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1.
J Hazard Mater ; 441: 129846, 2023 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-36063712

RESUMO

Exhaust emissions from gasoline vehicles are one of the major contributors to aerosol particles observed in urban areas. It is well-known that these tiny particles are associated with air pollution, climate forcing, and adverse health effects. However, their toxicity and bioreactivity after atmospheric ageing are less constrained. The aim of the present study was to investigate the chemical and toxicological properties of fresh and aged particulate matter samples derived from gasoline exhaust emissions. Chemical analyses showed that both fresh and aged PM samples were rich in organic carbon, and the dominating chemical species were n-alkane and polycyclic aromatic hydrocarbons. Comparisons between fresh and aged samples revealed that the latter contained larger amounts of oxygenated compounds. In most cases, the bioreactivity induced by the aged PM samples was significantly higher than that induced by the fresh samples. Moderate to weak correlations were identified between chemical species and the levels of biomarkers in the fresh and aged PM samples. The results of the stepwise regression analysis suggested that n-alkane and alkenoic acid were major contributors to the increase in lactate dehydrogenase (LDH) levels in the fresh samples, while polycyclic aromatic hydrocarbons (PAHs) and monocarboxylic acid were the main factors responsible for such increase in the aged samples.


Assuntos
Poluentes Atmosféricos , Hidrocarbonetos Policíclicos Aromáticos , Aerossóis/análise , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Alcanos/análise , Carbono/análise , Gasolina/análise , Gasolina/toxicidade , Hong Kong , Lactato Desidrogenases/análise , Material Particulado/análise , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Emissões de Veículos/análise , Emissões de Veículos/toxicidade
2.
J Hazard Mater ; 441: 129792, 2023 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-36084470

RESUMO

Cooking Oil Fumes (COFs) contain carcinogenic organic substances such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs), of which 2-Amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) is known as mainly meat-borne carcinogens. In this work, to identify the mechanisms to induce the inflammation response in human lung cells (A549) exposed to COFs, we investigated the physicochemical and biological characteristics of COFs generated with PhIP precursors (L-phenylalanine, creatinine, and glucose) at high cooking temperatures (300 °C and 600 °C). Interestingly, we found that PhIP was not formed both at 300 °C and 600 °C, while a large number of carbon nanoparticles were generated from soybean oil containing the PhIP precursors at 600 °C. From the biological analysis, COFs generated with the PhIP precursors at 600 °C induced the most significant pro-inflammatory cytokine (IL-6). This result indicates that the particulate matter in COFs generated with the PhIP precursors above the smoke temperature is the primary factor directly affecting the lung inflammatory response rather than PhIP. This study demonstrates for the first time a novel principle of the inflammatory response that the PhIP precursors can aggravate lung injury by affecting the physical properties of COFs depending on cooking temperature. Therefore, our finding is a significant result of overcoming the bias in previous studies focusing only on the chemical toxicity of PhIP in the inflammatory response of COFs.


Assuntos
Material Particulado , Hidrocarbonetos Policíclicos Aromáticos , Aminas/análise , Carbono/análise , Carcinógenos/análise , Culinária , Creatinina/análise , Glucose , Humanos , Inflamação/induzido quimicamente , Interleucina-6 , Pulmão , Carne/análise , Material Particulado/análise , Material Particulado/toxicidade , Fenilalanina , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Fumaça/análise , Óleo de Soja/análise , Temperatura
3.
J Hazard Mater ; 442: 130087, 2023 01 15.
Artigo em Inglês | MEDLINE | ID: mdl-36206715

RESUMO

Environmental persistent free radicals (EPFRs) are new environmental health risk substances in the atmosphere, and their oxidative toxicity (OT) has not been strongly confirmed. In this study, the fugitive characteristics of EPFRs in road dust in a metropolitan city located in northwest China, and their potential oxidative toxicity were investigated. The results showed that the road dust contains Carbon-centered EPFRs with the mean mass concentration of (6.6 ± 5.0) × 1017 spins/g. EPFRs in road dust are degradable and have a half-life of 4.5 years. The water insoluble (WIS) components contribute 71% to the oxidative toxicity of road dust and show a rapid toxicity generation process, while the oxidative toxicity generation rate of water-soluble dust is more stable. Based on the positive matrix factorization (PMF) model, the contribution of EPFRs-dominated factors to Total-OT and WIS-OT is 17.3% and 33.3%, respectively. The PMF model results indicated that different types of EPFRs contributed differently to the oxidative toxicity of road dust and Carbon-centered EPFRs are more likely to participate in reactive oxygen species generation. Our results highlight that the EPFRs are an important contributor to the oxidative toxicity of atmospheric particulate matter, and their oxidative toxicity is dependent on the types of free radicals. It also provides an important insight into the influence of other potentially toxic substances on the oxidative toxicity of atmospheric PM.


