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Air pollution is a significant concern for human health, particularly in relation to cardiovascular damage. Currently, the precise mechanisms underlying myocardial tissue injury induced by air pollution remain to be fully elucidated. Oil mist particulate matter (OMPM) is a key environmental factor that has been linked to increased mortality from cardiovascular diseases. The research aims to explore the detrimental effects and underlying molecular mechanisms of OMPM exposure on myocardial tissue. In this study, we established exposure models with different concentrations of OMPM both in vivo and in vitro to assess their deleterious effects on myocardial tissue. The results indicated that OMPM exposure induced alterations in myocardial enzymes and large accumulation of lipid droplets in rat myocardial tissue, with a dose-dependent increase in cell apoptosis, oxidative stress, and inflammatory responses, accompanied by mitochondrial structural damage and dysfunction. Proteomic analysis suggested that OMPM induced myocardial tissue damage is closely associated with changes in mitochondrial biological functions and fatty acid metabolism, possibly through inhibition of the PPAR signaling pathway. Further experiments using a PPARα agonist (WY-14643) and PPARα siRNA transfection cell model demonstrated that WY-14643 could mitigate abnormal fatty acid metabolism, mitochondrial dysfunction, and cell apoptosis caused by OMPM exposure. Overall, the study suggests that OMPM exposure disrupts myocardial fatty acid metabolism, contributes to mitochondrial damage and dysfunction through targeted inhibition of the PPAR signaling pathway, and ultimately results in cardiomyocyte apoptosis and myocardial tissue injury., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Exposure to fine atmospheric particulate matter (PM) is known to induce lung inflammation and injury; however, the way in which sophisticated endogenous lung repair and regenerative programs respond to this exposure remains unknown. In this study, we established a whole-body mouse exposure model to mimic real scenarios. Exposure to fine PM (PM with an aerodynamic diameter ≤ 2.5 µm [PM 2.5 ]; mean 1.05 mg/m 3 ) for 1-month elicited inflammatory infiltration and epithelial alterations in the lung, which were resolved 6 months after cessation of exposure. Immune cells that responded to PM 2.5 exposure mainly included macrophages and neutrophils. During PM 2.5 exposure, alveolar epithelial type 2 cells initiated rapid repair of alveolar epithelial mucosa through proliferation. However, the reparative capacity of airway progenitor cells (club cells) was impaired, which may have been related to the oxidative production of neutrophils or macrophages, as suggested in organoid co-cultures. These data suggested that the pulmonary toxic effects of short-term exposure to fine atmospheric PM at a certain dosage could be overcome through tissue reparative mechanisms., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Non-coding RNAs appear to be involved in the regulation of the nervous system. However, no competing endogenous RNA (ceRNA) network related to PM 2.5 damage in the hippocampal function has yet been constructed. Herein, we used whole-transcriptome sequencing technology to systematically study the ceRNA network in rat hippocampi after PM 2.5 exposure. We identified 100 circRNAs, 67 lncRNAs, 28 miRNAs, and 539 mRNAs and constructed the most comprehensive ceRNA network to date, to our knowledge. Gene Ontology and KEGG analyses showed that the network molecules are involved in synapses, neural projections, and neural development and involve signal pathways such as the synaptic vesicle cycle. Finally, the expression of the differentially expressed RNAs confirmed by quantitative real-time PCR was consistent with the sequencing data. This study systematically dissected the ceRNA atlas related to cognitive memory function in the hippocampal tissue of PM 2.5 -exposed rats for the first time, to our knowledge, and promotes the development of potential new treatments for cognitive impairment., (Copyright © 2021 Elsevier Inc. All rights reserved.)

