Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 3.453
Filtrar
1.
Chemosphere ; 262: 128404, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33182127

RESUMO

BACKGROUND: Reduced growth velocity before birth increases the risk of adverse health outcomes in adult life. However, until recently, there has been a lack of studies demonstrating the impact of prenatal PM2.5 exposure on fetal growth velocity. METHODS: The current study was embedded in a previous cohort built between January 1, 2014, and April 30, 2015, in Shanghai First Maternity and Infant Hospital, China, in 6129 eligible singleton pregnancies. The PM2.5 concentration was estimated by an inverse distance weighted method according to the residential addresses of the participants. Repeated fetal biometry measurements, including head circumference (HC), abdominal circumference (AC), femur length (FL), and biparietal diameter (BPD), were measured through ultrasound between 14 and 41 gestational weeks. A principal component analysis through conditional expectation for sparse longitudinal data was used to estimate the corresponding velocities. RESULTS: A total of 22782 ultrasound measurements were conducted among 6129 participants with a median of 2 and a maximum of 9 measurements. With each 10 µg/m3 increase in cumulative PM2.5 exposure, the velocity of HC, AC FL and BPD decreased by 0.12 mm/week, 0.17 mm/week, 0.02 mm/week and 0.02 mm/week, respectively, on average. The results of the Generalized Functional Concurrent Model showed that the velocity decreased significantly with PM2.5 exposure between 22 and 32 gestational weeks, which might be the potential sensitive exposure window. CONCLUSIONS: There are negative associations between prenatal exposure to PM2.5 and fetal growth velocity, and the late second trimester and early third trimester might be the potential sensitive window.


Assuntos
Poluentes Atmosféricos/toxicidade , Exposição Materna , Material Particulado/toxicidade , Efeitos Tardios da Exposição Pré-Natal , Adulto , China , Estudos de Coortes , Feminino , Desenvolvimento Fetal , Idade Gestacional , Humanos , Masculino , Material Particulado/análise , Gravidez , Segundo Trimestre da Gravidez , Terceiro Trimestre da Gravidez , Ultrassonografia Pré-Natal/métodos
2.
Sci Total Environ ; 753: 141774, 2021 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-33207436

RESUMO

Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical composition, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1 (PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In particular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regulatory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu winter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5; and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contributes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.


Assuntos
Poluentes Atmosféricos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , China , Monitoramento Ambiental , Regulação da Expressão Gênica , Humanos , Material Particulado/análise , Material Particulado/toxicidade , Estações do Ano , Fatores de Transcrição
3.
Sci Total Environ ; 753: 141980, 2021 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-33207456

RESUMO

The algae biological pump (ABP) effect for hydrophobic organic contaminants in deep oligotrophic lakes and oceans has been well studied. Suspended particulate matter (SPM) plays a connective role in ABP processes. However, little is known about the impacts of ABP effect on the occurrence, source apportionment and toxicity of SPM-bound polycyclic aromatic hydrocarbons (PAHs) in a typically shallow eutrophic lake under strong anthropogenic emissions of PAHs. In this study, we study this gap knowledge on the eutrophic Lake Chaohu, China. SPM-bound PAHs in Lake Chaohu were controlled by anthropogenic emissions in all seasons. Apparent ABP effect only occurred in spring and summer in lake area. Algae blooms in spring and summer significantly increased 46.5% ± 7.9% (mean ± standard deviation) and 19.8% ± 2.4% of Σ21 SPM-bound PAHs, and greatly enhanced their toxicity (1.98 ± 0.46 times in spring and 32.9% ± 4.2% in summer). Therefore, there need more attentions focusing on the coupling effect of persistent toxic substances such as PAHs and harmful algae blooms in aquatic environment for sustainable development. The apparent ABP effect had little influence on their source apportionment. However, it may cause a regime shift for the source apportionment on a short-term scale. Further study could pay more attentions on in-depth and short-term studies on ABP effect.


Assuntos
Proteínas de Membrana Transportadoras , Hidrocarbonetos Policíclicos Aromáticos , Poluentes Químicos da Água , China , Monitoramento Ambiental , Sedimentos Geológicos , Lagos/análise , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Poluentes Químicos da Água/análise , Poluentes Químicos da Água/toxicidade
4.
Sci Total Environ ; 750: 142347, 2021 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-33182206

