Investigating environmentally persistent free radicals (EPFRs) emissions of 3D printing process.

In recent years, the emission of particles and gaseous pollutants from 3D printing has attracted much attention due to potential health risks. This study investigated the generation of environmentally persistent free radicals (EPFRs, organic free radicals stabilized on or inside particles) in total particulate matter (TPM) released during the 3D printing process. Commercially available 3D printer filaments, made of acrylonitrile-butadiene-styrene (ABS) in two different colors and metal content, ABS-blue (19.66 µg/g Cu) and ABS-black (3.69 µg/g Fe), were used for printing. We hypothesized that the metal content/composition of the filaments contributes not only to the type and number of EPFRs in TPM emissions, but also impacts the overall yield of TPM emissions. TPM emissions during printing with ABS-blue (11.28 µg/g of printed material) were higher than with ABS-black (7.29 µg/g). Electron paramagnetic resonance (EPR) spectroscopy, employed to measure EPFRs in TPM emissions of both filaments, revealed higher EPFR concentrations in ABS-blue TPM (6.23 × 1017 spins/g) than in ABS-black TPM (9.72 × 1016 spins/g). The presence of copper in the ABS-blue contributed to the formation of mostly oxygen-centered EPFR species with a g-factor of ~2.0041 and a lifetime of 98 days. The ABS-black EPFR signal had a lower g-factor of ~2.0011, reflecting the formation of superoxide radicals during the printing process, which were shown to have an "estimated tentative" lifetime of 26 days. Both radical species (EPFRs and superoxides) translate to a potential health risk through inhalation of emitted particles.

Biochar-Associated Free Radicals Reduce Soil Bacterial Diversity: New Insight into Ecoenzymatic Stoichiometry.

The toxicity of environmentally persistent free radicals (EPFRs), often generated during biochar production, on soil bacteria is still not truly reflected when considering the conditions in real soil. Herein, the influence of free radicals within biochar on soil bacteria was investigated from the perspectives of enzyme activity, community structure, and ecoenzymatic stoichiometry. Biochar addition enhanced the contents of EPFRs and derived hydroxyl radicals (•OH) in the soil, while it reduced bacterial alpha diversity by 5.06-35.44%. The results of redundancy analysis and inhibition experiments collectively demonstrated the key role of EPFRs and •OH in reducing the bacterial alpha diversity. Specifically, EPFRs and •OH increased the stoichiometric imbalance by promoting the release of dissolved organic carbon and ammonium N, thus aggravating the P limitation in soil. This was further confirmed by increased alkaline phosphatase activity from 702 to 874 nmol g-1 h-1. The P limitation induced by EPFRs and •OH decreased the bacterial alpha diversity, as evidenced by the negative correlation between P limitation and bacterial alpha diversity (r2 = -0.931 to -0.979, P < 0.01) and the structural equation model. The obtained results demonstrate a ubiquitous but previously overlooked mechanism for bacterial toxicity of biochar-associated free radicals, providing scientific guidance for safe utilization of biochar.

Outdoor Health Risk of Atmospheric Particulate Matter at Night in Xi'an, Northwestern China.

The deterioration of air quality via anthropogenic activities during the night period has been deemed a serious concern among the scientific community. Thereby, we explored the outdoor particulate matter (PM) concentration and the contributions from various sources during the day and night in winter and spring 2021 in a megacity, northwestern China. The results revealed that the changes in chemical compositions of PM and sources (motor vehicles, industrial emissions, coal combustion) at night lead to substantial PM toxicity, oxidative potential (OP), and OP/PM per unit mass, indicating high oxidative toxicity and exposure risk at nighttime. Furthermore, higher environmentally persistent free radical (EPFR) concentration and its significant correlation with OP were observed, suggesting that EPFRs cause reactive oxygen species (ROS) formation. Moreover, the noncarcinogenic and carcinogenic risks were systematically explained and spatialized to children and adults, highlighting intensified hotspots to epidemiological researchers. This better understanding of day-night-based PM formation pathways and their hazardous impact will assist to guide measures to diminish the toxicity of PM and reduce the disease led by air pollution.

Adjuvant effect of inhaled particulate matter containing free radicals following house-dust mite induction of asthma in mice.