PM 2.5 and formaldehyde (FA) are major outdoor and indoor air pollutants in China, respectively, and both are known to be harmful to human health and to be carcinogenic. Of all the known chronic health effects, leukaemia is one of the most serious health risks associated with these two pollutants. To explore the influence and underlying mechanisms of exposure to formaldehyde and PM 2.5 on hematopoietic toxicity, we systematically studied the toxicity induced in hematopoietic organs: bone marrow (BM); spleen; and myeloid progenitor cells (MPCs). Male Balb/c mice were exposed to: PM 2.5 (20, 160 μg/kg·d) at a dose of 40 μL per mouse or formaldehyde (0.5, 3.0 mg/m 3 ) for 8 h per day for 2 weeks or co-exposed to formaldehyde and PM 2.5 (20 μg/kg·d PM 2.5  + 0.5 mg/m 3 FA, 20 μg/kg·d PM 2.5  + 3 mg/m 3 FA, 160 μg/kg·d PM 2.5  + 0.5 mg/m 3 FA, 160 μg/kg·d PM 2.5  + 3 mg/m 3 FA) for 2 weeks. Similar toxic effects were found in the formaldehyde-only and PM 2.5 -only groups, including significant decrease of blood cells and MPCs, along with decreased expression of hematopoietic growth factors. In addition, individual exposure of formaldehyde or PM 2.5 increased oxidative stress, DNA damage and immune system disorder by destroying the balance of Th1/Th2, and Treg/Th17. DNA repair was markedly inhibited by deregulating the mammalian target of rapamycin (mTOR) pathway. Combined exposure to PM 2.5 and formaldehyde led to more severe effects. Administration of Vitamin E (VE) was shown to attenuate these effects. In conclusion, our findings suggested that PM 2.5 and formaldehyde may induce hematopoietic toxicity by reducing the expression of hematopoietic growth factors, increasing oxidative stress and DNA damage, activating the 'immune imbalance' pathway and suppressing the DNA-repair related mTOR pathway. The hematopoietic toxicity induced by combined exposure of PM 2.5 and formaldehyde might provide further insights into the increased incidence of hematological diseases, including human myeloid leukaemia., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Epidemiological studies have revealed that ambient fine particulate matter (PM2.5) exposure is closely associated with autism spectrum disorder (ASD). However, there is a relative paucity of laboratory data to support this epidemic finding. In order to assess the relationship between PM2.5 exposure and ASD, neonatal male Sprague-Dawley rats were chosen and exposed to PM2.5 (2 or 20 mg/kg body weight, once a day) by intranasal instillation from postnatal day 8 to 22. It was found that when exposed to PM2.5 in the early neonatal period for two weeks, both groups of the exposure rats manifested typical behavioral features of autism, including communication deficits, poor social interaction, and novelty avoidance. And, we further found, among five ASD candidate genes we chose, both the mRNA level and protein expression of SH3 and multiple ankyrin repeat domains 3 (Shank3) decreased significantly in the rat hippocampus after high dose of PM2.5 exposure. Moreover, results showed that PM2.5-exposure significantly increased the levels of proinflammatory cytokines, interleukin 1β, interleukin 6, and tumor necrosis factor alpha in the hippocampus and prefrontal cortex. The expression of glial fibrillary acidic protein and ionized calcium-binding adapter molecule, markers of astrocytes and microglial cell activation, respectively, also increased in the exposed animals. Our work provides new data on the link between postnatal exposure to ambient PM2.5 and the onset of ASD-like symptoms in human beings, and the increased inflammatory response and abnormalities in Shank3 expression in the brain may contribute to the mechanisms of PM2.5 exposure-induced ASD.

Asthma is a complex pulmonary inflammatory disease that can be promoted by air pollutants such as PM2.5 and formaldehyde (FA). However, existent experimental evidence principally focuses on the negative influence of a single air pollutant, neglecting the possible synergistic effect in biological responses to mixture of these pollutants, a more common situation in our daily life. In this study, allergic Balb/c mice were exposed to a mixture of PM2.5 and FA, and their toxicological effects and mechanisms were explored. It is demonstrated that the combined exposure to PM2.5 and FA can greatly aggravate allergic asthma in mice. When compared with exposure to PM2.5 or FA alone, the co-exposure showed a certain synergistic effect. Increased levels of ROS, inflammatory factors and total serum immunoglobulin E were concomitant with this deterioration. Furthermore, results suggested that co-exposure exacerbated the activation of TRPV1 signal pathways, with an enhancement in substance P and calcitonin gene-related peptide production, which contributed to inflammation in asthma by neurogenic inflammation. The study also proved that capsazepine treatment could reduce the levels of not only pro-inflammatory neuropeptides, but also oxidative stress. It is concluded that co-exposure to PM2.5 and FA exacerbated allergic asthma through oxidative stress and enhanced TRPV1 activation.

Growing concern has been raised over the potential hazard of nanoparticles (NPs) on human health from ambient particulate air pollution. Silicon dioxide (SiO 2 ) NPs are one of the most widely used nanoparticles in many sectors of industry. Research on NPs has focused mainly on their toxicity in organs. Meanwhile, NPs are present in the air year-round, but are more serious in winter. Thus, the aim of this study was to evaluate the inflammatory response to SiO 2 NPs using in vivo test systems. The composition of particulate matter is complicated; however, elemental silicon accounts for a significant proportion. Cold exposure can induce many kinds of systemic reactions. Thus, the second aim of this study was also to evaluate the combined effect of NPs and cold exposure on human health. There is little research on the combined effects of nanoparticles and cold on inflammation. Sprague-Dawley rats were randomly divided into four groups: those exposed to SiO 2 NPs by intratracheal instillation, those exposed to at 4 °C 4 h/day for 4 weeks, a combined SiO 2 NPs and cold exposure group, and a control group. Inflammatory cell infiltration in the lungs was mainly observed after exposure to SiO 2 NPs or cold. Hematoxylin and eosin staining revealed that inflammation of the lungs was more serious in the combined group. In the white adipose tissue and brown adipose tissue of the combined groups, the mRNA expressions of pro-inflammatory cytokines were upregulated. In conclusion, SiO 2 NPs combined with cold exposure induced a stronger systemic inflammatory response, accompanied by more serious health hazards.

