Long-term phototransformation of microplastics under simulated sunlight irradiation in aquatic environments: Roles of reactive oxygen species

Photoaged polystyrene microplastics serve as photosensitizers that enhance cimetidine photolysis in an aqueous environment

New insights on metal ions accelerating the aging behavior of polystyrene microplastics: Effects of different excess reactive oxygen species

Environmentally persistent free radicals (EPFRs) are a recently recognized component of particulate matter that cause respiratory and cardiovascular toxicity. The mechanism of EPFR toxicity appears to be related to their ability to generate reactive oxygen species (ROS), causing oxidative damage. EPFRs were shown to affect cytochrome P450 (P450) function, inducing the expression of some forms through the Ah receptor. However, another characteristic of EPFRs is their ability to inhibit P450 activities. CYP2E1 is one of the P450s that is inhibited by EPFR (MCP230, the laboratory-generated EPFR made by heating silica 5% copper oxide, and silica [<0.2 μm in diameter] and 2-monochlorophenol at ≥230 °C) exposure. Because CYP2E1 is also known to generate ROS, it is important to understand the ability of EPFRs to influence the function of this enzyme and to identify the mechanisms involved. CYP2E1 was shown to be inhibited by EPFRs and to a lesser extent by non-EPFR particles. Because EPFR-mediated inhibition was more robust at subsaturating NADPH-P450 reductase (POR) concentrations, disruption of POR•CYP2E1 complex formation and electron transfer were examined. Surprisingly, neither complex formation nor electron transfer between POR and CYP2E1 was inhibited by EPFRs. Examination of ROS production showed that MCP230 generated a greater amount of ROS than the non-EPFR control particle (CuO-Si). When a POR/CYP2E1-containing reconstituted system was added to the pollutant-particle systems, there was a synergistic stimulation of ROS production. The results indicate that EPFRs cause inhibition of CYP2E1-mediated substrate metabolism, yet do not alter electron transfer and actually stimulate ROS generation. Taken together, the results are consistent with EPFRs affecting CYP2E1 function by inhibiting substrate metabolism and increasing the generation of ROS. SIGNIFICANCE STATEMENT: Environmentally persistent free radicals affect CYP2E1 function by inhibition of monooxygenase activity. This inhibition is not due to disruption of the POR•CYP2E1 complex or inhibition of electron transfer but due to the uncoupling of NADPH and oxygen consumption from substrate metabolism to the generation of reactive oxygen species. These results show that environmentally persistent free radicals block the metabolism of foreign compounds and synergistically stimulate the formation of reactive oxygen species that lead to oxidative damage within the organism.

Role of polystyrene microplastics in sunlight-mediated transformation of silver in aquatic environments: Mechanisms, kinetics and toxicity

Particulate matter (PM) is emitted during the combustion of fuels and wastes. PM exposure exacerbates pulmonary diseases, and the mechanism may involve oxidative stress. At lower combustion temperatures such as occurs in the cool zone of a flame, aromatic compounds chemisorb to the surface of metal-oxide-containing PM, resulting in the formation of surface-stabilized environmentally persistent free radicals (EPFR). Prior studies showed that PM-containing EPFR redox cycle to produce reactive oxygen species (ROS), and after inhalation, EPFR induce pulmonary inflammation and oxidative stress. Our objective was to elucidate mechanisms linking EPFR-induced oxidant injury with increased cytokine production by pulmonary epithelial cells. We thus treated human bronchial epithelial cells with EPFR at sub-toxic doses and measured ROS and cytokine production. To assess aryl hydrocarbon receptor (AhR) activity, cells were transfected with a luciferase reporter for xenobiotic response element activation. To test whether cytokine production was dependent upon AhR activation or oxidative stress, some cells were co-treated with an antioxidant or an AhR antagonist. EPFR increased IL-6 release in an ROS and AhR- and oxidant-dependent manner. Moreover, EPFR induced an AhR activation that was dependent upon oxidant production, since antioxidant co-treatment blocked AhR activation. On the other hand, EPFR treatment increased a cellular ROS production that was at least partially attenuated by AhR knockdown using siRNA. While AhR activation was correlated with an increased expression of oxidant-producing enzymes like cytochrome P450 CYP1A1, it is possible that AhR activation is both a cause and effect of EPFR-induced ROS. Finally, lipid oxidation products also induced AhR activation. ROS-dependent AhR activation may be a mechanism for altered epithelial cell responses after EPFR exposure, potentially via formation of bioactive lipid or protein oxidation products.

