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1.
Chemosphere ; 286(Pt 1): 131614, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34325257

RESUMO

Particulate matter (PM)-induced airway inflammation contributes to the development and exacerbation of chronic airway diseases. Circular RNA (circRNA) is a new class of non-coding RNA that participates in gene regulation in various respiratory diseases, but the regulatory role of circRNA in PM-induced airway inflammation has not been fully elucidated. In this study, we performed the human circRNA microarray to reveal differentially expressed circRNAs in PM-induced human bronchial epithelial cells (HBECs). A total of 176 upregulated and 15 downregulated circRNAs were identified. Of these, a new circRNA termed circTXNRD1 was upregulated by PM exposure in a dose- and time-dependent manner. Knockdown of circTXNRD1 significantly attenuated PM-induced expression of proinflammatory cytokine interleukin 6 (IL-6). CircRNA pull-down, dual-luciferase reporter assay and fluorescence in situ hybridization showed that circTXNRD1 acted as an endogenous sponge to decrease miR-892a levels in HBECs. Downregulation of miR-892a could increase cyclooxygenase-2 (COX-2) expression and eventually promote IL-6 secretion in PM-induced HBECs. Taken together, our findings reveal circTXNRD1 as a novel inflammatory mediator in PM-induced inflammation in HBECs via regulating miR-892a/COX-2 axis. These results provide new insight into the biological mechanism underlying PM-induced inflammation in chronic airway diseases.


Assuntos
MicroRNAs , RNA Circular , Ciclo-Oxigenase 2/genética , Células Epiteliais , Humanos , Hibridização in Situ Fluorescente , Inflamação/induzido quimicamente , Inflamação/genética , MicroRNAs/genética , Material Particulado/toxicidade , RNA/genética
2.
Sci Total Environ ; 803: 149790, 2022 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-34481165

RESUMO

BACKGROUND: Several studies have examined whether air pollution is associated with adverse births outcomes, but it is not clear if socioeconomic status (SES) modifies this relationship. OBJECTIVES: We investigated if maternal education and area-level socioeconomic status modified the relationship between ozone, nitrogen dioxide and particulate matter with aerodynamic diameter <10 µm (PM10) on preterm births (PTB; gestational age <37 weeks) and term low birth weight (TLBW; weight < 2500 g on term deliveries). METHODS: Analyses were based on almost 1 million singleton live births in São Paulo municipality between 2011 and 2016. The final sample included 979,306 births for PTB analysis and 888,133 for TLBW analysis. Exposure to PM10, NO2 and O3 were based on date of birth and estimated for the entire gestation and for each trimester. Multilevel logistic regression models were conducted to examine the effect of air pollutants on both adverse birth outcomes and whether it was modified by individual and area-level SES. RESULTS: In fully adjusted models, over the entire pregnancy, a 10 µg/m3 increase in O3 and PM10 was associated with increased chance of PTB (odds ratio; OR = 1.14 CI 1.13, 1.16 and 1.08 CI = 1.02, 1.15 respectively) and PM10 with TLBW (OR = 1.08 CI 1.03, 1.14). Associations were modified by maternal educational and area-level SES for both outcomes. Mothers of lower education had an additional chance of PTB and TLBW due to PM10 exposure (OR = 1.04 CI 1.04, 1.05 and 1.10 CI 1.08, 1.14 respectively), while mothers living in low SES areas have an additional chance for TLBW (OR = 1.05 CI 1.03, 1.06). Similar modification effects were found for O3 exposure. Trimester specific associations were weaker but followed a similar pattern. CONCLUSION: Socioeconomic status modifies the effect of air pollution on adverse birth outcomes. Results indicate that mothers with lower SES may be more susceptible to air pollution effects.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Brasil , Feminino , Humanos , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Classe Social
3.
Sci Total Environ ; 804: 150091, 2022 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-34517316