INTRODUCTION: Exposures to particulate matter (PM) from combustion sources can exacerbate preexisting asthma. However, the cellular and molecular mechanisms by which PM promotes the exacerbation of asthma remain elusive. We used a house dust mite (HDM)-induced mouse model of asthma to test the hypothesis that inhaled DCB230, which are PM containing environmentally persistent free radicals (EPFRs), will aggravate asthmatic responses. METHODS: Groups of 8-10-week-old C57BL/6 male mice were exposed to either air or DCB230 aerosols at a concentration of 1.5 mg/m3 4 h/day for 10 days with or without prior HDM-induction of asthma. RESULTS: Aerosolized DCB230 particles formed small aggregates (30-150 nm). Mice exposed to DCB230 alone showed significantly reduced lung tidal volume, overexpression of the Muc5ac gene, and dysregulation of 4 inflammation related genes, Ccl11, Ccl24, Il-10, and Tpsb2. This suggests DCB230 particles interacted with the lung epithelium inducing mucous hypersecretion and restricting lung volume. In addition to reduced lung tidal volume, compared to respective controls, the HDM + DCB230-exposed group exhibited significantly increased lung tissue damping and up-regulated expression of Muc5ac, indicating that in this model, mucous hypersecretion may be central to pulmonary dysfunction. This group also showed augmented lung eosinophilic inflammation accompanied by an up-regulation of 36 asthma related genes. Twelve of these genes are part of IL-17 signaling, suggesting that this pathway is critical for DCB230 induced toxicity and adjuvant effects in lungs previously exposed to HDM. CONCLUSION: Our data indicate that inhaled DCB230 can act as an adjuvant, exacerbating asthma through IL-17-mediated responses in a HDM mouse model.

Contamination profiles and potential health risks of environmentally persistent free radicals in PM2.5 over typical central Chinese megacity.

As one of the most important transportation hubs and industrial bases in China, Zhengzhou has suffered from serious PM2.5 pollution for a long time. However, the investigation of contamination status and possible exposure risks of environmentally persistent free radicals (EPFRs) in PM2.5 from Zhengzhou is rare. In this work, a comprehensive study of pollution levels, seasonal variations, sources, and potential health risks of PM2.5-bound EPFRs in Zhengzhou was conducted for the first time. The atmospheric concentrations of EPFRs in PM2.5 from Zhengzhou ranged from 1.732 × 1012 spin m-3 to 7.182 × 1014 spin m-3 between 2019 and 2020. Relatively serious contamination was noticed in winter and spring. Primary fossil fuel combustion and Fe-mediated secondary formation were apportioned as possible sources of PM2.5-bound EPFRs in Zhengzhou. Moreover, to avert the bias of the toxicity assessment induced by utilization of incompletely extracted EPFRs from sample filter, simulatively generated EPFRs were applied to toxicological evaluations (cell viability and reactive oxygen species assays). Corresponding experimental dosages were based on the estimated adults' annual exposure amounts of EPFRs in real PM2.5 samples. The results elucidated that EPFRs might cause growth inhibition and oxidative stress of human lung cells, suggesting the possible exposure-induced health concerns for local people in Zhengzhou. This study provides practical information of real contamination status of PM2.5-bound EPFRs in Zhengzhou, which is favorable to local air pollution control and reduction of exposure risks on public health in central China.

Pollution characteristics and sources of environmentally persistent free radicals and oxidation potential in fine particulate matter related to city lockdown (CLD) in Xi'an, China.