RESUMO

BACKGROUND: Short-term exposure to PM2.5 has been widely associated with human morbidity and mortality. However, most up-to-date research was conducted at a daily timescale, neglecting the intra-day variations in both exposure and outcome. As an important fraction in PM2.5, PM1 has not been investigated about the very acute effects within a few hours. METHODS: Hourly data for size-specific PMs (i.e., PM1, PM2.5, and PM10), all-cause emergency department (ED) visits and meteorological factors were collected from Guangzhou, China, 2015-2016. A time-stratified case-crossover design with conditional logistic regression analysis was performed to evaluate the hourly association between size-specific PMs and ED visits, adjusting for hourly mean temperature and relative humidity. Subgroup analyses stratified by age, sex and season were conducted to identify potential effect modifiers. RESULTS: A total of 292,743 cases of ED visits were included. The effects of size-specific PMs exhibited highly similar lag patterns, wherein estimated odds ratio (OR) experienced a slight rise from lag 0-3 to 4-6 h and subsequently attenuated to null along with the extension of lag periods. In comparison with PM2.5 and PM10, PM1 induced slightly larger effects on ED visits. At lag 0-3 h, for instance, ED visits increased by 1.49% (95% confidence interval: 1.18-1.79%), 1.39% (1.12-1.66%) and 1.18% (0.97-1.40%) associated with a 10-µg/m3 rise, respectively, in PM1, PM2.5 and PM10. We have detected a significant effect modification by season, with larger PM1-associated OR during the cold months (1.017, 1.013 to 1.021) compared with the warm months (1.010, 1.005 to 1.015). CONCLUSIONS: Our study provided brand-new evidence regarding the adverse impact of PM1 exposure on human health within several hours. PM-associated effects were significantly more potent during the cold months. These findings may aid health policy-makers in establishing hourly air quality standards and optimizing the allocation of emergency medical resources.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/análise , China , Estudos Cross-Over , Serviço Hospitalar de Emergência , Exposição Ambiental/análise , Humanos , Material Particulado/análise , Material Particulado/toxicidade
5.
Sci Total Environ ; 750: 141700, 2021 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-32861077

RESUMO

Despite adverse health effects, ultrafine particulate matter (UFP), i.e., PM less than 0.1 µm in diameter, is an emerging pollutant not subject to regulation. UFP may cause both lung inflammation and cardiopulmonary disease and may enter the brain directly via the olfactory bulb, affecting the nervous system. In highly urbanized environments, diesel and gasoline vehicles are among the major sources of UFP including combustion-generated solid particle pollutant and metal-based particles. Metal-based UFP are of much concern, as they may promote inflammation and DNA damage via oxidative stress with generation of free radicals and reactive oxygen species (ROS). We used the honeybee as an alternative sampling system of UFP in an area of the Po Valley (Northern Italy), which is subject to intense traffic. Worker bees are widely recognised as efficient samplers of air pollutants, including airborne PM. During flight and foraging activity, pubescence of the bees promotes the accumulation of electrical charge on the body's surface, enhancing attraction to air pollutants. Bees living near the main Italian highway, the Autostrada A1, displayed a contamination of nanosized Fe-oxides/hydroxides and baryte. Sources of Fe-bearing and baryte ultrafine particles are primarily the vehicles speeding on the motorway. Pollen collected by forager bees and honey produced by the bee colony displayed contamination by nanosized Fe-oxides/hydroxides and baryte. Such a contamination exposes pollinators and humans to UFP ingestion, endangering the safety of food produced at traffic-influenced sites. Given the global spread of traffic, our findings suggest that exposure and environmental impact of ultrafine Fe-oxides/hydroxides and baryte are potentially ubiquitous, although usually overlooked in environmental policy discussions.


Assuntos
Poluentes Atmosféricos , Emissões de Veículos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Animais , Abelhas , Poeira , Humanos , Itália , Tamanho da Partícula , Material Particulado/análise , Material Particulado/toxicidade , Emissões de Veículos/análise , Emissões de Veículos/toxicidade
6.
Artigo em Inglês | MEDLINE | ID: mdl-33202948

RESUMO

Growing evidence links prenatal exposure to particulate matter (PM2.5) with reduced lung function and incidence of pulmonary diseases in infancy and childhood. However, the underlying biological mechanisms of how prenatal PM2.5 exposure affects the lungs are incompletely understood, which explains the lack of an ideal in vitro lung development model. Human pluripotent stem cells (hPSCs) have been successfully employed for in vitro developmental toxicity evaluations due to their unique ability to differentiate into any type of cell in the body. In this study, we investigated the developmental toxicity of diesel fine PM (dPM2.5) exposure during hPSC-derived alveolar epithelial cell (AEC) differentiation and three-dimensional (3D) multicellular alveolar organoid (AO) development. We found that dPM2.5 (50 and 100 µg/mL) treatment disturbed the AEC differentiation, accompanied by upregulation of nicotinamide adenine dinucleotide phosphate oxidases and inflammation. Exposure to dPM2.5 also promoted epithelial-to-mesenchymal transition during AEC and AO development via activation of extracellular signal-regulated kinase signaling, while dPM2.5 had no effect on surfactant protein C expression in hPSC-derived AECs. Notably, we provided evidence, for the first time, that angiotensin-converting enzyme 2, a receptor to mediate the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2) entry into target cells, and the cofactor transmembrane protease serine 2 were significantly upregulated in both hPSC-AECs and AOs treated with dPM2.5. In conclusion, we demonstrated the potential alveolar development toxicity and the increase of SARS-Cov-2 susceptibility of PM2.5. Our findings suggest that an hPSC-based 2D and 3D alveolar induction system could be a useful in vitro platform for evaluating the adverse effects of environmental toxins and for virus research.