RESUMO

BACKGROUND: Ambient air pollution exposure has been associated with higher mortality risk in numerous studies. We assessed potential variability in the magnitude of this association for non-accidental, cardiovascular disease, respiratory disease, and lung cancer mortality in a country-wide administrative cohort by exposure assessment method and by adjustment for geographic subdivisions. METHODS: We used the Belgian 2001 census linked to population and mortality register including nearly 5.5 million adults aged ≥30 (mean follow-up: 9.97 years). Annual mean concentrations for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) were assessed at baseline residential address using two exposure methods; Europe-wide hybrid land use regression (LUR) models [100x100m], and Belgium-wide interpolation-dispersion (RIO-IFDM) models [25x25m]. We used Cox proportional hazards models with age as the underlying time scale and adjusted for various individual and area-level covariates. We further adjusted main models for two different area-levels following the European Nomenclature of Territorial Units for Statistics (NUTS); NUTS-1 (n = 3), or NUTS-3 (n = 43). RESULTS: We found no consistent differences between both exposure methods. We observed most robust associations with lung cancer mortality. Hazard Ratios (HRs) per 10 µg/m3 increase for NO2 were 1.060 (95%CI 1.042-1.078) [hybrid LUR] and 1.040 (95%CI 1.022-1.058) [RIO-IFDM]. Associations with non-accidental, respiratory disease and cardiovascular disease mortality were generally null in main models but were enhanced after further adjustment for NUTS-1 or NUTS-3. HRs for non-accidental mortality per 5 µg/m3 increase for PM2.5 for the main model using hybrid LUR exposure were 1.023 (95%CI 1.011-1.035). After including random effects HRs were 1.044 (95%CI 1.033-1.057) [NUTS-1] and 1.076 (95%CI 1.060-1.092) [NUTS-3]. CONCLUSION: Long-term air pollution exposure was associated with higher lung cancer mortality risk but not consistently with the other studied causes. Magnitude of associations varied by adjustment for geographic subdivisions, area-level socio-economic covariates and less by exposure assessment method.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Censos , Estudos de Coortes , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Humanos , Material Particulado/análise , Material Particulado/toxicidade
4.
Sci Total Environ ; 806(Pt 1): 150214, 2022 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-34571223

RESUMO

Fuel exhaust particulate matter (FEPM) is an important source of air pollution worldwide. However, the comparative and mechanistic toxicity of FEPMs emitted from combustion of different fuels is still not fully understood. This study employed pathway-based approaches via human cells to evaluate mechanistic toxicity of FEPMs. The results showed that FEPMs caused concentration-dependent (0.1-200 µg/mL) cytotoxicity and oxidative stress. FEPMs at low concentration (10 µg/mL) induced cell cycle arrest in S and G2 phases, while high level of FEPMs (200 µg/mL) caused cell cycle arrest in G1 phase. Different FEPMs induced distinct expression profiles of toxicity-related genes, illustrating different toxic mechanisms. Furthermore, FEPMs inhibited the phosphorylation of protein kinase A (PKA), which related with reproductive toxicity. Spearman rank correlations among the chemicals carried by FEPMs and the toxic effects revealed that PAHs and metals promoted cell cycle arrest in the G1 phase and suppressed PKA activity. Furthermore, PAHs (Nap and Acy) and metals (Al and Pb) in FEPMs were highly and positively correlated with the expression of genes involved in apoptosis, ER stress, metal stress and inflammation. Our findings offered more mechanistic information of FEPMs at the level of subcellular toxicity and help to better understand their potential health effects.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Hidrocarbonetos Policíclicos Aromáticos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Humanos , Material Particulado/análise , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/análise , Emissões de Veículos/análise , Emissões de Veículos/toxicidade
5.
Environ Res ; 203: 111930, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34425111

RESUMO

In June 2020, we published a review focused on assessing the influence of various air pollutants on the transmission of SARS-CoV-2, and the severity of COVID-19 in patients infected by the coronavirus. The results of most of those reviewed studies suggested that chronic exposure to certain air pollutants might lead to more severe and lethal forms of COVID-19, as well as delays/complications in the recovery of the patients. Since then, a notable number of studies on this topic have been published, including also various reviews. Given the importance of this issue, we have updated the information published since our previous review. Taking together the previous results and those of most investigations now reviewed, we have concluded that there is a significant association between chronic exposure to various outdoor air pollutants: PM2.5, PM10, O3, NO2, SO2 and CO, and the incidence/risk of COVID-19 cases, as well as the severity/mortality of the disease. Unfortunately, studies on the potential influence of other important air pollutants such as VOCs, dioxins and furans, or metals, are not available in the scientific literature. In relation to the influence of outdoor air pollutants on the transmission of SARS-CoV-2, although the scientific evidence is much more limited, some studies point to PM2.5 and PM10 as potential airborne transmitters of the virus. Anyhow, it is clear that environmental air pollution plays an important negative role in COVID-19, increasing its incidence and mortality.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , COVID-19 , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Humanos , Incidência , Material Particulado/análise , Material Particulado/toxicidade , SARS-CoV-2
6.
Environ Pollut ; 292(Pt A): 118349, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34653588