Assuntos
Poluentes Atmosféricos , Poeira , Poeira/análise , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Espécies Reativas de Oxigênio , Material Particulado/toxicidade , Material Particulado/análise , Radicais Livres , Monitoramento Ambiental , China , Carbono , Água
4.
J Hazard Mater ; 441: 129874, 2023 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-36084462

RESUMO

Wood burning is a major source of ambient particulate matter (PM) and has been epidemiologically linked to adverse pulmonary health effects, however the impact of fuel and burning conditions on PM properties has not been investigated systematically. Here, we employed our recently developed integrated methodology to characterize the physicochemical and biological properties of emitted PM as a function of three common hardwoods (oak, cherry, mesquite) and three representative combustion conditions (flaming, smoldering, incomplete). Differences in PM and off-gas emissions (aerosol number/mass concentrations; carbon monoxide; volatile organic compounds) as well as inorganic elemental composition and organic carbon functional content of PM0.1 were noted between wood types and combustion conditions, although the combustion scenario exerted a stronger influence on the emission profile. More importantly, flaming combustion PM0.1 from all hardwoods significantly stimulated the promoter activity of Sterile Alpha Motif (SAM) pointed domain containing ETS (E-twenty-six) Transcription Factor (SPDEF) in human embryonic kidney 293 (HEK-293 T) cells, a biomarker for mucin gene expression associated with mucus production in pulmonary diseases. However, no bioactivity was observed for smoldering and incomplete combustion, which was likely driven by differences in the organic composition of PM0.1. Detailed chemical speciation of organic components of wood smoke is warranted to identify the individual compounds that drive specific biological responses.


Assuntos
Poluentes Atmosféricos , Compostos Orgânicos Voláteis , Poluentes Atmosféricos/análise , Monóxido de Carbono/análise , Células HEK293 , Humanos , Mucinas/análise , Material Particulado/análise , Material Particulado/toxicidade , Aerossóis e Gotículas Respiratórios , Fumaça/análise , Fatores de Transcrição , Compostos Orgânicos Voláteis/análise , Madeira/química
5.
J Environ Sci (China) ; 124: 451-461, 2023 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-36182153

RESUMO

Inflammation is a major adverse outcome induced by inhaled particulate matter with a diameter of ≤ 2.5 µm (PM2.5), and a critical trigger of most PM2.5 exposure-associated diseases. However, the key molecular events regulating the PM2.5-induced airway inflammation are yet to be elucidated. Considering the critical role of circular RNAs (circRNAs) in regulating inflammation, we predicted 11 circRNAs that may be involved in the PM2.5-induced airway inflammation using three previously reported miRNAs through the starBase website. A novel circRNA circ_0008553 was identified to be responsible for the PM2.5-activated inflammatory response in human bronchial epithelial cells (16HBE) via inducing oxidative stress. Using a combinatorial model PM2.5 library, we found that the synergistic effect of the insoluble core and loaded Zn2+ ions at environmentally relevant concentrations was the major contributor to the upregulation of circ_0008553 and subsequent induction of oxidative stress and inflammation in response to PM2.5 exposures. Our findings provided new insight into the intervention of PM2.5-induced adverse outcomes.


Assuntos
MicroRNAs , RNA Circular , Células Epiteliais/metabolismo , Humanos , Inflamação/induzido quimicamente , MicroRNAs/metabolismo , Estresse Oxidativo , Material Particulado/toxicidade , Zinco/toxicidade
6.
J Toxicol Environ Health B Crit Rev ; 25(8): 422-444, 2022 Nov 17.
Artigo em Inglês | MEDLINE | ID: mdl-36351256

RESUMO

The complex, variable mixtures present in fine particulate matter (PM2.5) have been well established, and associations between chemical constituents and human health are expanding. In the past decade, there has been an increase in PM2.5 toxicology studies that include chemical analysis of samples. This investigation is a crucial component for identifying the causal constituents for observed adverse health effects following exposure to PM2.5. In this review, investigations of PM2.5 that used both in vivo models were explored and chemical analysis with a focus on respiratory, cardiovascular, central nervous system, reproductive, and developmental toxicity was examined to determine if chemical constituents were considered in the interpretation of the toxicity findings. Comparisons between model systems, PM2.5 characteristics, endpoints, and results were made. A vast majority of studies observed adverse effects in vivo following exposure to PM2.5. While limited, investigations that explored connections between chemical components and measured endpoints noted significant associations between biological measurements and a variety of PM2.5 constituents including elements, ions, and organic/elemental carbon, indicating the need for such analysis. Current limitations in available data, including relatively scarce statistical comparisons between collected toxicity and chemical datasets, are provided. Future progress in this field in combination with epidemiologic research examining chemical composition may support regulatory standards of PM2.5 to protect human health.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Humanos , Material Particulado/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise
7.
Int J Mol Sci ; 23(21)2022 Oct 27.
Artigo em Inglês | MEDLINE | ID: mdl-36361823