The toxic effects of coal combustion related fine particulate matter (PM2.5), collected from Datong, Shanxi province, China, on nematode Caenorhabditis elegans were investigated. Exposure to PM2.5 resulted in deficits in development, reproduction, locomotion behavior, and lifespan, and induction of intestinal autofluorescence or reactive oxygen species (ROS) production. Prolonged exposure to PM2.5 led to more severe toxicity on nematodes than acute exposure. In addition, exposure to PM2.5 induced altered expression patterns of genes required for the control of oxidative stress. Reduction in mean defecation cycle length and developmental deficits in AVL and DVB neurons, which are involved in the control of defecation behavior, were also triggered by PM2.5 exposure. Thus, oxidative stress and abnormal defecation behavior may contribute greatly to the toxicity of coal combustion related PM2.5 in nematodes. The results also imply that the long-term adverse effects of coal combustion related PM2.5 on environmental organisms should be carefully considered., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Numerous studies have demonstrated the toxic effects of fine particle matter less than 2.5 μm (PM2.5) on health of human. However, little information is available on PM2.5 ecotoxicity. We employed Caenorhabditis elegans to investigate the adverse effects of traffic-related PM2.5 on exposed animals and their progeny. Acute exposure to high concentrations of PM2.5 in the range of mg/L caused adverse effects on development, lifespan, reproduction, and locomotion behavior of nematodes. In contrast, prolonged exposure to low concentrations of PM2.5 in the range of μg/L resulted in adverse effects on development, lifespan, reproduction, locomotion behavior, and intestinal development of nematodes. Prolonged exposure to PM2.5 could even cause adverse effects on lifespan, reproduction, locomotion behavior, and intestinal development in progeny of exposed nematodes. PM2.5 toxicity was only partially recovered in progeny of exposed nematodes. For the PM2.5 toxicity on nematodes and their progeny, we hypothesize that it might be the combinational effects of oxidative stress, damage on intestinal barrier, and abnormal defecation behavior. Our data here imply the potential toxic effects of long-term exposure to traffic-related PM2.5 on environmental organisms. Our results further highlight the possible crucial roles of biological barrier and defecation behavior in regulating the PM2.5 toxicity., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Metabolites produced by the human gut microbiota play an important role in fighting and intervening in inflammatory diseases. It remains unknown whether immune homeostasis is influenced by increasing concentrations of air pollutants such as oil mist particulate matters (OMPM). Herein, we report that OMPM exposure induces a hyperlipidemia-related phenotype through microbiota dysregulation-mediated downregulation of the anti-inflammatory short-chain fatty acid (SCFA)–GPR43 axis and activation of the inflammatory pathway. A rat model showed that exposure to OMPM promoted visceral and serum lipid accumulation and inflammatory cytokine upregulation. Furthermore, our research indicated a reduction in both the "healthy" microbiome and the production of SCFAs in the intestinal contents following exposure to OMPM. The SCFA receptor GPR43 was downregulated in both the ileum and white adipose tissues (WATs). The OMPM treatment mechanism was as follows: the gut barrier was compromised, leading to increased levels of lipopolysaccharide (LPS). This increase activated the Toll-like receptor 4 Nuclear Factor-κB (TLR4-NF-κB) signaling pathway in WATs, consequently fueling hyperlipidemia-related inflammation through a positive-feedback circuit. Our findings thus imply that OMPM pollution leads to hyperlipemia-related inflammation through impairing the microbiota-SCFAs-GPR43 pathway and activating the LSP-induced TLR4-NF-κB cascade; our findings also suggest that OMPM pollution is a potential threat to humanmicrobiota dysregulation and the occurrence of inflammatory diseases. [Display omitted] • OMPM can induce hyperlipidaemia-related inflammation and macrophage infiltration. • OMPM can disturb gut microbiota to inhibit anti-inflammatory SCFAs-GPR43 signaling. • OMPM can impair the intestinal barrier to release LPS into serum. • OMPM can activate the LPS-TLR4/NF-κB pathway to induce body inflammation. [ABSTRACT FROM AUTHOR]

Sidestream cigarette smoke, the major component of environmental tobacco smoke, is a complex and reactive aerosol. The particulate matter (PM) in sidestream smoke is one of the carriers of chemical constituents. However, particle size-dependent toxicological effects of PM are poorly understood. In this study, we evaluated the relationship between the PM size and in vitro cytotoxicity and mutagenicity of sidestream cigarette smoke. A NanoMoudi-II 125A was used to collect PM samples ranging from 10 nm to 10 μm. The in vitro toxicity of PM was evaluated using a neutral red cytotoxicity assay and Salmonella mutagenicity assay. The results showed that the cytotoxicity and mutagenicity of PM larger than 1 μm was significantly lower than PM sized 10 nm-1 μm. Furthermore, there was a noticeable trend that the smaller the size of the PM of sidestream cigarette smoke, the greater the toxicity. This study suggests that the toxicity of PM in sidestream cigarette smoke is size-dependent. [ABSTRACT FROM AUTHOR]