RESUMO

The adverse effects of fine atmospheric particulate matter with aerodynamic diameters of ≤2.5 µm (PM2.5) are closely associated with particulate chemicals. In this study, PM2.5 samples were collected from highway and industry sites in Hangzhou, China, during the autumn and winter, and their cytotoxicity and pulmonary toxicity and endocrine-disrupting potential (EDP) were evaluated in vitro and in vivo; the particulate polycyclic aromatic hydrocarbons (PAHs), phthalate esters (PAEs), and heavy metals were then characterized. The toxicological results suggested that the PM2.5 from highway site induced higher cytotoxicity (cell viability inhibition, intracellular oxidative stress, and cell membrane injury) and pulmonary toxicity (inflammatory response (IR) and oxidative stress (OS)) than the samples from industry site, while the PM2.5 from industry site exhibited higher EDP (estrogenic and anti-androgenic activity). The cytotoxicity and pulmonary toxicity of PM2.5 in the winter were higher than those in the autumn, while no seasonal difference in the endocrine-disrupting potential was observed (p > 0.05). The Pearson correlation analysis between the biological effects and particulate chemicals revealed that the PM2.5-induced inflammatory response and oxidative stress were closely associated with the particulate PAHs and heavy metals (Pearson correlation coefficients: rIR, PAHs = 0.822-0.988, rIR, heavy metals = 0.895-0.971, rOS, PAHs = 0.843-0.986, and rOS, heavy metals = 0.887-0.933), while particulate di (2-ethylhexyl)phthalate (DEHP) substantially contributed to the EDP of PM2.5 (rEDP, DEHP = 0.981). This study indicated that the toxicity and EDP of PM2.5 could vary with the surrounding environment and season, which was closely associated with the variations of particulate chemicals. Further studies are needed to clarify the associations between the harmful effects of PM2.5 and other contributing factors.


Assuntos
Poluentes Atmosféricos , Metais Pesados , Hidrocarbonetos Policíclicos Aromáticos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Animais , China , Monitoramento Ambiental , Ésteres/toxicidade , Humanos , Metais Pesados/análise , Metais Pesados/toxicidade , Camundongos , Material Particulado/análise , Material Particulado/toxicidade , Ácidos Ftálicos , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Estações do Ano
7.
Environ Pollut ; 292(Pt A): 118320, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34634399

RESUMO

Particulate matter with a diameter of less than 2.5 µm or PM2.5 is recognized worldwide as a cause of public health problems, mainly associated with respiratory and cardiovascular diseases. There is accumulating evidence to show that exposure to PM2.5 has a crucial causative role in various neurological disorders, the main ones being dementia and Alzheimer's disease (AD). PM2.5 can activate glial and microglial activity, resulting in neuroinflammation, increased intracellular ROS production, and ultimately neuronal apoptosis. PM2.5 also causes the alteration of neuronal morphology and synaptic changes and increases AD biomarkers, including amyloid-beta and hyperphosphorylated-tau, as well as raising the levels of enzymes involved in the amyloidogenic pathway. Clinical trials have highlighted the correlation between exposure to PM2.5, dementia, and AD diagnosis. This correlation is also displayed by concordant evidence from animal models, as indicated by increased AD biomarkers in cerebrospinal fluid and markers of vascular injury. Blood-brain barrier disruption is another aggravated phenomenon demonstrated in people at risk who are exposed to PM2.5. This review summarizes and discusses studies from in vitro, in vivo, and clinical studies on causative relationships of PM2.5 exposure to AD-related neuropathology. Conflicting data are also examined in order to determine the actual association between ambient air pollution and neurodegenerative diseases.