RESUMO

BACKGROUND: An emerging body of evidence indicates an association between anthropogenic particulate matter (PM) and neurodegeneration. Although the historical focus of PM toxicity has been on the cardiopulmonary system, ultrafine PM particles can also exert detrimental effects in the brain. However, only a few studies are available on the harmful interaction between PM and CNS and on the putative pathomechanisms. METHODS: Ultrafine PM particles with a diameter < 0.1 µm (PM0.1) and nanoparticles < 20 nm (NP20) were sampled in a lab-scale combustion system. Their effect on cell tracking in the space was studied by time-lapse and high-content microscopy in NSC-34 motor neurons while pHrodo™ Green conjugates were used to detect PM endocytosis. Western blotting analysis was used to quantify protein expression of lysosomal channels (i.e., TRPML1 and TPC2) and autophagy markers. Current-clamp electrophysiology and Fura2-video imaging techniques were used to measure membrane potential, intracellular Ca2+ homeostasis and TRPML1 activity in NSC-34 cells exposed to PM0.1 and NP20. RESULTS: NP20, but not PM0.1, reduced NSC-34 motor neuron movement in the space. Furthermore, NP20 was able to shift membrane potential of motor neurons toward more depolarizing values. PM0.1 and NP20 were able to enter into the cells by endocytosis and exerted mitochondrial toxicity with the consequent stimulation of ROS production. This latter event was sufficient to determine the hyperactivation of the lysosomal channel TRPML1. Consequently, both LC3-II and p62 protein expression increased after 48 h of exposure together with AMPK activation, suggesting an engulfment of autophagy. The antioxidant molecule Trolox restored TRPML1 function and autophagy. CONCLUSIONS: Restoring TRPML1 function by an antioxidant agent may be considered a protective mechanism able to reestablish autophagy flux in motor neurons exposed to nanoparticles.


Assuntos
Material Particulado , Canais de Potencial de Receptor Transitório , Material Particulado/toxicidade , Material Particulado/análise , Antioxidantes/farmacologia , Lisossomos/metabolismo , Autofagia , Neurônios Motores/metabolismo , Canais de Potencial de Receptor Transitório/metabolismo
8.
Ecotoxicol Environ Saf ; 247: 114231, 2022 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-36327781

RESUMO

PM2.5 pollution is related to neurotoxic and vascular effects in eye diseases such as glaucoma. This study investigates the adverse effects of PM2.5 exposure on visual function and retinal neurons. A versatile aerosol concentration enrichment system was used to expose mice to either control air or PM2.5 polluted air. Six months after PM2.5 exposure, visual function was measured by electroretinography (ERG). Hematoxylin and eosin staining and immunofluorescence staining were used for histopathological analysis. Protein markers of apoptosis, astrocytic reactivity, inflammatory cytokines, lipid peroxidation, protein nitration and DNA damage response were quantified with ELISA, western blot or detected using immunofluorescence and immunohistochemistry. After six months of exposure, PM2.5-exposed mice responded poorly to light stimuli compared with those exposed to the control air. PM2.5 exposure caused retinal thinning and reduction in the expression of retinal ganglion cell-selective marker RNA-binding protein with multiple splicing (RBPMS). Further, positive TUNEL staining was observed in the inner nucleus and outer nuclear layers of the retinae after exposure to PM2.5, which was accompanied by the activation of apoptosis signaling molecules p53, caspase-3 and Bax. PM2.5 induced the release of inflammatory cytokines including tumor necrosis factor-α and cleaved interleukin-1ß. Furthermore, increased levels of 8-OHdG and γ-H2AX in the mouse retinea were indicative of DNA single and double strand breaks by PM2.5 exposure, which activated PARP-1 mediated DNA damage and repair. In conclusion, this study demonstrates sub-chronic systemic exposure to concentrated PM2.5 causes visual dysfunction and retinal neuronal degeneration. DATA AVAILABILITY: The datasets during and/or analyzed during the current study available from the corresponding author on reasonable request.


