels, spatial distribution, and influencing factors, as well as associated health risks in the Chinese population. The median concentrations of Σparabens and triclocarban were 14.0 and 0.03 µg/L, respectively. Methyl paraben was the predominant compound. Subjects in western China were more exposed to parabens, possibly due to climate differences resulting in higher consumption of personal care products. Subjects who were female, aged 18-44 years, or had a higher education level were found to have higher paraben concentrations. The frequency of drinking bottled water was positively associated with paraben exposure. The assessment of health risk based on urinary paraben concentrations indicated that 0.8 % of the subjects had a hazard index exceeding one unit, while Monte Carlo analysis suggested that 3.6 % of the Chinese population exposure to parabens had a potential non-carcinogenic risk. This large-scale biomonitoring study will help to understand the exposure levels of parabens and triclocarban in the Chinese general population and provide supporting information for government decision-making.

[Application of multiomics mass spectrometry in the research of chemical exposome].

Environmental factors, such as environmental pollutants, behaviors, and lifestyles, are the leading causes of chronic noncommunicable diseases. Estimates indicate that approximately 50% of all deaths worldwide can be attributed to environmental factors. The exposome is defined as the totality of human environmental (i.e., all nongenetic) exposures from conception, including general external exposure (e.g., climate, education, and urban environment), specific external exposure (e.g., pollution, physical activity, and diet), and internal exposure (e.g., metabolic factors, oxidative stress, inflammation, and protein modification). As a new paradigm, this concept aims to comprehensively understand the link between human health and environmental factors. Therefore, a comprehensive measurement of the exposome, including accurate and reliable measurements of exposure to the external environment and a wide range of biological responses to the internal environment, is of great significance. The measurement of the general external exposome depends on advances in environmental sensors, personal-sensing technologies, and geographical information systems. The determination of exogenous chemicals to which individuals are exposed and endogenous chemicals that are produced or modified by external stressors relies on improvements in methodology and the development of instrumental approaches, including colorimetric, chromatographic, spectral, and mass-spectrometric methods. This article reviews the research strategies for chemical exposomes and summarizes existing exposome-measurement methods, focusing on mass spectrometry (MS)-based methods. The top-down and bottom-up approaches are commonly used in exposome studies. The bottom-up approach focuses on the identification of chemicals in the external environment (e.g., soil, water, diet, and air), whereas the top-down approach focuses on the evaluation of endogenous chemicals and biological processes in biological samples (e.g., blood, urine, and serum). Low- and high-resolution MS (LRMS and HRMS, respectively) have become the most popular methods for the direct measurement of exogenous and endogenous chemicals owing to their superior sensitivity, specificity, and dynamic range. LRMS has been widely applied in the targeted analysis of expected chemicals, whereas HRMS is a promising technique for the suspect and unknown screening of unexpected chemicals. The development of MS-based multiomics, including proteomics, metabolomics, epigenomics, and spatial omics, provides new opportunities to understand the effects of environmental exposure on human health. Metabolomics involves the sum of all low-molecular-weight metabolites in a living system. Nontargeted metabolomics can measure both endogenous and exogenous chemicals, which would directly link exposure to biological effects, internal dose, and disease pathobiology, whereas proteomics could play an important role in predicting potential adverse health outcomes and uncovering molecular mechanisms. MS imaging (MSI) is an emerging technique that provides unlabeled in-depth measurements of endogenous and exogenous molecules directly from tissue and cell sections without changing their spatial information. MSI-based spatial omics, which has been widely applied in biomarker discovery for clinical diagnosis, as well as drug and pollutant monitoring, is expected to become an effective method for exposome measurement. Integrating these response measurements from metabolomics, proteomics, spatial omics, and epigenomics will enable the generation of new hypotheses to discover the etiology of diseases caused by chemical exposure. Finally, we highlight the major challenges in achieving chemical exposome measurements.

Co-precipitation of Cd with struvite during phosphorus recovery.