Abstract. A series of emission control measures implemented by the Chinese government have effectively reduced air pollution by multiple pollutants in many regions of the country in recent decades. However, the impacts of these control measures on environmental persistent free radicals (EPFRs) and reactive oxygen species (ROSs), the two groups of chemical species that are known to be linked with adverse human health effects, are still not clear. In this study, we investigated the levels, patterns, and sources of EPFRs and gas- and particle-phase ROSs (referred to as G-ROSs and P-ROSs, respectively) in Beijing during the 2015 China Victory Day Parade period when short-term air quality control measures were imposed. EPFRs in the non-control period (NCP) tended to be radicals centered on a mixture of carbon and oxygen, while those in the control period (CP) were mainly oxygen-centered free radicals. The contribution of G-ROSs to the atmospheric oxidizing capacity increased, and that of P-ROSs decreased during the CP compared to the NCP. The strict control measures reduced ambient EPFRs, G-ROSs, and P-ROSs by 18.3 %, 24.1 %, and 46.9 %, respectively; these amounts were smaller than the decreases in most other measured pollutants. Although particle-matter-based air quality control measures have performed well in achieving “Parade Blue”, it is difficult to simultaneously reduce the negative impacts of the atmosphere on human health. The Parade Blue days were largely attributed to the dramatic reduction in secondary aerosols, which were also largely responsible for EPFR and ROS reductions. Compared to the cases during the NCP, the source-sector-based concentrations of PM2.5, EPFRs, G-ROSs, and P-ROSs during the CP were reduced by 78.7 %–80.8 % when coming from secondary aerosols, by 59.3 %–65.0 % when coming from dust sources, by 65.3 %–67.0 % when coming from industrial emissions, and by 32.6 %–43.8 % when coming from vehicle emissions, while concentrations from other sources increased by 1.61 %–71.5 %. Vehicle emissions and other sources may play complex roles in air quality and public health. This insight will prompt policymakers to reevaluate current air quality management strategies to more effectively address the challenges posed by pollutants such as EPFRs and ROSs.

Environmentally persistent free radicals (EPFRs) are a new class of pollutants that have been identified as potential environmental contaminants due to their persistence and ability to generate reactive oxygen species (ROS) that cause oxidative stress in living organisms. This study investigates the formation and behavior of EPFRs during the photodegradation of organic pollutants, emphasizing the role of metal ions, precursor concentration, and environmental conditions. Results show that light exposure significantly enhances pollutant degradation rates, EPFR yield, and formation speed, though it simultaneously shortens EPFR lifespan due to reactive oxygen species (ROS) generation. In dark conditions, EPFR formation is slower but results in more stable radicals. Metal ions play a pivotal role, with Cu(II) exhibiting the highest EPFR generation capacity due to its strong electron-accepting properties, surpassing Zn(II) and Na(I), highlighting that metal ions with greater oxidizing potential enhance EPFR formation. The precursor, as both reaction product and reactant, plays a dual role in EPFR formation. Individual compounds like anthracene (ANT) yield stable carbon-centered radicals, while mixtures of polycyclic aromatic hydrocarbons (PAHs) produce more complex radical spectra. The study of the influencing factors and transformation mechanisms of EPFR generation in soil can provide a more comprehensive understanding of the environmental behavior of new pollutants, provide a scientific basis for sustainable development, and be of great significance for the assessment and management of environmental risks and the protection of the ecological environment.