Assuntos
Poluição do Ar , Material Particulado , Camundongos , Animais , Material Particulado/toxicidade , Retina , Coloração e Rotulagem , Hematoxilina
9.
Ecotoxicol Environ Saf ; 247: 114266, 2022 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-36334339

RESUMO

Particulate matter 2.5 (PM2.5) is a widely known atmospheric pollutant which can induce the aging-related pulmonary diseases such as acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and interstitial pulmonary fibrosis (IPF). In recent years, with the increasing atmospheric pollution, airborne fine PM2.5, which is an integral part of air pollutants, has become a thorny problem. Hence, this study focused on the effect of PM2.5 on cellular senescence in the lung, identifying which inflammatory pathway mediated PM2.5-induced cellular senescence and how to play a protective role against this issue. Our data suggested that PM2.5 induced time- and concentration-dependent increasement in the senescence of A549 cells. Using an inhibitor of cGAS (PF-06928215) and an inhibitor of NF-κB (BAY 11-7082), it was revealed that PM2.5-induced senescence was regulated by inflammatory response, which was closely related to the cGAS/STING/NF-κB pathway activated by DNA damage. Moreover, our study also showed that the pretreatment with selenomethionine (Se-Met) could inhibit inflammatory response and prevent cellular senescence by hindering cGAS/STING/NF-κB pathway in A549 cells exposed to PM2.5. Furthermore, in vivo C57BL/6J mice model demonstrated that aging of mouse lung tissue caused by PM2.5 was attenuated by decreasing cGAS expression after Se-Met treatment. Our findings indicated that selenium made a defense capability for PM2.5-induced cellular senescence in the lung, which provided a novel insight for resisting the harm of PM2.5 to human health.


Assuntos
NF-kappa B , Selenometionina , Humanos , Animais , Camundongos , Camundongos Endogâmicos C57BL , Material Particulado/toxicidade , Senescência Celular , Antioxidantes , Nucleotidiltransferases , Pulmão
10.
Ecotoxicol Environ Saf ; 247: 114253, 2022 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-36343449

RESUMO

BACKGROUND: Ambient fine particulate matter (PM2.5) exposure increases local and systemic interleukin-6 (IL-6). However, the pathogenic role of IL-6 signalling following PM2.5 exposure, particularly in the development of pulmonary dysfunction and abnormal glucose homeostasis, has hardly been investigated. RESULTS: In the study, IL-6 receptor (IL-6R)-deficient (IL-6R-/-) and wildtype littermate (IL-6R+/+) mice were exposed to concentrated ambient PM2.5 (CAP) or filtered air (FA), and their pulmonary and metabolic responses to these exposures were analyzed. Our results demonstrated that IL-6R deficiency markedly alleviated PM2.5 exposure-induced increases in lung inflammatory markers including the inflammation score of histological analysis, the number of macrophages in bronchoalveolar lavage fluid (BALF), and mRNA expressions of TNFα, IL-1ß and IL-6 and abnormalities in lung function test. However, IL-6R deficiency did not reduce the hepatic insulin resistance nor systemic glucose intolerance and insulin resistance induced by PM2.5 exposure. CONCLUSION: Our findings support the crucial role of IL-6 signalling in the development of pulmonary inflammation and dysfunction due to PM2.5 exposure but question the putative central role of pulmonary inflammation for the extra-pulmonary dysfunctions following PM2.5 exposure, providing a deep mechanistic insight into the pathogenesis caused by PM2.5 exposure.


Assuntos
Resistência à Insulina , Interleucina-6 , Animais , Camundongos , Interleucina-6/genética , Receptores de Interleucina-6 , Inflamação/induzido quimicamente , Homeostase , Material Particulado/toxicidade , Glucose
11.
Int J Immunopathol Pharmacol ; 36: 3946320221137464, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36347039

RESUMO

Particulate matter 2.5 (PM2.5)-induced pulmonary inflammation is an important issue worldwide. NLRP3 inflammasome activation has been found to be involved in pulmonary inflammation development. However, whether PM2.5 induces pulmonary inflammation by activating the NLRP3 inflammasome has not yet been fully elucidated. This study researched whether PM2.5 induces the NLRP3 inflammasomes activation to trigger pulmonary inflammation.Mice and MH-S cells were exposed to PM2.5, BOX5, and Rapamycin. Hematoxylin and eosin staining was performed on the lung tissues of mice. M1 macrophage marker CD80 expression in the lung tissues of mice and LC3B expression in MH-S cells was detected by immunofluorescence. IL-1ß level in the lavage fluid and MH-S cells were detected by enzyme-linked immunosorbent assay. Protein expression was detected by Western blot. Autophagy assay in MH-S cells was performed by LC3B-GFP punctae experiment.PM2.5 exposure induced the lung injury of mice and increased NLRP3, P62, Wnt5a, LC3BII/I, and CD80 expression and IL-1ß release in the lung tissues. PM2.5 treatment increased NLRP3, pro-caspase-1, cleaved caspase-1, Pro-IL-1ß, Pro-IL-18, P62, LC3BII/I, and Wnt5a expression, IL-1ß release, and LC3B-GFP punctae in MH-S cells. However, BOX5 treatment counteracted this effect of PM2.5 on lung tissues of mice and MH-S cells. Rapamycin reversed the effect of BOX5 on PM2.5-induced lung tissues of mice and MH-S cells.PM2.5 activated the NLRP3 inflammasome and IL-1ß release in MH-S cells by facilitating the autophagy via activating Wnt5a. The findings of this study provided a new clue for the treatment of pulmonary inflammation caused by PM2.5.