Assuntos
Infecções por Coronavirus , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Pandemias , Material Particulado/toxicidade , Peptidil Dipeptidase A/genética , Células-Tronco Pluripotentes/efeitos dos fármacos , Pneumonia Viral , Betacoronavirus , Células Epiteliais/efeitos dos fármacos , Humanos , Organoides/efeitos dos fármacos , Regulação para Cima , Emissões de Veículos/toxicidade
7.
Biomed Environ Sci ; 33(9): 680-689, 2020 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-33106213

RESUMO

Objective: To investigate the effect of c-fos gene silencing on differentially expressed proteins (DEPs) in human bronchial epithelial (HBE) cells after exposure to fine particulate matter (PM 2.5). Methods: HBE cells and c-fos-silenced HBE cells were exposed to 50 µg/mL PM 2.5, LC-MS/MS and tandem mass tag (TMT) labeling methods were combined with bioinformatics methods, and DEPs and interaction networks were identified. Results: In the HBE group, 414 DEPs were screened, of which 227 were up-regulated and 187 down-regulated. In the c-fos silenced HBE group, 480 DEPs were screened, including 240 up-regulated proteins and 240 down-regulated proteins. KEGG annotations showed that DEPs in the HBE group are mainly concentrated in the glycolysis/gluconeogenesis pathway and those in the c-fos silenced group are concentrated mainly in endoplasmic reticulum and the processing of proteins. Additionally, the abnormal expression of GPRC5C, DKK4, and UBE2C was identified in top 15 DEPs. After constructing the protein interaction network, 20 Hub proteins including HNRNPA2B1, HNRNPL, RPS15A, and RPS25 were screened from the HBE group and the c-fos silenced HBE group. Conclusion: c-fos gene affected the expression of cancer-related proteins. Our results provided a scientific basis for further study of PM 2.5-induced carcinogenesis mechanism.


Assuntos
Poluentes Atmosféricos/toxicidade , Brônquios/efeitos dos fármacos , Regulação da Expressão Gênica , Inativação Gênica , Genes fos/genética , Material Particulado/toxicidade , Mucosa Respiratória/efeitos dos fármacos , Brônquios/metabolismo , Células Cultivadas , Humanos , Proteômica , Mucosa Respiratória/metabolismo
8.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 36(3): 240-244, 2020 May.
Artigo em Chinês | MEDLINE | ID: mdl-32981279

RESUMO

Objective: To investigate the inflammatory mechanism of nasal instillation of fine particulate matter (PM2.5)on hippocampal tissue injury in mice.Methods: Thirty C57BL/6J mice were randomly divided into 3 groups(n=10):control group, low-dose group, high-dose group. The nasal instillation doses of PM2.5 in the low-dose group and the high-dose group were 1.5 mg/kg BW and 7.5 mg/kg BW, respectively, and the control group was given saline with an equal volume. Saline was sprayed once every other time for 12 times. The serum levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) were determined by ELISA method. HE staining and electron microscopy were used to observe the pathological changes and ultrastructure of lung tissue and hippocampus. The inflammatory cytokine levels in hippocampus were detected by antibody chip technique. Results: There was no significant effect of PM2.5 nasal instillation on serum TNF-α, IL-1ß and IL-6 levels (P>0.05), and there was no obvious pathological changes in lung tissue structure. In hippocampus, low-dose and high-dose PM2.5 exposure could lead to disordered neuronal arrangement in the hippocampal CA3 region, and there were neurological changes around the neuron cells and ultrastructural changes such as edema around small blood vessels. Compared with the control group, the levels of inflammatory cytokines such as CX3CL1, CSF2 and TECK in the low-dose group were increased significantly (P <0.05), while sTNFR1 was decreased significantly (P<0.05); the inflammatory factors CX3CL1, CSF2, and TCA-3 were significantly increased in the high-dose group (P<0.05), while leptin, MIG, and FASLG were significantly decreased (P<0.05). Conclusion: Nasal instillation of PM2.5 can induce tissue damage in the hippocampus of mice, and its mechanism of action may be the olfactory brain pathway. The increasing of TNF-α and IL-6 and the decreasing of sTNFR1 and FASLG may be involved in inflammatory mechanisms.