Assuntos
Poluição do Ar , Doença de Alzheimer , Poluição do Ar/efeitos adversos , Peptídeos beta-Amiloides , Animais , Cognição , Humanos , Material Particulado/toxicidade
8.
Chemosphere ; 286(Pt 3): 131963, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426263

RESUMO

BACKGROUND: Exposure to air pollution has been linked with altered immune function in adults, but little is known about its effects on early life. This study aimed to investigate the effects of exposure to air pollution during prenatal and postnatal windows on cell-mediated immune function in preschoolers. METHODS: Pre-school aged children (2.9 ± 0.5 y old, n = 391) were recruited from a mother-child cohort study in Wuhan, China. We used a spatial-temporal land use regression (LUR) model to estimate exposures of particulate matter with aerodynamic diameters ≤2.5 µm (PM2.5) and ≤10 µm (PM10), and nitrogen dioxide (NO2) during the specific trimesters of pregnancy and the first two postnatal years. We measured peripheral blood T lymphocyte subsets and plasma cytokines as indicators of cellular immune function. We used multiple informant models to examine the associations of prenatal and postnatal exposures to air pollution with cell-mediated immune function. RESULTS: Prenatal exposures to PM2.5, PM10, and NO2 during early pregnancy were negatively associated with %CD3+ and %CD3+CD8+ cells, and during late pregnancy were positively associated with %CD3+ cells. Postnatal exposures to these air pollutants during 1-y or 2-y childhood were positively associated with IL-4, IL-5, IL-6, and TNF-α. We also observed that the associations of prenatal or postnatal air pollution exposures with cellular immune responses varied by child's sex. CONCLUSIONS: Our results suggest that exposure to air pollution during different critical windows of early life may differentially alter cellular immune responses, and these effects appear to be sex-specific.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Criança , Pré-Escolar , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Humanos , Imunidade Celular , Masculino , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Gravidez
9.
Sci Total Environ ; 804: 150216, 2022 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-34520930

RESUMO

European harbours are known to contribute to air quality degradation. While most of the literature focuses on emissions from stacks or logistics operations, ship refit and repair activities are also relevant aerosol sources in EU harbour areas. Main activities include abrasive removal of filler and spray painting with antifouling coatings/primers/topcoats. This work aimed to assess ultrafine particle (UFP) emissions from ship maintenance activities and their links with exposure, toxicity and health risks for humans and the aquatic environment. Aerosol emissions were monitored during mechanical abrasion of surface coatings under real-world operating conditions in two scenarios in the Mallorca harbour (Spain). Different types of UFPs were observed: (1) highly regular (triangular, hexagonal) engineered nanoparticles (Ti-, Zr-, Fe-based), embedded as nano-additives in the coatings, and (2) irregular, incidental particles emitted directly or formed during abrasion. Particle number concentrations monitored were in the range of industrial activities such as drilling or welding (up to 5 ∗ 105/cm3, mean diameters <30 nm). The chemical composition of PM4 aerosols was dominated by metallic tracers in the coatings (Ti, Al, Ba, Zn). In vitro toxicity of PM2 aerosols evidenced reduced cell viability and a moderate potential for cytotoxic effects. While best practices (exhaust ventilation, personal protective equipment, dust removal) were in place, it is unlikely that exposures and environmental release can be fully avoided at all times. Thus, it is advisable that health and safety protocols should be comprehensive to minimise exposures in all types of locations (near- and far-field) and periods (activity and non-activity). Potential release to coastal surface waters of metallic engineered and incidental nanomaterials, as well as fine and coarse particles (in the case of settled dust), should be assessed and avoided.


Assuntos
Monitoramento Ambiental , Soldagem , Aerossóis/análise , Humanos , Tamanho da Partícula , Material Particulado/análise , Material Particulado/toxicidade
10.
Chemosphere ; 286(Pt 2): 131833, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426128