Levels, spatial distribution, and source identification of airborne environmentally persistent free radicals from tree leaves

Microplastics (MPs) are presumed to be inert during aging under ambient conditions. In this study, four types of virgin MPs, including polystyrene (PS), phenol-formaldehyde resin (PF), polyethylene (PE), and polyvinyl chloride (PVC), were aged under simulated solar light irradiation. Surprisingly, several environmentally persistent free radicals (EPFRs), which are considered to be a type of emerging contaminant, were detected on the irradiated PS and PF, rather than PE and PVC, by electron paramagnetic resonance (EPR) spectroscopy. Depending on the photoaging duration time, the characteristic g-factors of the EPFRs produced on PS and PF were 2.0044-2.0049 and 2.0043-2.0044, respectively. The generated EPFRs on PS and PF decayed rapidly at the initial stage and then slowly disappeared with the elapsed aging time. Analyses by attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR), X-ray photoelectron spectroscopy (XPS), nuclear magnetic resonance (NMR), and gel permeation chromatography (GPC) suggested that MPs might experience chemical chain scission, O2/H2O addition, and EPFR formation under the light irradiation. Accompanying with the formation of EPFRs, reactive oxygen species, such as O2•- and •OH, were also observed. The findings provide a novel insight to evaluate the potential hazards of MPs to organisms and ecosystems.

Environmentally persistent free radicals (EPFRs) are stable free radicals formed on particulate matter (PM) through processes such as combustion and pyrolysis. These free radicals are generated on transition metal oxide surfaces in the presence of aromatic precursors. Exposure to EPFRs occurs primarily via inhalation of PM deriving from combustion, traffic, industrial activities, and both indoor and outdoor burning. Other environmental factors that might generate EPFRs are radon, electronic and tobacco cigarettes. EPFRs exhibit unexpectedly long half-lives, ranging from several weeks to, in some cases, several years. EPFRs may be carbon-centered, oxygen-centered or mixed, identified by g-values exhibited in electron paramagnetic resonance analysis. The radicals undergo redox cycling within aqueous solutions and in biological tissues/fluids triggering production of reactive oxygen species (ROS), comprised primarily of hydroxyl, superoxide, and peroxyl radicals. The stability of EPFRs, their association with PM2.5, and their ability to generate ROS may pose significant concerns for human health. To determine whether there are sufficient data for risk assessment, recent advances were examined in the following important aspects of EPFR research: (1) atmospheric chemistry, (2) human exposures, (3) animal toxicity, and (4) epidemiology. Our review found insufficient epidemiological and exposure studies; however, toxicological data in animals suggested that EPFR inhalation contributes to cardiovascular, respiratory, and metabolic diseases. Although EPFRs are not currently surveyed by a regulatory monitoring system, data indicate their widespread presence in the environment and their potential to initiate/exacerbate diseases.

Polyaromatic hydrocarbons and microplastics are common atmospheric pollutants, but their interaction processes and influence on one another under sunlight irradiation are unknown. Herein, the synergistic transformation of polystyrene microplastics (PS-MP) adsorbed with benzo[a]pyrene (B[a]P) was studied upon exposure to simulated sunlight. During this process, B[a]P accelerated the photoaging process of PS-MP. UV-visible near-infrared diffuse reflectance spectrometer (UV-vis RDS) analysis of the PS-MP/B[a]P complex revealed that B[a]P and its photodegradation products containing chromophore groups, such as ethers, ketones, carboxylic compounds, and aromatic compounds, significantly expanded the wavelength range and enhanced the absorption intensity of sunlight by PS-MP. Moreover, the absorbed light energy was transferred to PS-MP in the form of energy or electrons, which expedited the bond breaking of PS-MP and generated additional binding sites for oxygen. Meanwhile, direct photolysis of B[a]P was initially impeded by PS-MP due to its shielding effects. Subsequently, reactive oxygen species (ROS) induced by persistent free radicals (PFRs) on the photoaged PS-MP promoted B[a]P degradation. The synergistic interaction between PS-MP and B[a]P enhanced PFRs and ROS generation, potentially elevating their environmental risk. This research offered novel perspectives on ecological behavior and the associated risks of MP with exogenous organic pollutants.

Elucidating the role of overlooked environmentally persistent free radicals and reactive chlorine species on photoaged chlorine-containing microplastics: New insights into formation mechanisms and health risks.

A short review on environmental distribution and toxicity of the environmentally persistent free radicals

What are the drivers of tetracycline photolysis induced by polystyrene microplastic?

Can the concentration of environmentally persistent free radicals describe its toxicity to Caenorhabditis elegans? Evidence provided by neurotoxicity and oxidative stress