Assuntos
Inflamassomos , Pneumonia , Humanos , Inflamassomos/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Material Particulado/toxicidade , Interleucina-1beta/metabolismo , Caspase 1/metabolismo , Pneumonia/induzido quimicamente , Pneumonia/metabolismo , Autofagia , Sirolimo/efeitos adversos , Proteína Wnt-5a
12.
Part Fibre Toxicol ; 19(1): 66, 2022 Nov 23.
Artigo em Inglês | MEDLINE | ID: mdl-36419123

RESUMO

BACKGROUND: Traffic-related air pollution (TRAP) exposure causes adverse effects on wellbeing and quality of life, which can be studied non-invasively using self-reported symptoms. However, little is known about the effects of different TRAP concentrations on symptoms following controlled exposures, where acute responses can be studied with limited confounding. We investigated the concentration-response relationship between diesel exhaust (DE) exposure, as a model TRAP, and self-reported symptoms. METHODS: We recruited 17 healthy non-smokers into a double-blind crossover study where they were exposed to filtered air (FA) and DE standardized to 20, 50, 150 µg/m3 PM2.5 for 4 h, with a ≥ 4-week washout between exposures. Immediately before, and at 4 h and 24 h from the beginning of the exposure, we administered visual analog scale (VAS) questionnaires and grouped responses into chest, constitutional, eye, neurological, and nasal categories. Additionally, we assessed how the symptom response was related to exposure perception and airway function. RESULTS: An increase in DE concentration raised total (ß ± standard error = 0.05 ± 0.03, P = 0.04), constitutional (0.01 ± 0.01, P = 0.03) and eye (0.02 ± 0.01, P = 0.05) symptoms at 4 h, modified by perception of temperature, noise, and anxiety. These symptoms were also correlated with airway inflammation. Compared to FA, symptoms were significantly increased at 150 µg/m3 for the total (8.45 ± 3.92, P = 0.04) and eye (3.18 ± 1.55, P = 0.05) categories, with trends towards higher values in the constitutional (1.49 ± 0.86, P = 0.09) and nasal (1.71 ± 0.96, P = 0.08) categories. CONCLUSION: DE exposure induced a concentration-dependent increase in symptoms, primarily in the eyes and body, that was modified by environmental perception. These observations emphasize the inflammatory and sensory effects of TRAP, with a potential threshold below 150 µg/m3 PM2.5. We demonstrate VAS questionnaires as a useful tool for health monitoring and provide insight into the TRAP concentration-response at exposure levels relevant to public health policy.


Assuntos
Qualidade de Vida , Emissões de Veículos , Humanos , Emissões de Veículos/toxicidade , Emissões de Veículos/análise , Estudos Cross-Over , Método Duplo-Cego , Material Particulado/toxicidade
13.
Inflamm Res ; 71(12): 1433-1448, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36264363

RESUMO

INTRODUCTION: Cardiovascular diseases (CVD) have been associated with high exposure to fine particulate air pollutants (PM2.5). Alveolar macrophages are the first defense against inhaled particles. As soon as they phagocytize the particles, they reach an inflammatory phenotype, which affects the surrounding cells and associates with CVD. Not coincidentally, CVD are marked by a depleted heat shock response (HSR), defined by a deficit in inducing 70-kDa heat shock protein (HSP70) expression during stressful conditions. HSP70 is a powerful anti-inflammatory chaperone, whose reduced levels trigger a pro-inflammatory milieu, cellular senescence, and a senescence-associated secretory phenotype (SASP). However, whether macrophage senescence is the main mechanism by which PM2.5 propagates low-grade inflammation remains unclear. OBJECTIVE AND DESIGN: In this article, we review evidence supporting that chronic exposure to PM2.5 depletes HSR and determines the ability to solve the initial stress. RESULTS AND DISCUSSION: When exposed to PM2.5, macrophages increase the production of reactive oxygen species, which activate nuclear factor-kappa B (NF-κB). NF-κB is naturally a pro-inflammatory factor that drives prostaglandin E2 (PGE2) synthesis and causes fever. PGE2 can be converted into prostaglandin A2, a powerful inducer of HSR. Therefore, when transiently activated, NF-κB can trigger the anti-inflammatory response through negative feedback, by inducing HSP70 expression. However, when chronically activated, NF-κB heads a set of pathways involved in mitochondrial dysfunction, endoplasmic reticulum stress, unfolded protein response, inflammasome activation, and apoptosis. During chronic exposure to PM2.5, cells cannot properly express sirtuin-1 or activate heat shock factor-1 (HSF-1), which delays the resolution phase of inflammation. Since alveolar macrophages are the first immune defense against PM2.5, we suppose that the pollutant impairs HSR and, consequently, induces cellular senescence. Accordingly, senescent macrophages change its secretory phenotype to a more inflammatory one, known as SASP. Finally, macrophages' SASP would propagate the systemic inflammation, leading to endothelial dysfunction and atherosclerosis.