The impact of COVID-19 control on air quality have been prevalent for the past two years, however few studies have explored the toxicity of atmospheric particulate matter during the epidemic control. Therefore, this research highlights the characteristics and sources of oxidative potential (OP) and the new health risk substances environmentally persistent free radicals (EPFRs) in comparison to city lockdown (CLD) with early days of 2019-2020. Daily particulate matter (PM2.5) samples were collected from January 14 to February 3, 2020, with the same period during 2019 in Xi'an city. The results indicated that the average concentration of PM2.5 decreased by 48% during CLD. Concentrations of other air pollutants and components, such as PM10, NO2, SO2, WSIs, OC and EC were also decreased by 22%, 19%, 2%, 17%, 6%, and 4% respectively during the CLD, compared to the same period in 2019. Whereas only O3 increased by 30% during CLD. The concentrations of EPFRs in PM2.5 was considerably lower than in 2019, which decreased by 12% during CLD. However, the OP level was increased slightly during CLD. Moreover, both EPFRs/PM and DTTv/PM did not decrease or even increase significantly, manifesting that the toxicity of particulate matter has not been reduced by more gains during the CLD. Based on PMF analysis, during the epidemic period, the contribution of traffic emission is significantly reduced, while EPFRs and DTTv increased, which consist of significant O3 and secondary aerosols. This research leads to able future research on human health effect of EPFRs and oxidative potential and can be also used to formulate the majors to control EPFRs and OP emissions, suggest the need for further studies on the secondary processing of EPFRs and OP during the lockdown period in Xi'an. .The COVID-19 lockdown had a significant impact on both social and economic aspects. The city lockdown, however, had a positive impact on the environment and improved air quality, however, no significant health benefits were observed in Xi'an, China.

Insight into urban PM2.5 chemical composition and environmentally persistent free radicals attributed human lung epithelial cytotoxicity.

Fine particulate matter (PM2.5) is detrimental to the human respiratory system. However, the toxicity of PM2.5 and its associated potentially harmful species, notably novel pollutants like environmentally persistent free radicals (EPFRs), remains unclear. Therefore, one-year site monitoring and ambient air PM2.5 sampling in the Nanjing urban area was designed to investigate the relationships between chemical compositions (carbon fractions, metallic elements, and water-soluble ions) and EPFRs, and change in cytotoxicity with varying PM2.5 components. Oxidative stress (reactive oxygen species, ROS), inflammatory injury (IL-6 and TNF-α), and membrane injury (LDH) of human lung epithelial cells (A549) induced by PM2.5 were analyzed using in vitro cytotoxicity test. Both the composition and toxicity of PM2.5 from different seasons were compared. The average daily exposure of urban PM2.5 associated EPFRs load in Nanjing were 2.29 × 1011 spin m-3. Their exposure concentration and cytotoxic damage ability were stronger in the cold season than warm. The particle compositions of metals and carbon fractions were significantly positively correlated with EPFRs. The airborne EPFRs, organic carbon (OC), and heavy metal Cu, As, and Pb may pose principal cell damage ability, which is worthy of further study interlinking aerosol pollution and health risks.

Genomic Basis for Individual Differences in Susceptibility to the Neurotoxic Effects of Diesel Exhaust.

Air pollution is a known environmental health hazard. A major source of air pollution includes diesel exhaust (DE). Initially, research on DE focused on respiratory morbidities; however, more recently, exposures to DE have been associated with neurological developmental disorders and neurodegeneration. In this study, we investigated the effects of sub-chronic inhalation exposure to DE on neuroinflammatory markers in two inbred mouse strains and both sexes, including whole transcriptome examination of the medial prefrontal cortex. We exposed aged male and female C57BL/6J (B6) and DBA/2J (D2) mice to DE, which was cooled and diluted with HEPA-filtered compressed air for 2 h per day, 5 days a week, for 4 weeks. Control animals were exposed to HEPA-filtered air on the same schedule as DE-exposed animals. The prefrontal cortex was harvested and analyzed for proinflammatory cytokine gene expression (Il1ß, Il6, Tnfα) and transcriptome-wide response by RNA-seq. We observed differential cytokine gene expression between strains and sexes in the DE-exposed vs. control-exposed groups for Il1ß, Tnfα, and Il6. For RNA-seq, we identified 150 differentially expressed genes between air and DE treatment related to natural killer cell-mediated cytotoxicity per Kyoto Encyclopedia of Genes and Genomes pathways. Overall, our data show differential strain-related effects of DE on neuroinflammation and neurotoxicity and demonstrate that B6 are more susceptible than D2 to gene expression changes due to DE exposures than D2. These results are important because B6 mice are often used as the default mouse model for DE studies and strain-related effects of DE neurotoxicity warrant expanded studies.

Risk evaluation of environmentally persistent free radicals in airborne particulate matter and influence of atmospheric factors.