During the struvite recovery process, Cd, a hazardous metal commonly found in waste streams, can be sequestered by struvite. This study investigated the influence of Cd2+ on the precipitation of struvite. Quantitative X-ray diffraction (QXRD) results showed that the purity of struvite decreased from 99.1% to 73.6% as Cd concentration increased from 1 to 500 µM. Scanning electron microscopy (SEM) revealed a roughened surface of struvite, and X-ray photoelectron spectroscopy (XPS) analysis indicated that the peak area ratio of Cd-OH increased from 19.4% to 51.3%, while the area ratio of Cd-PO4 decreased from 86.6% to 48.7% as Cd concentrations increased from 10 to 500 µM. The findings suggested that Cd2+ disrupted the crystal growth of struvite, and mainly combined with -OH and -PO4 to form amorphous Cd-bearing compounds co-precipitated with struvite. Additionally, Mg-containing amorphous phases were formed by incorporating Mg2+ with -OH and -PO4 during struvite formation.

Emission characteristics of (halogenated) polycyclic aromatic hydrocarbons during printed circuit board combustion and estimated emission intensity of a typical e-waste dismantling site in South China.

The pollution of polycyclic aromatic hydrocarbons (PAHs) and halogenated PAHs (Cl/Br-PAHs) caused by electronic waste dismantling activities have attracted considerable attention. The present study investigated the emissions and formation of PAHs and Cl/Br-PAHs based on the combustion of printed circuit boards simulating electronic waste dismantling process. The emission factor of ΣPAHs was 648 ± 56 ng/g, which was much lower than that of ΣCl/Br-PAHs (8.80 × 104 ± 9.14 × 103 ng/g). From 25 to 600 °C, the emission rate of ΣPAHs reached a sub-peak of 7.39 ± 1.85 ng/(g•min) at 350 °C, then increased gradually with the fastest rate of 19.9 ± 21.8 ng/(g•min) at 600 °C, whereas that of ΣCl/Br-PAHs was the fastest at 350 °C with a rate of 597 ± 106 ng/(g•min), then decreased gradually. The present study suggested that the formation pathways of PAHs and Cl/Br-PAHs are by de novo synthesis. Low molecular weight PAHs were readily partitioned into gas and particle phases, whereas high molecular weight fused PAHs were only detected in oil phase. However, the proportion of Cl/Br-PAHs in particle and oil phases were different from that of gas phase, whereas similar to that of the total emission. In addition, PAH and Cl/Br-PAH emission factors were used to estimate the emission intensity of pyrometallurgy project in Guiyu Circular Economy Industrial Park, and it was shown that approximately 1.30 kg PAHs and 176 kg Cl/Br-PAHs would be emitted annually. This study revealed that Cl/Br-PAHs would be formed by de novo synthesis, and for the first time provided the emission factors of Cl/Br-PAHs during the heat treatment process of printed circuit board, as well as estimated the contribution of pyrometallurgy, a new electronic waste recovery technology, to environmental Cl/Br-PAH pollution, which provides potential scientific information for governmental decision-making on the control of Cl/Br-PAHs.

A large-scale nationwide study of urinary phenols in the Chinese population.

Bisphenol A (BPA), tetrabromobisphenol A (TBBPA), and their substitutes are commonly used in everyday products. However, large-scale internal exposure levels of them in China, the factors influencing on them, and the associated health risks were not systematically investigated still. In the present study, there were 1157 morning urine samples collected from residents of 26 provincial capitals in China for the measurement of BPA and seven bisphenol analogues, as well as TBBPA and its substitutes, i.e., tetrachlorobisphenol A and 4,4'-sulphonylbis(2,6-dibromophenol). The concentrations of Σ8bisphenols and Σ3TBBPAs ranged from

Maternal transfer of resorcinol-bis(diphenyl)-phosphate perturbs gut microbiota development and gut metabolism of offspring in rats.

Resorcinol-bis(diphenyl)-phosphate (RDP), an emerging organophosphate flame retardant, is increasingly used as a primary alternative for decabromodiphenyl ether and is frequently detected in global environmental matrices. However, the long-term effects of its exposure to humans remain largely unknown. To investigate its intergenerational transfer capacity and health risks, female Sprague Dawley rats were orally exposed to RDP from the beginning of pregnancy to the end of the lactation period. The RDP content, gut microbiota homeostasis, and metabolic levels were determined. RDP accumulation occurred in the livers of maternal rats and offspring and increased with exposure time. 16S rRNA gene sequencing showed that exposure to RDP during pregnancy and/or lactation significantly disrupted gut microbiota homeostasis, as evidenced by decreased abundance and diversity. In particular, the abundance of Turicibacter, Adlercreutzia, and YRC22 decreased, correlating significantly with glycollipic metabolism. This finding was consistent with the reduced levels of short-chain fatty acids, the crucial gut microbial metabolites. Meanwhile, RDP exposure resulted in changes in gut microbiome-related metabolism. Nine critical overlapping KEGG metabolic pathways were identified, and the levels of related differential metabolites decreased. Our results suggest that the significant adverse impacts of RDP on gut microbiota homeostasis and metabolic function may increase the long-term risks related to inflammation, obesity, and metabolic diseases.

Estimation of indoor soil/dust-skin adherence factors and health risks for adults and children in two typical cities in southern China.

Soil/dust (SD) skin adherence is key dermal exposure parameter used for calculating the health risk of dermal exposure to contaminants. However, few studies of this parameter have been conducted in Chinese populations. In this study, forearm SD samples were randomly collected using the wipe method from population in two typical cities in southern China as well as office staff in a fixed indoor environment. SD samples from the corresponding areas were also sampled. The wipes and SD were analyzed for tracer elements (aluminum, barium, manganese, titanium, and vanadium). The SD-skin adherence factors were 14.31 µg/cm2 for adults in Changzhou, 7.25 µg/cm2 for adults in Shantou, and 9.37 µg/cm2 for children in Shantou, respectively. Further, the recommended values for indoor SD-skin adherence factors for adults and children in Southern China were calculated to be 11.50 µg/cm2 and 9.37 µg/cm2, respectively, which were lower than the U.S. Environmental Protection Agency (USEPA) recommended values. And the SD-skin adherence factor value for the office staff was small (1.79 µg/cm2), but the data were more stable. In addition, PBDEs and PCBs in dust samples from industrial and residential area in Shantou were also determined, and health risks were assessed using the dermal exposure parameters measured in this study. None of the organic pollutants posed a health risk to adults and children via dermal contact. These studies emphasized the importance of localized dermal exposure parameters, and further studies should be conducted in the future.

Emission and gas-particle partitioning characteristics of atmospheric halogenated and organophosphorus flame retardants in decabromodiphenyl ethane-manufacturing functional areas.

The emission and gas-particle partitioning characteristics in various functional areas of production lines are still unknown. However, flame-retardant manufacturing activities are the primary emission source of flame retardants. Thus, fine particles and gases were investigated in three functional areas of a decabromodiphenyl ethane production line, i.e., polybrominated diphenyl ethers (PBDEs), novel brominated flame retardants (NBFRs), dechlorane plus (DPs), and organophosphorus flame retardants (OPFRs) in a flame-retardant manufacturing factory. High levels of PBDEs (8.02 × 103-4.16 × 104 pg/m3), NBFRs (6.05 × 103-1.92 × 105 pg/m3), and DPs (89.5-5.20 × 103 pg/m3) were found in various functional areas, suggesting manufacturing activities were a primary emission source. In contrast, OPFRs were derived from long-range transport or other non-industrial sources. Varied concentrations of PBDEs, NBFRs, and DPs were observed in different production lines, higher in the reaction zone area than others. As the predominant compounds, decabromodiphenyl ether, decabromodiphenyl ethane, syn-DP, and tris(chloropropyl) phosphate accounted for 54.7%, 89.3%, 93.4%, and 34.7% of PBDEs, NBFRs, DPs, and OPFRs, respectively. Three models were used to predict the gas-particle partitioning of the halogenated flame retardants emitted from manufacturing activities. The Li-Jia Empirical Model predicted the gas-particle partitioning behavior well. This research shows that the adsorption-desorption process of the halogenated flame retardants between the gaseous and particulate phases did not reach equilibrium.

Xanthine-derived reactive oxygen species exacerbates adipose tissue disorders in male db/db mice induced by real-ambient PM2.5 exposure.

Epidemiological and experimental data have associated exposure to fine particulate matter (PM2.5) with various metabolic dysfunctions and diseases, including overweight and type 2 diabetes. Adipose tissue is an energy pool for storing lipids, a necessary regulator of glucose homeostasis, and an active endocrine organ, playing an essential role in developing various related diseases such as diabetes and obesity. However, the molecular mechanisms underlying PM2.5-impaired functions in adipose tissue have rarely been explored. In this work, metabolomics based on liquid chromatography-mass spectrometry was performed to study the adverse impacts of PM2.5 exposure on brown adipose tissue (BAT) and white adipose tissue (WAT) in the diabetic mouse model. We found the effects of PM2.5 exposure by comparing the different metabolites in both adipose tissues of male db/db mice using real-ambient PM2.5 exposure. The results showed that PM2.5 exposure changed the purine metabolism in mice, especially the dramatic increase of xanthine content in both WAT and BAT. These changes led to significant oxidative stress. Then the results from real-time quantitative polymerase chain reaction showed that PM2.5 exposure could cause the production of inflammatory factors in both adipose tissues. Moreover, the increased reactive oxygen species (ROS) promoted triglyceride accumulation in WAT and inhibited its decomposition, causing increased WAT content in db/db mice. In addition, PM2.5 exposure significantly suppressed thermogenesis and affected energy metabolism in the BAT of male db/db mice, which may deteriorate insulin sensitivity and blood glucose regulation. This research demonstrated the impact of PM2.5 on the adipose tissue of male db/db mice, which may be necessary for public health.

DEHP exposure elevated cardiovascular risk in obese mice by disturbing the arachidonic acid metabolism of gut microbiota.

Phthalate esters (PAEs) are one of the significant classes of emerging contaminants that are increasingly detected in environmental and human samples. Nevertheless, the current toxicity studies rarely report how PAEs affect the cardiovascular system, especially in obese individuals. In this study, diet-induced obese mice and corresponding normal mice were exposed to di(2-ethylhexyl) phthalate (DEHP) by oral gavage at environmentally relevant concentrations and key characteristics of cardiovascular risk were examined. The 16S rRNA and high-resolution mass spectrometry were used to investigate the alterations in the gut microbial profile and metabolic homeostasis. The results indicated that the cardiovascular system of fat individuals was more susceptible to DEHP exposure than mice in the lean group. 16S rRNA-based profiling and correlation analysis collectively suggested DEHP-induced gut microbial remodeling in fed a high-fat diet mice, represented by the abundance of the genus Faecalibaculum. Using metagenomic approaches, Faecalibaculum rodentium was identified as the top-ranked candidate bacterium. Additionally, metabolomics data revealed that DEHP exposure altered the gut metabolic homeostasis of arachidonic acid (AA), which is associated with adverse cardiovascular events. Finally, cultures of Faecalibaculum rodentium were treated with AA in vitro to verify the role of Faecalibaculum rodentium in altering AA metabolism. Our findings provide novel insights into DEHP exposure induced cardiovascular damage in obese individuals and suggest that AA could be used as a potential modulator of gut microbiota to prevent related diseases.

Associated long-term effects of decabromodiphenyl ethane on the gut microbial profiles and metabolic homeostasis in Sprague-Dawley rat offspring.

Decabromodiphenyl ethane (DBDPE) as a widely used brominated flame retardant is harmful to human health due to its toxicity, including cardiovascular toxicity, reproductive toxicity, and hepatotoxicity. However, the knowledge of the long-term effects and structural and metabolic function influence on gut microbiota from DBDPE exposure remains limited. This study was mainly aimed at the gut microbiome and fecal metabolome of female rats and their offspring exposed to DBDPE in early life. 16S rRNA gene sequencing demonstrated that maternal DBDPE exposure could increase the α-diversity of gut microbiota in immature offspring while decreasing the abundance of Bifidobacterium, Clostridium, Muribaculum, Escherichia, and Lactobacillus in adult offspring. The nonmetric multidimensional scaling showed a consistency in the alternation of ß-diversity between pregnant rats and their adult offspring. Furthermore, the short-chain fatty acids produced by gut microbiota dramatically increased in adult offspring after maternal DBDPE exposure, revealing that DBDPE treatment disrupted the gut microbial compositions and altered the gut community's metabolic functions. Untargeted metabolomics identified 41 differential metabolites and seven metabolic pathways between adult offspring from various groups. Targeted metabolomic showed that maternal high dose DBDPE exposure obviously decreased the level of glutathione, taurine, and l-carnitine in their adult offspring, which verified the correlation between weight loss and amino acid metabolites. An interesting link between some gut bacteria (especially the Firmicutes) and fecal metabolites demonstrated the shifts in gut microbiota may drive the metabolic process of fecal metabolites. The current findings provide new insight into long-term effects on human health.

A Novel Strategy to Directly Quantify Polyethylene Microplastics in PM2.5 Based on Pyrolysis-Gas Chromatography-Tandem Mass Spectrometry.

The broad application of plastic products has resulted in a considerable release of microplastics (MPs) into the ecosystem. While MPs in other environmental matrices (e.g., soil and water) have been studied for a long time, the atmospheric fine particulate matter (PM2.5)-bound MPs are rarely investigated due to the lack of an appropriate analytical approach. The prevalently used visual and spectroscopic means (e.g., optical microscopy, Fourier-transform infrared spectroscopy, and Raman spectroscopy) suffer from obvious drawbacks that cannot precisely detect MPs of tiny sizes and provide quantitative information. In the present study, a novel strategy that does not require sample pretreatment was developed to first effectuate accurate quantification of polyethylene MP (PE-MP) in PM2.5 based on pyrolysis-gas chromatography-tandem mass spectrometry (Pyr-GC-MS/MS). It featured acceptable recoveries (97%-110%), high sensitivity (LOD = 1 pg), and qualified precisions (RSD of 3%-13%). Employing this approach, for the first time, exact atmospheric concentrations of PE-MPs in PM2.5 from megacities in North (Zhengzhou and Taiyuan) and South (Guangzhou) China were obtained, and relatively serious pollution was found in Taiyuan. The 100% sample detection rates also suggested the widespread occurrence and possible human exposure risks of PM2.5-bound PE-MPs. In brief, the new strategy could conduct direct, sensitive, and accurate quantification of PE-MP in PM2.5, favoring further studies of environmental fates, distributions, and toxicities of atmospheric MPs.

Proliferation toxicity and mechanism of novel mixed bromine/chlorine transformation products of tetrabromobisphenol A on human embryonic stem cell.

Mixed bromine/chlorine transformation products of tetrabromobisphenol A (ClyBrxBPAs) are mixed halogenated-type compounds recently identified in electronic waste dismantling sites. There are a lack of toxicity data on these compounds. To study their development toxicity, the proliferation toxicity was investigated using human embryonic stem cells (hESC) exposed to the lowest effective dose of two ClyBrxBPA analogues (2-chloro-2',6-dibromobisphenol A and 2,2'-dichloro-6-monobromobisphenol A). For comparison, tetrabromobisphenol A, 2,2',6-tribromobisphenol A, and bisphenol A were also assessed. It was observed that ClyBrxBPAs inhibited hESCs proliferation in a concentration-dependent manner. The cell bioaccumulation efficiency of ClyBrxBPAs was higher than that of tetrabromobisphenol A. Also, ClyBrxBPAs were more toxic than tetrabromobisphenol A, with 2,2'-dichloro-6-monobromobisphenol A exhibiting the most potent toxicity. Furthermore, flow cytometry and oxidative stress results showed that increased reactive oxygen species raised the degree of apoptosis and reduced DNA synthesis. Metabolomics analysis on the effect of ClyBrxBPAs on metabolic pathway alteration showed that ClyBrxBPAs mainly interfered with four metabolic pathways related to amino acid metabolism and biosynthesis. These results provide an initial perspective on the proliferation toxicity of ClyBrxBPAs, indicating development toxicity in children.

Contribution and Effects of PM2.5-Bound Lead to the Cardiovascular Risk of Workers in a Non-Ferrous Metal Smelting Area Considering Chemical Speciation and Bioavailability.

Lead is known to have toxic effects on the cardiovascular system. Owing to its high concentration, transmission range, and absorption efficiency in organisms, inhalation of fine particulate matter (PM2.5)-bound lead (PM2.5-Pb) may cause significant cardiovascular damage. However, the contribution and adverse effects of PM2.5-Pb on workers and residents in non-ferrous metal smelting areas are not fully understood. In this work, the concentration and chemical speciation of PM2.5-Pb were analyzed to determine its pollution characteristics at a typical non-ferrous metal smelting site. A panel study conducted among factory workers revealed that PM2.5-Pb exposure makes an important contribution to the human absorption of Pb. Although the chemical speciation of PM2.5-Pb suggested poor water solubility, a high bioavailability was observed in mice (tissue average value: 50.1%, range: 31.1-71.1%) subjected to inhalation exposure for 8 weeks. Based on the bioavailability data, the relationship between PM2.5-Pb exposure and cardiovascular damage was evaluated in animal simulation experiments. Finally, a damage threshold and cardiovascular-specific risk assessment model were established for the non-ferrous metal smelting area. Our project not only accurately estimates the risk of PM2.5-bound heavy metals on the cardiovascular system but also offers a scientific basis for future prevention and therapy of PM2.5-Pb-related diseases.

Temporal trends and health risks of organophosphorus flame retardants in fishes in Taihu Lake from 2013 to 2018.

Organophosphorus flame retardants (OPFRs) are synthetic, physical additive flame retardants widely detected in the environment. To investigate the temporal trends of OPFRs in Taihu regions and the associated health risks from fish consumption, 150 fish samples of five species were collected from Taihu Lake in China from 2013 to 2018. Eight OPFRs were measured, having 2-ethylhexyl diphenyl phosphate (90.7%) and tris (1,3-dichloro-2 propyl) phosphate (21.5%) as the most and least frequently detected OPFRs, respectively. Among the eight OPFRs, tris (chloropropyl) phosphate concentration (446 pg/g, wet weight) was higher than others. The maximum cumulative concentration of the OPFRs (∑8OPFRs) was observed in large icefish (1.69 × 103 pg/g), while silver carp (841 pg/g) had the lowest. For the temporal trends, higher levels of ∑8OPFRs (1.91 × 103 pg/g) were detected in 2013 than in other years, although no significant change in the trend occurred over time. The estimated daily intake of OPFRs from large icefish consumption was 1.20 × 103 pg/kg-bw/day, higher than that of other fish species. The Monte Carlo simulations showed that ≤0.3% of adults and children would suffer non-cancer health risks from OPFRs via fish consumption. This study provides the first data on temporal trends of OPFRs in Taihu Lake.

Azole-Induced Color Vision Deficiency Associated with Thyroid Hormone Signaling: An Integrated In Vivo, In Vitro, and In Silico Study.

Azoles that are used in pesticides, pharmaceuticals, and personal care products can have toxic effects on fish. However, there is no information regarding azole-induced visual disorder associated with thyroid disruption. We evaluated changes in retinal morphology, optokinetic response, transcript abundance of the genes involved in color perception and hypothalamic-pituitary-thyroid (HPT) axis, and thyroid hormone (TH) levels in zebrafish larvae exposed to common azoles, such as climbazole (CBZ, 0.1 and 10 µg/L) and triadimefon (TDF, 50 and 500 µg/L), at environmentally relevant and predicted worst-case environmental concentrations. Subsequently, the effect of azoles on TH-dependent GH3 cell proliferation and thyroid receptor (TR)-regulated transcriptional activity, as well as the in silico binding affinity between azoles and TR isoforms, was investigated. Azole exposure decreased cell densities of the ganglion cell layer, inner nuclear layer, and photoreceptor layer. Zebrafish larvae exposed to environmentally relevant concentrations of CBZ and TDF showed a decrease in optokinetic response to green-white and red-white stripes but not blue-white stripes, consistent with disturbance in the corresponding opsin gene expression. Azole exposure also reduced triiodothyronine levels and concomitantly increased HPT-related gene expression. Molecular docking analysis combined with in vitro TR-mediated transactivation and dual-luciferase reporter assays demonstrated that CBZ and TDF exhibited TR antagonism. These results are comparable to those obtained from a known TR antagonist, namely, TR antagonist 1, as a positive control. Therefore, damage to specific color perception by azoles appears to result from lowered TH signaling, indicating the potential threat of environmental TH disruptors to the visual function of fish.

The protective effects of taurine and fish oil supplementation on PM2.5-induced heart dysfunction among aged mice: A random double-blind study.

As it is nearly impossible to reduce PM2.5 concentrations in most cities to safe limits in a short period of time, dietary supplementation presents a promising approach for mitigating the adverse effects of PM2.5 exposure. A cross-sectional study showed that the elderly population of Linfen (PM2.5: 102 µg/m3) exhibited significantly lower serum taurine levels, as well as higher oxidative stress levels and cardiovascular health risks, than the corresponding population in Guangzhou (PM2.5: 39 µg/m3). We conducted a random double-blind study on aged mice that employed a "real-world" PM2.5 exposure system to simulate the conditions of Linfen with the aim of investigating the protective effects of taurine and fish oil supplementation on PM2.5-induced heart dysfunction. When compared with the placebo group, supplementation with taurine and fish oil not only maintained normal taurine levels, but also suppressed oxidative stress and inflammation in aged mice subjected to high concentrations of PM2.5. Variations in heart rate, contractile function, cardiac oxidative stress, inflammation and fibrosis among different groups of aged mice were used to clarify the beneficial effects of taurine and fish oil supplementation. Our results not only revealed the protective effects of taurine and fish oil supplementation on heart dysfunction induced by PM2.5 exposure from the aged mice experiments and also provided new means for the elderly to resist PM2.5 pollution at the individual level.

Beyond Substituted p-Phenylenediamine Antioxidants: Prevalence of Their Quinone Derivatives in PM2.5.

Substituted para-phenylenediamine (PPD) antioxidants have been extensively used to retard oxidative degradation of tire rubber and were found to pervade multiple environmental compartments. However, there is a paucity of research on the environmental occurrences of their transformation products. In this study, we revealed the co-occurrence of six PPD-derived quinones (PPD-Qs) along with eight PPDs in fine particulate matter (PM2.5) from two Chinese megacities, in which N,N'-bis(1,4-dimethylpentyl)-p-phenylenediamine quinone (77PD-Q) was identified and quantified for the first time. Prevalent occurrences of these emerging PPD-Qs were found in Taiyuan (5.59-8480 pg/m3) and Guangzhou (3.61-4490 pg/m3). Significantly higher levels of PPDs/PPD-Qs were observed at a roadside site, implying the possible contribution of vehicle emissions. Correlation analysis implied potential consistencies in the fate of these PPD-Qs and suggested that most of them were originated from the transformation of their parent PPDs. For different subpopulation groups under different exposure scenarios, the estimated daily intakes of PPD-Qs (0.16-1.25 ng kgbw-1 day-1) were comparable to those of their parent PPDs (0.19-1.41 ng kgbw-1 day-1), suggesting an important but overlooked exposure caused by novel PPD-Qs. Given the prolonged exposure of these antioxidants and their quinone derivatives to traffic-relevant occupations, further investigations on their toxicological and epidemiological effects are necessary.