Assuntos
Lesões Encefálicas , Hipocampo , Material Particulado , Administração Intranasal , Animais , Lesões Encefálicas/induzido quimicamente , Lesões Encefálicas/fisiopatologia , Citocinas/sangue , Hipocampo/efeitos dos fármacos , Hipocampo/lesões , Pulmão/efeitos dos fármacos , Pulmão/patologia , Lesão Pulmonar/patologia , Camundongos , Camundongos Endogâmicos C57BL , Material Particulado/toxicidade
9.
Environ Res ; 191: 110177, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32931792

RESUMO

BACKGROUND: The risk of infection and death by COVID-19 could be associated with a heterogeneous distribution at a small area level of environmental, socioeconomic and demographic factors. Our objective was to investigate, at a small area level, whether long-term exposure to air pollutants increased the risk of COVID-19 incidence and death in Catalonia, Spain, controlling for socioeconomic and demographic factors. METHODS: We used a mixed longitudinal ecological design with the study population consisting of small areas in Catalonia for the period February 25 to May 16, 2020. We estimated Generalized Linear Mixed models in which we controlled for a wide range of observed and unobserved confounders as well as spatial and temporal dependence. RESULTS: We have found that long-term exposure to nitrogen dioxide (NO2) and, to a lesser extent, to coarse particles (PM10) have been independent predictors of the spatial spread of COVID-19. For every 1 µm/m3 above the mean the risk of a positive test case increased by 2.7% (95% credibility interval, ICr: 0.8%, 4.7%) for NO2 and 3.0% (95% ICr: -1.4%,7.44%) for PM10. Regions with levels of NO2 exposure in the third and fourth quartile had 28.8% and 35.7% greater risk of a death, respectively, than regions located in the first two quartiles. CONCLUSION: Although it is possible that there are biological mechanisms that explain, at least partially, the association between long-term exposure to air pollutants and COVID-19, we hypothesize that the spatial spread of COVID-19 in Catalonia is attributed to the different ease with which some people, the hosts of the virus, have infected others. That facility depends on the heterogeneous distribution at a small area level of variables such as population density, poor housing and the mobility of its residents, for which exposure to pollutants has been a surrogate.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Infecções por Coronavirus , Pandemias , Pneumonia Viral , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Betacoronavirus , Exposição Ambiental/análise , Humanos , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Espanha/epidemiologia
10.
Ecotoxicol Environ Saf ; 203: 111044, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888613

RESUMO

BACKGROUND: Exposure to ambient fine particulate matter (PM2.5) is associated with various adverse health outcomes. Although several mechanisms have been proposed including oxidative stress and inflammatory responses, the exact mechanism is still unknown. Few studies have investigated the mechanism linking PM2.5 and blood pressure (BP). In this study, we measured urinary metabolites and BP -related renin-angiotensin-aldosterone system (RAAS) to investigate the associations between ambient PM2.5 exposure and BP in healthy C57BL/6 mice. METHODS: The C57BL/6 mice were exposed to ambient concentrated PM2.5 or filtered air (FA) for 16 weeks. Systolic BP and diastolic BP were measured by noninvasive BP system. The urine metabolites were quantified using the untargeted metabolomics approach. The expression of RAAS-related proteins angiotensin-converting enzyme (ACE)2, angiotensin (Ang) II, Ang (1-7) and aldosterone (ALD) were measured using Western blot and ELISA kits. RESULTS: The metabolomics analysis demonstrated that PM2.5 exposure induced significant changes of some metabolites in urine, including stress hormones, amino acids, fatty acids, and lipids. Furthermore, there was an elevation of BP, increase of serous Ang II and ALD, along with the decrease of ACE2 and Ang (1-7) in kidney in the PM2.5-exposed mice compared with FA-exposed mice. CONCLUSIONS: The results demonstrated that PM2.5 exposure-induced BP elevation might be associated with RAAS activation. Meanwhile, PM2.5 exposure-induced changes of stress hormone and lipid metabolism might mediate the activation of RAAS. The results suggested that the systemic stress hormone and lipid metabolism was associated with the development of hypertension.


Assuntos
Poluentes Atmosféricos/toxicidade , Angiotensina I/metabolismo , Pressão Sanguínea/efeitos dos fármacos , Hipertensão/induzido quimicamente , Material Particulado/toxicidade , Fragmentos de Peptídeos/metabolismo , Peptidil Dipeptidase A/metabolismo , Acetilglucosaminidase/urina , Angiotensina I/sangue , Animais , Biomarcadores/sangue , Biomarcadores/urina , Hipertensão/urina , Metabolismo dos Lipídeos/efeitos dos fármacos , Masculino , Metaboloma/efeitos dos fármacos , Metabolômica , Camundongos , Camundongos Endogâmicos C57BL , Fragmentos de Peptídeos/sangue , Peptidil Dipeptidase A/sangue , Sistema Renina-Angiotensina/efeitos dos fármacos , beta-Galactosidase/urina
11.
Ecotoxicol Environ Saf ; 205: 111125, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32949841