Assuntos
Poluição do Ar , Aterosclerose , Pneumonia , Humanos , NF-kappa B/metabolismo , Dinoprostona , Resposta ao Choque Térmico , Macrófagos/metabolismo , Inflamação/metabolismo , Material Particulado/toxicidade , Anti-Inflamatórios , Poluição do Ar/efeitos adversos
14.
J Epidemiol Community Health ; 76(12): 984-990, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36198486

RESUMO

BACKGROUND: Despite ambient air pollution being associated with various adverse cardiovascular outcomes, the acute effects of ambient air pollution on hospital readmissions for heart failure (HF) among post-discharge patients with hypertension remain less understood. METHODS: We conducted a time-stratified case-crossover study among 3660 subjects 60 years or older who were admitted to hospital for HF after discharge for hypertension in Guangzhou, China during 2016-2019. For each subject, individualised residential exposures to ambient particulate matter with an aerodynamic diameter ≤1 µm (PM1), ≤2.5 µm (PM2.5), ≤10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO) and ozone were extracted from our validated grid dataset. RESULTS: An IQR increase of lag 04-day exposure to PM1 (IQR: 11.6 µg/m3), PM2.5 (IQR 21.9 µg/m3), PM10 (IQR 35.0 µg/m3), SO2 (IQR 4.4 µg/m3), NO2 (IQR 23.3 µg/m3) and CO (IQR 0.25 mg/m3) was significantly associated with a 9.77% (95% CI 2.21% to 17.89%), 8.74% (95% CI 1.05% to 17.00%), 13.93% (95% CI 5.36% to 23.20%), 10.81% (95% CI 1.82% to 20.60%), 14.97% (95% CI 8.05% to 22.34%) and 7.37% (95% CI 0.98% to 14.16%) increase in odds of HF readmissions, respectively. With adjustment for other pollutants, the association for NO2 exposure remained stable, while the associations for PM1, PM2.5, PM10, SO2 and CO exposures became insignificant. Overall, an estimated 19.86% of HF readmissions were attributable to NO2 exposure, while reducing NO2 exposure to the WHO and China air quality standards would avoid 12.87% and 0.54% of readmissions, respectively. No susceptible populations were observed by sex, age or season. CONCLUSION: Short-term exposure to ambient NO2 was significantly associated with an increased odds of HF readmissions among post-discharge patients with hypertension in older Chinese adults.


Assuntos
Poluição do Ar , Exposição Ambiental , Insuficiência Cardíaca , Idoso , Humanos , Pessoa de Meia-Idade , Assistência ao Convalescente , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , China/epidemiologia , Estudos Cross-Over , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Insuficiência Cardíaca/epidemiologia , Insuficiência Cardíaca/terapia , Hipertensão/epidemiologia , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Alta do Paciente , Readmissão do Paciente/estatística & dados numéricos
15.
Environ Res ; 215(Pt 3): 114360, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36184965

RESUMO

Recently, elevated blood pressure (BP) and hypertension (HTN) have caused a huge burden of health loss. Previous studies used ambient air pollutants as a proxy for individual exposure, limiting the assessment of its multiple exposure to health effects. For the first time, this study constructed individual PM2.5 component (SO42-, NO3-, NH4+, OM, and BC) exposure model DAG (Directed Acyclic Graph), DAG-oriented generalized linear model and random forest model, and explored the effects of single and multiple exposures to PM2.5 components on BP at different stages by the generalized linear model (GLM) and Quantile g-Computation (QgC) model based on a large cohort study in China. We defined BP in four stages according to the 2017 ACC/AHA guidelines. After excluding the lack of key information, the cohort analyses ultimately included 9031 participants. Our results showed that the individual PM2.5 component exposure model had good efficacy. Single or multiple exposure to PM2.5 components had significant positive effects on normal BP to elevated BP and elevated BP to stage 1 HTN. In addition, males, the elderly and urban residents were more sensitive to PM2.5 components. This study provided implications for environmental exposure assessment and control of particulate pollution in the future.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Hipertensão , Idoso , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Pressão Sanguínea , China/epidemiologia , Cidades , Estudos de Coortes , Exposição Ambiental/análise , Humanos , Hipertensão/induzido quimicamente , Hipertensão/epidemiologia , Masculino , Pessoa de Meia-Idade , Material Particulado/análise , Material Particulado/toxicidade
16.
Dis Markers ; 2022: 7098463, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36204510