RESUMO

Due to the poor living and healthcare conditions, preterm birth (PTB) in rural population is a pressing health issue. However, PTB studies in rural population are rare. To explore the effects of air pollutants on PTB in rural population, we collected 697,316 medical records during 2014-2016 based on the National Free Preconception Health Examination Project. Logistic regression models were used to estimate the association between air pollutants and PTB and the modifying effects of demographic characteristics. Relative contribution and principal component analysis-generalized linear model (PCA-GLM) analysis were used to explore the most significant air pollutant and gestational period. Our results demonstrated that PTB risk is positively associated with exposure to air pollutants including PM10, PM2.5, SO2, NO2, and CO, while negatively associated with O3 exposure (P < 0.05). In addition, we found that NO2 was the largest contributor to the risk of PTB caused by air pollutants (26.5%). The third trimester of pregnancy was the most sensitive exposure window. PCA-GLM analysis showed that the first component (a combination of PM, SO2, NO2, and CO) increased the risk of PTB. Moreover, we found that rural women who are younger, had higher educated, multi-parity, or smoke appeared to be more sensitive to the association between air pollutants exposure and PTB (P-interaction<0.05). Our findings suggested that increased air pollutants except O3 were associated with elevated PTB risk, especially among vulnerable mothers. Therefore, the effects of air pollutants exposure on PTB should be mitigated by restricting emission sources of NO2 and SO2 in rural population, especially during the third trimester.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Nascimento Prematuro , Efeitos Tardios da Exposição Pré-Natal , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , China/epidemiologia , Feminino , Humanos , Recém-Nascido , Exposição Materna/estatística & dados numéricos , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologia , População Rural
11.
Chemosphere ; 286(Pt 2): 131741, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34358888

RESUMO

Airborne particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs) and heavy metals (HMs) are significant contributors leading to many human health issues. Thus, this study was designed to perform chemical analysis and biological impact of airborne particulate matter 10 (PM10) in the World heritage City of Kandy City in Sri Lanka. 12 priority PAHs and 34 metals, including 10 highly toxic HMs were quantified. The biological effects of organic extracts were assayed using an in vitro primary porcine airway epithelial cell culture model. Cytotoxicity, DNA damage, and gene expressions of selected inflammatory and cancer-related genes were also assessed. Results showed that the total PAHs ranged from 3.062 to 36.887 ng/m3. The metals were dominated by Na > Ca > Mg > Al > K > Fe > Ti, while a few toxic HMs were much higher in the air than the existing ambient air quality standards. In the bioassays, a significant cytotoxicity (p < 0.05) was observed at 300 µg/mL treatment, and significant (p < 0.05) DNA damages were noted in all treatment groups. All genes assessed were found to be significantly up-regulated (p < 0.05) after 24 h of exposure and after 48 h, only TGF-ß1 and p53 did not significantly up-regulate (p < 0.05). These findings confirm that the Kandy city air contains potential carcinogenic and mutagenic compounds and thus, exposure to Kandy air may increase the health risks and respiratory tract-related anomalies.


Assuntos
Poluentes Atmosféricos , Metais Pesados , Hidrocarbonetos Policíclicos Aromáticos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Animais , Monitoramento Ambiental , Células Epiteliais , Humanos , Metais Pesados/análise , Metais Pesados/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Sistema Respiratório/química , Sri Lanka , Suínos
12.
J Hazard Mater ; 421: 126710, 2022 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-34332479

RESUMO

The particulate matter (PM) in livestock houses, one of the primary sources of atmospheric PM, is not only detrimental to the respiratory health of animals and farmworkers but also poses a threat to the public environment and public health and warrants increased attention. In this study, we investigated the variation in the pulmonary microbiome and metabolome in broiler chickens exposed to PM collected from a broiler house. We examined the pulmonary microbiome and metabolome in broilers, observing that PM induced a visible change in α and ß diversity. A total of 66 differential genera, including unclassified_f_Ruminococcaceae and Campylobacter, were associated with pulmonary inflammation. Untargeted metabolomics was utilised to identify 63 differential metabolites induced by PM and correlated with differential bacteria. We observed that PM resulted in injury of the broiler lung and disruption of the microbial community, as well as causing changes in the observed metabolites. These results imply that perturbations to the microbiome and metabolome may play pivotal roles in the mechanism underlying PM-induced broiler lung damage.


Assuntos
Metaboloma , Microbiota , Animais , Galinhas , Inflamação/induzido quimicamente , Pulmão , Material Particulado/toxicidade
13.
J Hazard Mater ; 421: 126760, 2022 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-34396970

RESUMO

Large amounts of epidemiological evidence have confirmed the atmospheric particulate matter (PM2.5) exposure was positively correlated with the morbidity and mortality of respiratory diseases. Nevertheless, its pathogenesis remains incompletely understood, probably resulting from the activation of oxidative stress, inflammation, altered genetic and epigenetic modifications in the lung upon PM2.5 exposure. Currently, biomarker investigations have been widely used in epidemiological and toxicological studies, which may help in understanding the biologic mechanisms underlying PM2.5-elicited adverse health outcomes. Here, the emerging biomarkers to indicate PM2.5-respiratory system interactions were summarized, primarily related to oxidative stress (ROS, MDA, GSH, etc.), inflammation (Interleukins, FENO, CC16, etc.), DNA damage (8-OHdG, γH2AX, OGG1) and also epigenetic modulation (DNA methylation, histone modification, microRNAs). The identified biomarkers shed light on PM2.5-elicited inflammation, fibrogenesis and carcinogenesis, thus may favor more precise interventions in public health. It is worth noting that some inconsistent findings may possibly relate to the inter-study differentials in the airborne PM2.5 sample, exposure mode and targeted subjects, as well as methodological issues. Further research, particularly by -omics technique to identify novel, specific biomarkers, is warranted to illuminate the causal relationship between PM2.5 pollution and deleterious lung outcomes.


Assuntos
Poluentes Atmosféricos , MicroRNAs , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Biomarcadores , Humanos , Pulmão , Estresse Oxidativo , Material Particulado/análise , Material Particulado/toxicidade
14.
Environ Pollut ; 292(Pt B): 118464, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34763019

RESUMO

The use of biomass for cooking and heating is considered an important factor associated with chronic obstructive pulmonary disease (COPD), but few studies have previously addressed its underlying mechanisms. Therefore, this research aimed to evaluate the effects of biomass-related PM2.5 (BRPM2.5) exposure on 16HBE human airway epithelial cells and in mice with regard to mitochondrial dysfunction. Our study indicated that BRPM2.5 exposure of 16HBE cells resulted in mitochondrial dysfunction, including decreased mitochondrial membrane potential, increased expression of fission proteins-phospho-DRP1, increased mitochondrial ROS (mtROS), and decreased levels of ATP. BRPM2.5 altered the mitochondrial metabolism of 16HBE cells by decreasing mitochondrial oxygen consumption and glycolysis. However, Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release. BRPM2.5 exposure resulted in abnormal mitochondrial morphological alterations both in 16HBE and in lung tissue. Taken together, these results suggest that BRPM2.5 has detrimental effects on human airway epithelial cells, leading to mitochondrial dysfunction, abnormal mitochondrial metabolism and altered mitochondrial dynamics. The present study provides the first evidence that disruption of mitochondrial structure and mitochondrial metabolism may be one of the mechanisms of BRPM2.5-induced respiratory dysfunction.


Assuntos
Células Epiteliais , Pulmão , Animais , Biomassa , Humanos , Pulmão/química , Camundongos , Material Particulado/análise , Material Particulado/toxicidade , Espécies Reativas de Oxigênio
15.
Chemosphere ; 287(Pt 3): 132269, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34562704

RESUMO

Studies have indicated that ambient pollutant exposure correlates with nasal disease, in which nasal mucosa microbiota play a crucial role. However, the association between exposure to real-ambient air pollutants and the composition of nasal mucosa microbiota has not been well studied. This study aimed to explore the composition of nasal mucosa microbiota after exposure to real-ambient air pollutants with a special system. We monitored PM2.5, O3, etc. in the system and confirmed PM2.5 and O3 were the main pollutants. SD rats were exposed to the system for 16 weeks in summer or 22 weeks in autumn-winter. The concentrations of PM2.5 were 24.00 µg/m3 in the Summer stage and 22.21 µg/m3 in the autumn-winter stage. The O3 concentrations were 25.46 and 13.55 µg/m3, respectively. Exposure altered bacterial beta diversity in the summer stage. There were 4 and 3 different bacteria at the king, order, family and genus levels between the two groups at the two stages, respectively. The abundance of opportunistic pathogens changed, Pseudomonas decreased in summer stage, and Bifidobacterium increased in the autumn-winter stage. The influence of the season on the nasal mucosa microbiota was analyzed. The alpha diversity of the autumn-winter stage was higher than that of the summer stage. LEfSe analysis revealed 34 differential bacterial taxa at the king, order, family and genus level in the two control groups and 31 of the two exposure groups, which were not the same as the bacteria between the control groups and exposure groups. We found that PM2.5 combined with O3 exposure was associated with the composition of the nasal mucosa microbiota and the abundance of opportunistic pathogens, in which season likely impacted the microbiota.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Animais , Bactérias/genética , Monitoramento Ambiental , Mucosa Nasal , Material Particulado/análise , Material Particulado/toxicidade , Ratos , Ratos Sprague-Dawley , Estações do Ano
16.
Chemosphere ; 286(Pt 1): 131566, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34293557