RESUMO

Dry eye syndrome (DES) is a multifactorial condition characterized by insufficient tear lubrication and eye irritation. Air pollutants, including particulate matter (PM), are an emerging threat to human health causing DES and other diseases. However, the pathogenic mechanisms of DES induced by PM exposure remain to be fully elucidated. Recent studies have attempted to create DES animal model using PM exposure. In this study, we explored a novel in vivo exposure model of DES, utilizing an inhalation device (aerosol exposure system) to reproduce the natural exposure to atmospheric PM. Rats were exposed to urban PM (UPM) using this aerosol system for 5 h per day over 5 days. Tear volume in UPM-exposed rats decreased significantly, whereas corneal irregularity and lissamine green staining significantly increased following UPM exposure. Additional effects observed following UPM exposure included apoptosis in the corneal epithelium and a decrease in the number of goblet cells in the conjunctiva. UPM also affected the stability of the tear film by disrupting its mucin-4 layer. In conclusion, aerosol exposure systems have proven effective as assessment tools for DES caused by PM.


Assuntos
Poluentes Atmosféricos/toxicidade , Túnica Conjuntiva/efeitos dos fármacos , Córnea/efeitos dos fármacos , Síndromes do Olho Seco/induzido quimicamente , Material Particulado/toxicidade , Aerossóis , Poluentes Atmosféricos/análise , Animais , Túnica Conjuntiva/metabolismo , Córnea/metabolismo , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Síndromes do Olho Seco/metabolismo , Feminino , Humanos , Mucina-4/metabolismo , Tamanho da Partícula , Material Particulado/análise , Ratos , Ratos Sprague-Dawley
12.
Ecotoxicol Environ Saf ; 205: 111327, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32961493

RESUMO

Exposure to PM2.5 can cause serious harm to the respiratory system. Until now, although many toxicological studies have shown that pulmonary fibrosis can be caused by long-term PM2.5 exposure, there is no evidence that Endothelial-Mesenchymal Transition (EndMT) can trigger the process of pulmonary fibrosis after exposure. LncRNAs are a class of non-coding RNAs detected in mammalian cells. Nevertheless, researchers have not found whether lncRNAs participate in PM2.5 induced EndMT during pathophysiological duration. The Balb/c mouse model was exposed to PM2.5 for 4 months by dynamic intoxication. The levels of specific endothelial and mesenchymal markers were evaluated by molecular biology experiments to elucidate the mechanisms of EndMT induced by PM2.5 in lung tissues. LncRNA microarray analysis of the established mouse model of PM2.5 exposure was performed. Based on a bioinformatics analysis and RT-qPCR analysis, lncRNA Gm16410 attracted our attention. The change of lncRNA Gm16410 in mouse pulmonary vascular endothelial cells (MHCs) exposed to PM2.5 was verified, and the mechanism of lncRNA Gm16410 in EndMT was discussed. The changes of cell function were evaluated by cell migration and proliferation experiments. The molecular biology experiments proved that PM2.5 induced EndMT by activating the TGF-ß1/Smad3/p-Smad3 pathway in vitro. The relationship of EndMT and lncRNA Gm16410 was verified in mouse lung tissues and MHC cells by PM2.5 exposure. The involvement of lncRNA Gm16410 in PM2.5-induced EndMT highlights the potential of lncRNA to promote pulmonary fibrosis under environmental pollution.


Assuntos
Material Particulado/toxicidade , RNA Longo não Codificante/metabolismo , Animais , Movimento Celular/efeitos dos fármacos , Células Endoteliais/metabolismo , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Humanos , Pulmão/metabolismo , Camundongos , Material Particulado/metabolismo , Fibrose Pulmonar/metabolismo , RNA Longo não Codificante/genética , Transdução de Sinais/efeitos dos fármacos , Proteína Smad3 , Fator de Crescimento Transformador beta1/metabolismo
13.
Toxicol Lett ; 334: 14-20, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32949622

RESUMO

Air pollution is known to trigger and exacerbate many respiratory diseases. The interaction between respiratory microbiome and host plays a significant role in maintaining airway immune homeostasis and health. Emerging evidence has revealed the associations of disturbances in the airway microbiome with air pollution and respiratory disease. However, respiratory microbiome has been an undervalued player in progressions of respiratory disease caused by air pollution. In this review, we summarize the current research advances with respect to the effects of air pollution on respiratory microbiome, then discuss the underlying mechanisms of air pollution induction of dysbiosis in respiratory microbiota and its links to respiratory diseases. This work may be helpful to deepening understanding the relationships between exposure, microbiome and airway disease and discovering new preventive and therapeutic strategies for air pollution-mediated respiratory disease.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Microbiota/efeitos dos fármacos , Material Particulado/toxicidade , Sistema Respiratório/efeitos dos fármacos , Doenças Respiratórias/induzido quimicamente , Humanos , Exposição por Inalação/efeitos adversos , Sistema Respiratório/microbiologia , Doenças Respiratórias/microbiologia
14.
Ecotoxicol Environ Saf ; 205: 111283, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32977282