RESUMO

Background: Lung fibrosis is a severe lung disorder featured by chronic nonspecific inflammation of the interstitial lung and deposition of collagen, leading to lung dysfunction. It has been identified that ferroptosis is involved in the progression of lung injury. Particulate matter (PM2.5) is reported to be correlated with the incidence of pulmonary fibrosis. However, mechanisms underlying ferroptosis in PM2.5-related lung fibrosis is unclear. In this study, we aimed to explore the effect of PM2.5 on ferroptosis in lung fibrosis and the related molecular mechanisms. Methods: PM2.5-treated mouse model and cell model were established. Fibrosis and tissue damage were measured by Masson's trichrome staining and HE staining. Fibrosis biomarkers, such as α-SMA, collagen I, and collagen III, were examined by histological analysis. The ferroptosis phenotypes, including the levels of iron, Fe2+, MDA, and GSH, were measured by commercial kits. ROS generation was checked by DCFH-DA. The oxidative stress indicators, 3-nitro-L-tyrosine (3'-NT), 4-HNE, and protein carbonyl, were checked by enzyme linked immunosorbent assay (ELISA). The thiobarbituric acid reactive substances (TBARS) and GSH/GSSG ratio were assessed by TBARS assay kit and GSH/GSSG assay kit, respectively. TGF-ß signaling was detected by Western blotting. Results: PM2.5 induced the lung injury and fibrosis in the mice model, along with elevated expression of fibrosis markers. PM2.5 enhanced oxidative stress in the lung of the mice. The SOD2 expression was reduced, and NRF2 expression was enhanced in the mice by the treatment with PM2.5. PM2.5 triggered ferroptosis, manifested as suppressed expression of GPX4 and SLC7A11, decreased levels of iron, Fe2+, and MDA, and increased GSH level in mouse model and cell model. The TGF-ß and Smad3 signaling was inhibited by PM2.5. ROS inhibitor NAC reversed PM2.5-regulated ROS and ferroptosis in primary mouse lung epithelial cells. Conclusions: Therefore, we concluded that PM2.5 exposure induced lung injury and fibrosis by inducing ferroptosis via TGF-ß signaling.


Assuntos
Ferroptose , Lesão Pulmonar , Fibrose Pulmonar , Animais , Colágeno Tipo I , Fibrose , Dissulfeto de Glutationa , Ferro , Lesão Pulmonar/induzido quimicamente , Camundongos , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Material Particulado/toxicidade , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/metabolismo , Espécies Reativas de Oxigênio , Substâncias Reativas com Ácido Tiobarbitúrico , Fator de Crescimento Transformador beta/genética , Fator de Crescimento Transformador beta/metabolismo
17.
Zhonghua Yu Fang Yi Xue Za Zhi ; 56(9): 1314-1322, 2022 Sep 06.
Artigo em Chinês | MEDLINE | ID: mdl-36207897

RESUMO

Objective: To reveal the crucial toxic components of ambient fine particles (PM2.5) that affect the maturation and differentiation of megakaryocytes. Methods: Human megakaryocytes were exposed to the organic fractions, metallic fractions and water-soluble fractions of PM2.5 at two exposure doses (i.e. actual air proportion concentration or the same concentration), respectively. The cell viability was performed to screen the non-cytotoxic levels of toxic components of PM2.5 using the CCK-8 assay. CellTiter-Blue assay, morphological observation, flow cytometry analysis and WGA staining assay were used to evaluate the cell morphological changes, occurrence of DNA ploidy, alteration in the expressions of biomarkers and platelet formation, which were key indicators of the maturation and differentiation of megakaryocytes. Results: Compared to the control group, both metallic and organic components of PM2.5 resulted in a lag in megakaryocytes with an increase in cell volume and the onset of DNA ploidy. Flow cytometry analysis showed that CD33 (the marker of myeloid-specific) decreased and CD41a (a megakaryocyte maturation-associated antigen) increased in metallic and organic components of PM2.5 treatment groups. Moreover, compared to the control group, budding protrusions increased in metallic and organic components of PM2.5 treatment groups. The water-soluble components had no effect on the maturation and differentiation of macrophages. Conclusion: Metallic and organic components of PM2.5 are the crucial toxic components that promote the maturation and differentiation of megakaryocytes.


Assuntos
Megacariócitos , Sincalida , Biomarcadores , DNA/análise , DNA/farmacologia , Humanos , Megacariócitos/química , Material Particulado/toxicidade , Sincalida/farmacologia , Água/farmacologia
18.
Environ Pollut ; 315: 120234, 2022 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-36195197

RESUMO

Asthma is a respiratory disease that can be exacerbated by certain environmental factors. Both formaldehyde (FA) and PM2.5, the most common indoor and outdoor air pollutants in mainland China, are closely associated with the onset and development of asthma. To date, however, there is very little report available on whether there is an exacerbating effect of combined exposure to FA and PM2.5 at ambient concentrations. In this study, asthmatic mice were exposed to 1 mg/m3 FA, 1 mg/kg PM2.5, or a combination of 0.5 mg/m3 FA and 0.5 mg/kg PM2.5, respectively. Results demonstrated that both levels of oxidative stress and inflammation were significantly increased, accompanied by an obvious decline in lung function. Further, the initial activation of p38 MAPK and NF-κB that intensified the immune imbalance of asthmatic mice were found to be visibly mitigated following the administration of SB203580, a p38 MAPK inhibitor. Noteworthily, it was found that combined exposure to the two at ambient concentrations could significantly worsen asthma than exposure to each of the two alone at twice the ambient concentration. This suggests that combined exposure to formaldehyde and PM2.5 at ambient concentrations may have a synergistic effect, thus causing more severe damage in asthmatic mice. In general, this work has revealed that the combined exposure to FA and PM2.5 at ambient concentrations can synergistically aggravate asthma via the p38 MAPK pathway in mice.


Assuntos
Poluentes Atmosféricos , Asma , Camundongos , Animais , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Formaldeído/toxicidade , Asma/metabolismo , Inflamação/induzido quimicamente , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Material Particulado/toxicidade
19.
J Environ Manage ; 324: 116371, 2022 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-36202035

RESUMO

Atmospheric particulate matter (PM) has a significant threat not only to human health but also to our environment. In Hungary, 54% of PM10 comes from residential combustion, which also includes the practice of household waste burning. Therefore, this work aims to investigate the quality of combustion through the flue gas concentrations (CO, CO2, O2) and to identify and evaluate the negative impacts of PM and PAHs generated during controlled lab-scale combustion of different mixed wastes (cardboard and glossy paper, polypropylene and polyethylene terephthalate, polyester and cotton). Mixed wastes were burnt in a lab-scale tubular furnace at different temperatures with 180 dm3/h air flow rate. Chemical analyses were coupled with ecotoxicological tests using the bioluminescent bacterium Vibrio fischeri. Ecotoxicity was expressed as toxic unit (TU) values, toxic equivalent factors (TEF) were also presented. During the combustion same amount of O2 enters the reaction, but a different amount CO2 is generated due to the C content of the sample. The waste with highest C-content related to the highest CO2 emission. Increasing the combustion temperature produces more PM-bound PAHs, which remains the same composition in the case of plastic and textile groups. The TU of solid contaminants decreases with increasing combustion temperature and increases with the minerals which are left behind in the water from the solid contaminants.


Assuntos
Poluentes Atmosféricos , Hidrocarbonetos Policíclicos Aromáticos , Humanos , Material Particulado/toxicidade , Material Particulado/análise , Dióxido de Carbono/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Temperatura , Plásticos , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise
20.
Ecotoxicol Environ Saf ; 246: 114151, 2022 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-36228359

RESUMO

The epidemiological evidence has linked prenatal exposure to fine particulate matter (PM2.5) pollution with neurological diseases in offspring. However, the biological process and toxicological mechanisms remain unclear. Tau protein is a neuronal microtubule-associated protein expressed in fetal brain and plays a critical role in mediating neuronal development. Aberrant expression of tau is associated with adverse neurodevelopmental outcomes. To study whether prenatal exposure to PM2.5 pollution induce tau lesion in mice offspring and elucidate the underlying pathogenic mechanism, we exposed pregnant mice to PM2.5 (3 mg/kg b.w.) by oropharyngeal aspiration every other day. The results indicate that prenatal PM2.5 exposure induced hyperphosphorylation of tau in the cortex of postnatal male offspring, which was accompanied by insulin resistance through the IRS-1/PI3K/AKT signaling pathway. Importantly, we further found that prenatal PM2.5 exposure induced mitochondrial dysfunction by disrupting mitochondrial ultrastructure and decreasing the expression of rate-limiting enzymes (CS, IDH2 and FH) in the Krebs cycle and the subunits of mitochondrial complex IV and V (CO1, CO4, ATP6, and ATP8) during postnatal neurodevelopment. The findings suggest that prenatal PM2.5 exposure could induce tauopathy-like changes in male offspring, in which mitochondrial dysfunction-induced insulin resistance might play an important role.


Assuntos
Resistência à Insulina , Efeitos Tardios da Exposição Pré-Natal , Animais , Feminino , Masculino , Camundongos , Gravidez , Mitocôndrias , Material Particulado/toxicidade , Fosfatidilinositol 3-Quinases , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Proteínas tau
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