RESUMO

It is well documented that fine particles matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) are associated with a range of adverse health outcomes. However, most epidemiologic studies have focused on understanding their additive effects, despite that individuals are exposed to multiple air pollutants simultaneously that are likely correlated with each other. Therefore, we applied a novel method - Bayesian Kernel machine regression (BKMR) and conducted a population-based cohort study to assess the individual and joint effect of air pollutant mixtures (PM2.5, O3, and NO2) on all-cause mortality among the Medicare population in 15 cities with 656 different ZIP codes in the southeastern US. The results suggest a strong association between pollutant mixture and all-cause mortality, mainly driven by PM2.5. The positive association of PM2.5 with mortality appears stronger at lower percentiles of other pollutants. An interquartile range change in PM2.5 concentration was associated with a significant increase in mortality of 1.7 (95% CI: 0.5, 2.9), 1.6 (95% CI: 0.4, 2.7) and 1.4 (95% CI: 0.1, 2.6) standard deviations (SD) when O3 and NO2 were set at the 25th, 50th, and 75th percentiles, respectively. BKMR analysis did not identify statistically significant interactions among PM2.5, O3, and NO2. However, since the small sub-population might weaken the study power, additional studies (in larger sample size and other regions in the US) are in need to reinforce the current finding.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Idoso , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Teorema de Bayes , Estudos de Coortes , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Humanos , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Ozônio/análise , Ozônio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade
17.
Chemosphere ; 286(Pt 1): 131615, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34303049

RESUMO

BACKGROUND: Systematic evaluations of the cumulative effects and mortality displacement of ambient particulate matter (PM) pollution on deaths are lacking. We aimed to discern the cumulative effect profile of PM exposure, and investigate the presence of mortality displacement in a large-scale population. METHODS: We conducted a time-series analysis with different exposure-lag models on 13 cities in Jiangsu, China, to estimate the effects of PM pollution on non-accidental, cardiovascular, and respiratory mortality (2015-2019). Over-dispersed Poisson generalized additive models were integrated with distributed lag models to estimate cumulative exposure effects, and assess mortality displacement. RESULTS: Pooled cumulative effect estimates with lags of 0-7 and 0-14 days were substantially larger than those with single-day and 2-day moving average lags. For each 10 µg/m3 increment in PM2.5 concentration with a cumulative lag of 0-7 days, we estimated an increase of 0.50 % (95 % CI: 0.29, 0.72), 0.63 % (95 % CI: 0.38, 0.88), and 0.50 % (95 % CI: 0.01, 1.01) in pooled estimates of non-accidental, cardiovascular, and respiratory mortality, respectively. Both PM10 and PM2.5 were associated with significant increases in non-accidental and cardiovascular mortality with a cumulative lag of 0-14 days. We observed mortality displacement within 30 days for non-accidental, cardiovascular, and respiratory deaths. CONCLUSIONS: Our findings suggest that risk assessment based on single-day or 2-day moving average lag structures may underestimate the adverse effects of PM pollution. The cumulative effects of PM exposure on non-accidental and cardiovascular mortality can last up to 14 days. Evidence of mortality displacement for non-accidental, cardiovascular, and respiratory deaths was found.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças Cardiovasculares , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Doenças Cardiovasculares/epidemiologia , China/epidemiologia , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Humanos , Mortalidade , Material Particulado/análise , Material Particulado/toxicidade
18.
Environ Pollut ; 292(Pt B): 118351, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34637830

RESUMO

Particulate matter exposure and related chemical changes in drinking water have been associated with health problems and inflammatory disorders. This study aimed to examine the effect of orally administered ash-water dilution on the gut of mice under normal and inflammatory conditions. Balb/c mice received ash-released soluble and dust-suspended components in the drinking water for 14 days. On day 7, animals were intrarectally instilled with TNBS in ethanol or flagellin from Salmonella typhimurium in PBS. At sacrifice, colon segments were collected and histologic damage, mRNA expression and cytokine levels in tissue were evaluated. In addition, these parameters were also evaluated in IL-10 null mice. We found that mice that received 5% w. fine-ash dilution in the drinking water worsened colitis signs. Weight loss, shortening of the colon, tissue edema with mucosa and submucosa cell infiltration and production of pro-inflammatory cytokines and chemokines were enhanced compared to control mice. A more pronounced inflammation was observed in IL-10 null mice. In addition, markers of NLRP3-dependent inflammasome activation were found in animals exposed to ash. In conclusion, ingestion of contaminated water with dust-suspended particulate matter enhanced the inflammatory response in the gut, probably due to alteration of the gut barrier and promoting an intense contact with the luminal content. This study critically appraises the response for fine particulate matter in uncommon illnesses reported for volcanic ash pollution. We suggest actions to enable better prediction and assessment the health impacts of volcanic eruptions.


Assuntos
Colite , Erupções Vulcânicas , Animais , Colite/induzido quimicamente , Inflamação/induzido quimicamente , Camundongos , Material Particulado/toxicidade
19.
Chemosphere ; 287(Pt 1): 131955, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34478962

RESUMO

PURPOSE: The aim of this study was to investigate the expression profiles of long noncoding RNAs (lncRNAs) in human corneal epithelial cells (HCECs) exposed to fine particulate matter (PM2.5) and to identify potential biological pathways involved in PM2.5-induced toxicity in HCECs. METHODS: Using RNA sequencing (RNA-seq) and hierarchy clustering analysis, lncRNA expression profiles in PM2.5-treated and untreated HCECs were examined. Gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to predict the role of altered lncRNAs in biological processes and pathways. A quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) assay was conducted to verify the RNA-seq results in HCECs and human corneal epithelial cell sheets. RESULTS: In total, 65 lncRNAs were altered in the PM2.5-treated HCECs, including 41 upregulated and 24 downregulated lncRNAs. The results of the qRT-PCR assay were consistent with those of the RNA-seq analysis. The expression of two significantly upregulated lncRNAs was confirmed in human corneal epithelial cell sheets. The GO analysis demonstrated that altered lncRNAs in the PM2.5-treated HCECs were significantly enriched in three domains: cellular component, molecular function, and biological process. The KEGG pathway analysis revealed enriched pathways of lncRNA co-expressed mRNAs, including cancer, RNA transport, and Rap1 signaling. CONCLUSIONS: Our results suggest that lncRNAs are involved in the pathogenesis of PM2.5-induced ocular diseases, exerting their effects through biological processes and pathogenic pathways. Among the altered lncRNAs, RP3-406P24.3 and RP11-285E9.5 may play significant roles in PM2.5-induced ocular surface injury.


Assuntos
RNA Longo não Codificante , Células Epiteliais , Perfilação da Expressão Gênica , Ontologia Genética , Humanos , Material Particulado/toxicidade , RNA Longo não Codificante/genética , RNA Mensageiro
20.
J Hazard Mater ; 422: 126771, 2022 01 15.
Artigo em Inglês | MEDLINE | ID: mdl-34391975

RESUMO

The present study investigates potential nanomaterial releases and occupational health risks across the lifecycle of nano-enabled building materials (NEBMs), namely, insulations and coatings. We utilized real-world degradation scenarios of a) sanding (mechanical), b) incineration (thermal), and c) accelerated UV-aging (environmental) followed by incineration. Extensive physicochemical characterization of the released lifecycle particulate matter (LCPM) was performed. The LCPM2.5 aerosol size fraction was used to assess the acute biological, cytotoxic and inflammatory effects on Calu-3 human lung epithelial cells. RNA-Seq analysis of exposed cells was performed to assess potential for systemic disease. Findings indicated that release dynamics and characteristics of LCPM depended on both the NEBM composition and the degradation scenario(s). Incineration emitted a much higher nanoparticle number concentration than sanding (nearly 4 orders of magnitude), which did not change with prior UV-aging. Released nanofillers during sanding were largely part of the matrix fragments, whereas those during incineration were likely physicochemically transformed. The LCPM from incineration showed higher bioactivity and inflammogenicity compared to sanding or sequential UV-aging and incineration, and more so when metallic nanofillers were present (such as Fe2O3). Overall, the study highlights the need for considering real-world exposure and toxicological data across the NEBM lifecycle to perform adequate risk assessments and to ensure workplace health and safety.


Assuntos
Saúde do Trabalhador , Material Particulado , Aerossóis/análise , Materiais de Construção , Humanos , Incineração , Material Particulado/toxicidade
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