RESUMO

Fine particulate matter (PM2.5) airborne pollution increases the risk of chronic respiratory diseases, such as idiopathic pulmonary fibrosis (IPF), which is characterized by non-specific inflammation of the interstitial lung and extensive deposition of collagen fibers. Type 2 alveolar epithelial cells (AEC2s) are alveolar stem cells in the adult lung that contribute to the lung repair process through complex signaling. Our previous studies demonstrated that OGG1, a kind of DNA repair enzyme, have a critical role in protecting cells from oxidative damage and apoptosis induced by PM2.5, but the contribution of OGG1 in proliferation and self-renewal of AEC2s is not known. Here, we constructed OGG1-/-mice to test the effect and mechanism of OGG1 on PM2.5-induced pulmonary fibrosis and injury in vivo. We detected proliferation and self-renewal of OGG1 overexpression or OGG1 knockout AEC2s after PM2.5 injury by flow cytometry and clone formation. We observed that knockout of OGG1 aggravated pulmonary fibrosis, oxidative stress, and AEC2 cell death in PM2.5-injured mice. In addition, OGG1 is required for the proliferation and renewal of AEC2s after PM2.5 injury. Overexpression of OGG1 promotes the proliferation and self-renewal of AEC2s by inhibiting PM2.5-mediated oxidative stress and NF-κB signaling hyperactivation in vitro. Furthermore, NF-κB inhibitors promoted proliferation and self-renewal of OGG1-deficient AEC2s cells after PM2.5 injury, and attenuated PM2.5-induced pulmonary fibrosis and injury in mice. These data establish OGG1 as a regulator of NF-κB signal that serves to regulate AEC2 cell proliferation and self-renewal, and suggest a mechanism that inhibition of the NF-κB signaling pathway may represent a potential therapeutic strategy for IPF patients with low-expression of OGG1.


Assuntos
Poluentes Atmosféricos/toxicidade , Células Epiteliais Alveolares/efeitos dos fármacos , Autorrenovação Celular/genética , DNA Glicosilases/metabolismo , Material Particulado/toxicidade , Fibrose Pulmonar/induzido quimicamente , Células-Tronco/efeitos dos fármacos , Células Epiteliais Alveolares/metabolismo , Células Epiteliais Alveolares/patologia , Animais , Apoptose/efeitos dos fármacos , Apoptose/genética , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/genética , DNA Glicosilases/genética , Humanos , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , NF-kappa B/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/genética , Fibrose Pulmonar/genética , Fibrose Pulmonar/patologia , Transdução de Sinais , Células-Tronco/metabolismo , Células-Tronco/patologia
15.
Environ Res ; 188: 109841, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32846635

RESUMO

BACKGROUND: Exposure to ambient air pollution is associated with cardiovascular risk, potentially via atherosclerosis promotion. The disease mechanisms underlying these associations remain uncertain. OBJECTIVES: We aim to investigate the relationship of air pollution and traffic proximity with subclinical atherosclerosis, using coronary plaque phenotypes to gain insight into potential mechanisms. METHODS: Coronary plaque total and component volumes, high-risk plaque (HRP) appearance, and luminal stenosis were characterized by coronary computed tomography angiography in 2279 patients with atherosclerosis at baseline between 2014 and 2017. Annual average exposure to air pollutants including fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) was estimated by air pollution models for individual participants. Multiple linear regression models were used to assess the association of each exposure with plaque phenotypes and coronary stenosis, controlling for potential confounders. Multiple logistic regression models were used to estimate associations with plaque vulnerability. RESULTS: The studied population was 60.2±9.2 years old. PM2.5 and NO2 concentrations were significantly associated with a 5.0% (95%CI: 0.3, 9.9%, per 15 µg/m3 increase for PM2.5), 12.0% (95%CI: 2.5, 22.5% per 20 µg/m3 for NO2) larger volume of non-calcified plaque, respectively. Increase in O3 concentration was associated with a 12.2% (95%CI: 2.2, 23.2%, per 5 µg/m3 O3) larger volume of calcified plaque and a 12.8% (95%CI: 0.9, 26.2%) greater lumen narrowing. Increased PM2.5 and NO2, was also associated with increase in HRP, determined by the napkin ring sign (odds ratio: 1.41 [95%CI: 1.10, 1.80] for PM2.5 and 1.78 [95%CI: 1.20, 2.63] for NO2) and positive remodeling index (OR: 1.11 [95%CI: 1.01, 1.21] for PM2.5 and 1.20 [95%CI: 1.02, 1.42] for NO2), respectively, indicating increased plaque vulnerability. CONCLUSION: Long-term exposures to air pollution were associated with greater plaque volume and luminal stenosis, and increased plaque vulnerability with attendant risk of plaque rupture and erosion.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Aterosclerose , Poluição Relacionada com o Tráfego , Idoso , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , China/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Pessoa de Meia-Idade , Dióxido de Nitrogênio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Fenótipo
16.
Environ Res ; 191: 110129, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32853663