Environmentally persistent free radicals (EPFRs) was considered unrecognized composition of air pollutants and might help explain the long-standing medical mystery of why non-smokers develop tobacco-related diseases like lung cancer. EPFRs in airborne fine particulate matter (PM2.5) can induce oxidative and DNA damage when inhaled. We assessed the inhalation risk of EPFRs in PM2.5 and factors influencing this risk in Beijing as a large city with frequent haze events. The average concentration of EPFRs in PM2.5 was 6.00 × 1017 spins/m3 in spring, autumn, and winter; lower concentrations were recorded in the summer. To estimate the daily inhalation risk of EPFRs in PM2.5, we used the equivalent EPFRs in cigarette tar. The average daily inhalation exposure of EPFRs in PM2.5 was estimated to be the equivalent of 33.1 cigarette tar EPFRs per day (range: 0.53-226.9) during both haze and non-haze days. The major factors influencing EPFR concentrations in the atmosphere were precipitation and humidity, which reduced airborne concentrations. Levels of PM2.5 and carbon monoxide were positively correlated with EPFR concentrations. The health risks of inhaling airborne EPFRs could be significant and should be recognized and quantified.

Exposure to environmentally persistent free radicals during gestation lowers energy expenditure and impairs skeletal muscle mitochondrial function in adult mice.

We have investigated the effects of in utero exposure to environmentally persistent free radicals (EPFRs) on growth, metabolism, energy utilization, and skeletal muscle mitochondria in a mouse model of diet-induced obesity. Pregnant mice were treated with laboratory-generated, combustion-derived particular matter (MCP230). The adult offspring were placed on a high-fat diet for 12 wk, after which we observed a 9.8% increase in their body weight. The increase in body size observed in the MCP230-exposed mice was not associated with increases in food intake but was associated with a reduction in physical activity and lower energy expenditure. The reduced energy expenditure in mice indirectly exposed to MCP230 was associated with reductions in skeletal muscle mitochondrial DNA copy number, lower mRNA levels of electron transport genes, and reduced citrate synthase activity. Upregulation of key genes involved in ameliorating oxidative stress was also observed in the muscle of MCP230-exposed mice. These findings suggest that gestational exposure to MCP230 leads to a reduction in energy expenditure at least in part through alterations to mitochondrial metabolism in the skeletal muscle.

Environmentally persistent free radical-containing particulate matter competitively inhibits metabolism by cytochrome P450 1A2.

Combustion processes generate different types of particulate matter (PM) that can have deleterious effects on the pulmonary and cardiovascular systems. Environmentally persistent free radicals (EPFRs) represent a type of particulate matter that is generated after combustion of environmental wastes in the presence of redox-active metals and aromatic hydrocarbons. Cytochromes P450 (P450/CYP) are membrane-bound enzymes that are essential for the phase I metabolism of most lipophilic xenobiotics. The EPFR formed by chemisorption of 2-monochlorophenol to silica containing 5% copper oxide (MCP230) has been shown to generally inhibit the activities of different forms of P450s without affecting those of cytochrome P450 reductase and heme oxygenase-1. The mechanism of inhibition of rat liver microsomal CYP2D2 and purified rabbit CYP2B4 by MCP230 has been shown previously to be noncompetitive with respect to substrate. In this study, MCP230 was shown to competitively inhibit metabolism of 7-benzyl-4-trifluoromethylcoumarin and 7-ethoxyresorufin by the purified, reconstituted rabbit CYP1A2. MCP230 is at least 5- and 50-fold more potent as an inhibitor of CYP1A2 than silica containing 5% copper oxide and silica, respectively. Thus, even though PM generally inhibit multiple forms of P450, PM interacts differently with the forms of P450 resulting in different mechanisms of inhibition. P450s function as oligomeric complexes within the membrane. We also determined the mechanism by which PM inhibited metabolism by the mixed CYP1A2-CYP2B4 complex and found that the mechanism was purely competitive suggesting that the CYP2B4 is dramatically inhibited when bound to CYP1A2.

Influence of microplastics and environmentally persistent free radicals on the ability of biochar components to promote degradation of antibiotics by activated peroxymonosulfate.

Microplastics (MPs) in sludge can affect the ability of biochar-activated peroxymonosulfate (PMS) to degrade antibiotics. In this work, biochar was prepared by mixing sludge and polystyrene (PS) through hydrothermal carbonization (HTC) and high-temperature pyrolysis processes. The resulting biochar was used to activate PMS to degrade ofloxacin (OFX), levofloxacin (LEV), and pefloxacin (PFX). The addition of PS significantly enhanced the ability of biochar/PMS to degrade antibiotics and the levels of environmentally persistent free radicals (EPFRs, 4.59 × 1020 spin/g) due to the decomposition of PS. The addition of PS resulted in a slight decrease in the specific surface area of biochar (2-3 m2/g on average), but a significant increase in the concentration of EPFRs increased the removal efficiency. The activation of PMS by biochar is dominated by free radicals, accounting for about 70%, in which SO4•- and •OH contribute the most and O2•- the least. However, 1O2 contributes 15-20% to the degradation of antibiotics in non-free radical processes. Overall, the process of biochar/PMS degradation of antibiotics is mainly dominated by free radicals, and the effect of non-free radicals is not obvious. Both hydrochar and pyrocarbon samples showed good hydrophilicity, and this property should improve the ability of active sites on biochar to degrade antibiotics. In the HTC process, PS can decompose during hydrochar preparation, with a maximum reduction value of 40.09%. The three-dimension excitation emission matrix fluorescence spectroscopy (3D-EEM) and total organic carbon (TOC) results show that the protein content in sludge plays a major role in reducing PS, with little effect of polysaccharide and SiO2. There are six to seven degradation intermediates of quinolone antibiotics, which are eventually degraded into CO2, H2O, and inorganic substances. The regeneration experiment showed good reusability of hydrochar and pyrocarbon, further demonstrating the suitability of biochar for the degradation of antibiotics.

Effects of excess sludge composting process, environmentally persistent free radicals, and microplastics on antibiotics degradation efficiency of aging biochar.

Simulation of microbial aging biochar in compost is an important index for evaluating the biochar degradation efficiency of antibiotics. In this study, biochar was prepared by adding microplastics (MPs) to sludge, and the degradation effect of biochar/(peroxymonosulfate, PMS) on antibiotics was evaluated during the compost aging process of biochar. After the compost aging of biochars, the antibiotic degradation efficiency of HPBC500, HPBC500 + polystyrene (PS), HPBC900/PMS, and HPBC900 + PS/PMS decreased by 6.47, 15.2, 10.16, and 10.33 %, respectively. Environmentally persistent free radicals (EPFRs) and defect structure were the main contributors to the activation of PMS. EPFRs produced through PS pyrolysis of biochar exhibited strong reactivity but poor stability during the degradation of antibiotics. Biochar enhanced the growth of microorganisms in compost but reduced its specific surface area. The antibiotic degradation efficiency of the biochar was positively correlated with the concentration of EPFRs. This study elucidated the durability of different biochar toward antibiotic degradation.

Formation and biotoxicity of environmentally persistent free radicals in steelworks soil under thermal treatment.

Thermal treatment are commonly used to address organic contaminated soils. In particular, the pyrolysis of organic substances can result in the creation of environmentally persistent free radicals (EPFRs). We investigated a steelworks site in Chongqing (China) to observe changes in EPFRs before and after thermal treatment. Our findings revealed that the EPFRs were carbon-centered radicals with a g-factor < 2.0030 and a spin density ranging from n.d.-5.23 × 1015 spins/mg. The formation of EPFRs was driving by polycyclic aromatic hydrocarbons (PAHs), Mn, Cu, and total organic carbon (TOC). Following the thermal treatment, the spin densities of EPFRs increased by a factor of 0.25 to 1.81, with maximum levels reached at 300 °C. High molecular weight PAHs exhibited high heat capacity, enabling the generation of more EPFRs. The thermal decay of EPFRs occurred in two stages, with the shortest 1/e lifetime lasting up to 16.8 h. Raising the temperature or prolonging time can significantly reduce EPFRs levels. Thermal treatment increased the generation of EPFRs, hydroxyl radicals (•OH) and superoxide radical (•O2-), leading to a decrease in bacterial luminescence. Specifically, •OH contributed to approximately 73% of the B. brilliantus inhibition. Our results highlight that the thermal treatment significantly enhance EPFRs concentrations, and the treated soil remained ecologically risky. The knowledge of the formation of EPFRs and their biotoxicity is shedding new light on the thermal treatment risk management.

Environmentally persistent free radicals on photoaged microplastics from disposable plastic cups induce the oxidative stress-associated toxicity.

Microplastics (MPs) are ubiquitous environmental contaminants that exerting multiple toxicological effects. Most studies have focused primarily on the models of unaged MPs and lack environmental relevance. The generation and toxicity of environmentally persistent free radicals (EPFRs) on photoaging MPs from disposable plastic cups (DPC-MPs) have not been well studied. Here, the formation of EPFRs on photoaged DPC-MPs and their toxic effects in nematodes were investigated. UV irradiation generated EPFRs, which influenced the characterization of DPC-MPs. Exposure to photoaged DPC-MPs at environmentally relevant concentrations （100-1000 µg/L） reduced the locomotion behavior, body length, and brood size. The Reactive oxygen species (ROS) production, lipofuscin accumulation, malondialdehyde (MDA), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were increased along with the downregulation of the expression levels of associated genes, such as clk-1, clt-1, and gst-4，in nematodes. Moreover, the toxicity and oxidative stress response of nematodes were significantly inhibited due to N-acetyl-l-cysteine (NAC). Pearson's correlation analysis revealed that the oxidative stress was significantly associated with adverse physiological effects. Therefore, EPFRs on photoaged DPC-MPs cause toxicity in nematodes, and oxidative stress is important for regulating toxicity. This study offers novel insights into the potential risks of DPC-MPs under UV irradiation, highlighting the need to consider the role of EPFRs in toxicity assessments of DPC-MPs.

Molecular characterization of diverse quinone analogs for discrimination of aerosol-bound persistent pyrolytic and photolytic radicals.

Aerosol-bound organic radicals, including environmentally persistent free radicals (EPFRs), are key components that affect climate, air quality, and human health. While putative structures have been proposed, the molecular characteristics of EPFRs remain unknown. Here, we report a surrogate method to characterize EPFRs in real ambient samples using mass spectrometry. The method identifies chemically relevant oxygenated polycyclic aromatic hydrocarbons (OxPAH) that interconvert with oxygen-centered EPFR (OC-EPFR). We found OxPAH compounds most relevant to OC-EPFRs are structurally rich and diverse quinones, whose diversity is strongly associated with OC-EPFR levels. Both atmospheric oxidation and combustion contributed to OC-EPFR formation. Redundancy analysis and photochemical aging model show pyrolytic sources generated more oxidized OC-EPFRs than photolytic sources. Our study reveals the detailed molecular characteristics of OC-EPFRs and shows that oxidation states can be used to identify the origins of OC-EPFRs, offering a way to track the development and evolution of aerosol particles in the environment.

Research of the impact of environmentally persistent free radicals on chemical element behaviour in the soil-plant system.

Environmentally persistent free radicals (EPFRs) may pose a potential risk to the ecosystem and human health via oxidation stress and are considered emerging contaminants. Being stable with a lifetime of minutes or several months and abundant in transitional matrices (e.g. biochar), EPFRs continue to affect deposits (e.g. soil) and related media (plants) when the transitional matrices (e.g. biochar) are applied. The impact of EPFR on the plant uptake of chemical elements (CEs) was studied in the field conditions where, for two years, biochar and fertilisers were applied to the agricultural soil for winter triticale cultivation. EPFRs determination methods, along with the element uptake indices (bioaccumulation and biophilicity) and the method of the dynamic factors were applied. Results have shown that EPFRs have influenced the soil properties relevant to CE soil bioavailability and bioaccumulation in plants. The impact of EPFRs on CE transport in the soil-plant system was observed to influence the biogeochemical behaviour of CEs in the soil-plant system. This work provides the first findings on EPFRs-induces changes on CE bioavailability and bioaccumulation intensity, indicating the higher plant uptake risk of some potentially toxic elements (such as Cr).

Phototransformation of tetrabromobisphenol A bis (allyl ether) in an aqueous solution: Role of environmentally persistent free radicals.

Tetrabromobisphenol A bis (allyl ether) (TBBPA-BAE) represents an extensively used brominated flame retardant (BFRs) in the production of many fields and their phototransformation in natural water is still unclear. The environmentally persistent free radicals (EPFRs) with preserved activities could exist in the environment for a long time and involve in the phototransformation of many organic pollutants. Here, the photodegradation of TBBPA-BAE with the degradation rate constant (k = 0.060 h-1) under simulate sunlight and the promoting effect of EPFRs on TBBPA-BAE photodegradation (k = 0.135 h-1) were investigated. According to the detected photogenerated electrons (e-) and singlet oxygen (1O2) rather than hydroxyl radicals (•OH) by the electron paramagnetic resonance (EPR), the effect mechanism may not be related to the typical •OH induced by EPFRs. The possible transformation pathways of the ether cleavage, hydrolysis and hydroxylation of propenyl bond and the debromination were proposed by the primary byproducts identified by UPLC-Q-Exactive Orbitrap MS. EPFRs caused a further debromination and ether cleavage and probably be due to EPFRs directly providing electrons to TBBPA-BAE which promoted the photodegradation of TBBPA-BAE, and their reaction mechanism needed further attention. Overall, this study provided useful information to understand the role of EPFRs on phototransformation of TBBPA-BAE in water.

The Effect of α-Fe2O3(0001) Surface Containing Hydroxyl Radicals and Ozone on the Formation Mechanism of Environmentally Persistent Free Radicals.

The formation of environmentally persistent free radicals (EPFRs) is mediated by the particulate matter's surface, especially transition metal oxide surfaces. In the context of current atmospheric complex pollution, various atmospheric components, such as key atmospheric oxidants ·OH and O3, are often absorbed on particulate matter surfaces, forming particulate matter surfaces containing ·OH and O3. This, in turn, influences EPFRs formation. Here, density functional theory (DFT) calculations were used to explore the formation mechanism of EPFRs by C6H5OH on α-Fe2O3(0001) surface containing the ·OH and O3, and compare it with that on clean surface. The results show that, compared to EPFRs formation with an energy barrier on a clean surface, EPFRs can be rapidly formed through a barrierless process on these surfaces. Moreover, during the hydrogen abstraction mechanism leading to EPFRs formation, the hydrogen acceptor shifts from a surface O atom on a clean surface to an O atom of ·OH or O3 on these surfaces. However, the detailed hydrogen abstraction process differs on surfaces containing oxidants: on surfaces containing ·OH, it occurs directly through a one-step mechanism, while, on surfaces containing O3, it occurs through a two-step mechanism. But, in both types of surfaces, the essence of this promotional effect mainly lies in increasing the electron transfer amounts during the reaction process. This research provides new insights into EPFRs formation on particle surfaces within the context of atmospheric composite pollution.

Ecotoxicity of three typical tire wear particles to periphytic biofilms: The potentiating role after natural water-incubation-aging.

Tire wear particles (TWPs), abundant in the aquatic environment, pose potential ecological risks, yet their implications have not been extensively studied. Rolling friction TWPs, sliding friction TWPs (S-TWPs) and cryogenically milled tire treads were used as research objects to study the ecotoxicity and difference of the above materials before and after aging in natural water (AS-TWPs) to the periphytic biofilm. The results showed that there were significant differences in the microstructure, surface elements, size, functional groups and environmentally persistent free radicals (EPFRs) of the three TWPs. After aging in natural water, the properties of the three TWPs mentioned above showed homogenization, but the EPFRs and reactive oxygen species (ROS) yield were different. After exposure to TWPs (10 mg L-1), total organic carbon and adenosine triphosphate decreased significantly (p < 0.05), and the production of extracellular polymeric substances (EPS) in the periphytic biofilm increased, in which the content of humic-like substance and proteins (tryptophan protein and humic acid-like substances) increased obviously. The increment of TB-EPS was higher than that of LB-EPS, and S-TWPs and AS-TWPs had the strongest promoting effect on EPS secretion. In addition, 10 mg L-1 TWPs caused massive cell death in the periphytic biofilm, which was more obvious in the S-TWPs and AS-TWPs exposure group. The toxic mechanism of TWPs promotes intracellular ROS accumulation and leads to the release of lactate dehydrogenase, which was attributed to the formation of EPFRs on the surface of TWPs and an increase in EPFRs intensity after aging in natural water. TWPs at environmentally relevant concentrations (0.1 mg L-1) had no biological toxicity to periphytic biofilms. This study fills the gap in the study of the surface structure characteristics of TWPs on the toxicity of periphytic biofilms, and is of great significance to the study of the aquatic toxicity mechanism of TWPs.