RESUMO

A new coronavirus (SARS-CoV-2) has determined a pneumonia outbreak in China (Wuhan, Hubei Province) in December 2019, called COVID-19 disease. In addition to the person-to person transmission dynamic of the novel respiratory virus, it has been recently studied the role of environmental factors in accelerate SARS-CoV-2 spread and its lethality. The time being, air pollution has been identified as the largest environmental cause of disease and premature death in the world. It affects body's immunity, making people more vulnerable to pathogens. The hypothesis that air pollution, resulting from a combination of factors such as meteorological data, level of industrialization as well as regional topography, can acts both as a carrier of the infection and as a worsening factor of the health impact of COVID-19 disease, has been raised recently. With this review, we want to provide an update state of art relating the role of air pollution, in particular PM2.5, PM10 and NO2, in COVID-19 spread and lethality. The Authors, who first investigated this association, often used different research methods or not all include confounding factors whenever possible. In addition, to date incidence data are underestimated in all countries and to a lesser extent also mortality data. For this reason, the cases included in the reviewed studies cannot be considered conclusive. Although it determines important limitations for direct comparison of results, and more studies are needed to strengthen scientific evidences and support firm conclusions, major findings are consistent, highlighting the important contribution of PM2.5 and NO2 as triggering of the COVID-19 spread and lethality, and with a less extent also PM10, although the potential effect of airborne virus exposure it has not been still demonstrated.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Infecções por Coronavirus , Pandemias , Pneumonia Viral , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Betacoronavirus , China/epidemiologia , Humanos , Dióxido de Nitrogênio , Material Particulado/análise , Material Particulado/toxicidade
17.
Environ Res ; 191: 110052, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-32860780

RESUMO

BACKGROUND: Ambient fine particulate matter (PM2.5) is associated with a wide range of acute and chronic health effects, including increased risk of respiratory infection. However, evidence specifically related to novel coronavirus disease (COVID-19) is limited. METHODS: COVID-19 case counts for 111 Canadian health regions were obtained from the COVID-19 Canada Open Data portal. Annual PM2.5 data for 2000-2016 were estimated from a national exposure surface based on remote sensing, chemical transport modelling and ground observations, and minimum and maximum temperature data for 2000-2015 were based on a national interpolated surface derived from thin-plate smoothing splines. Population counts and sociodemographic data by health region were obtained from the 2016 census, and health data (self-rated health and prevalence of smoking, obesity, and selected chronic diseases) by health region, were obtained from the Canadian Community Health Survey. Data on total number of COVID-19 tests and changes in mobility comparing post-vs. pre-introduction of social distancing measures were available by province. Data were analyzed using negative binomial regression models. RESULTS: After controlling for province, temperature, demographic and health characteristics and days since peak incidence by health region, long-term PM2.5 exposure exhibited a positive association with COVID-19 incidence (incidence rate ratio 1.07, 95% confidence interval 0.97-1.18 per µg/m3). This association was larger in magnitude and statistically significant in analyses excluding provinces that reported cases only for aggregated health regions, excluding health regions with less than median population density, and restricted to the most highly affected provinces (Quebec and Ontario). CONCLUSIONS: We observed a positive association between COVID-19 incidence and long-term PM2.5 exposure in Canadian health regions. The association was larger in magnitude and statistically significant in more highly affected health regions and those with potentially less exposure measurement error. While our results generate hypotheses for further testing, they should be interpreted with caution and require further examination using study designs less prone to bias.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Infecções por Coronavirus , Coronavirus , Pandemias , Pneumonia Viral , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Betacoronavirus , Exposição Ambiental/análise , Humanos , Incidência , Ontário , Material Particulado/análise , Material Particulado/toxicidade , Quebeque
18.
Environ Res ; 188: 109854, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32798957

RESUMO

Short-term exposure to air pollutants has been extensively related to daily mortality, however most of the evidence comes from studies conducted in major cities, and little is known on the extent of the spatial heterogeneity in the effects within areas including both urban and non-urban settings. We aimed to investigate the short-term association of air pollutants with daily cause-specific mortality in the Stockholm county, and to test whether an association exists also outside the metropolitan area. We used a spatiotemporal random forest model to predict daily concentrations of fine and inhalable particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2) and ozone (O3) at 1-km spatial resolution over Sweden for 2005-2016. We collected data on daily mortality for each small area for market statistics (SAMS) of the Stockholm county, to which we matched daily exposures to air pollutants and air temperature. We applied a case-crossover design to investigate the short-term association between the four pollutants and mortality from non-accidental, cardiovascular and respiratory causes. We compared the associations in and out the Stockholm urban area, by SAMS population density and across the 26 municipalities of the county. We found weak effects of most air pollutants on cause-specific mortality in the full year analysis, with estimates much larger and significant only during the warmer months (April to September): non-accidental mortality increased by 4.58% (95% confidence interval - 95% CI: 0.89%, 8.41%) and by 2.21% (95% CI: 0.71%, 3.73%) per 10 µg/m3 increase in lag 0-1 PM2.5 and O3, respectively. Associations were in general higher in the Stockholm city and in SAMS with high population density. When comparing the 26 municipalities, we didn't detect a significant heterogeneity in the short-term associations with air pollutants. In conclusion, we found a suggestion of a harmful role of air pollution also in non-urban areas, but the study was underpowered to draw firm conclusions. We consider this study as a pilot to investigate the spatial heterogeneity of the association between daily air pollution and mortality at the national level in Sweden.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Cidades , Mortalidade , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Ozônio/análise , Ozônio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Análise Espaço-Temporal , Suécia/epidemiologia , Fatores de Tempo
19.
Ecotoxicol Environ Saf ; 202: 110932, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800216

RESUMO

Adverse health effects arising from exposure to fine particulates have become a major concern. Angiogenesis is a vital physiological process for the growth and development of cells and structures in the human body, whereby excessive or insufficient vessel growth could contribute to pathogenesis of diseases. We therefore evaluated indirect effects of carbon black (CB) and inhalable airborne particles on the angiogenic ability of unexposed Human Umbilical Vein Endothelial Cells (HUVECs) by co-culturing HUVECs with pre-exposed Small Airway Epithelial Cells (SAECs). As endothelial cells are major components of blood vessels and potential targets of fine particles, we investigated if lung epithelial cells exposed to ambient PM2.5 surrogates could induce bystander effects on neighboring unexposed endothelial cells in an alveolar-capillary co-culture lung model. Epithelial exposure to CB at a non-toxic dose of 25 µg/mL reduced endothelial tube formation and cell adhesion in co-cultured HUVECs, and decreased expression of angiogenic genes in SAECs. Similarly, exposure of differentiated SAECs to PM2.5 surrogates reduced cell reproductive ability, adhesion and tube formation of neighboring HUVECs. This indicates epithelial exposure to CB and urban PM2.5 surrogates both compromised the angiogenic ability of endothelial cells through bystander effects, thereby potentially perturbing the ventilation-perfusion ratio and affecting lung function.


Assuntos
Poluentes Atmosféricos/toxicidade , Material Particulado/toxicidade , Testes de Toxicidade , Técnicas de Cocultura , Células Epiteliais , Células Endoteliais da Veia Umbilical Humana/citologia , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Pulmão/metabolismo , Neovascularização Patológica , Fuligem
20.
Chemosphere ; 261: 127635, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32768749

RESUMO

Ambient air pollution is recognized as a major threat to those with cardiovascular disease (CVD), especially among old adults within this high risk group. Heart rate variability (HRV) is a marker of cardiac autonomic system, which links air pollution and CVD. However, the relationship between PM and HRV has been inconsistently reported. To investigate the associations of PM2.5 and HRV in old adults whose average age was 55 years old or above, we conducted a meta-analysis of nineteen longitudinal studies including nine short-term and ten long-term studies. In the short-term exposure group, per 10 µg/m3 increase of PM2.5 was associated with decreases in the time-domain measurements, for SDNN -0.39% (95% CI: -0.72%, -0.06%) and for RMSSD -1.20% (95% CI: -2.17%, -0.23%) and in frequency-domain measurements, for LF -2.31% (95% CI: -3.85%, -0.77%) and for HF -1.87% (95% CI: -3.45%, -0.29%); In the long-term exposure group, per 10 µg/m3 increase of PM2.5 was associated with decreases in the time-domain measurements, for SDNN -0.92% (95% CI: -2.14%, 0.31%) and for RMSSD -1.96% (95% CI: -3.48%, -0.44%) and in frequency-domain measurements, for LF -2.78% (95% CI: -4.02%, -1.55%) and for HF -1.61% (95% CI: -4.02%, 0.80%). Exposure to PM2.5 is associated with decreased indicators of HRV in older adults suggesting an affected cardiac autonomic system upon exposure, which may explain the association between PM2.5 and risk of CVD in older adults. Long-term exposure to PM2.5 was more strongly associated with indicators of HRV than short-term exposure.


Assuntos
Exposição Ambiental/estatística & dados numéricos , Material Particulado/toxicidade , Idoso , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Biomarcadores , Feminino , Frequência Cardíaca , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Material Particulado/análise
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA