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1.
Chemosphere ; 235: 1134-1145, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31561304

RESUMO

Particulate matter (PM) from layer house has adverse effect on people and chicken respiratory health, which can further influence animal performance and reduce production efficiency. However, little study focus on the respiratory inflammation induced by PM2.5 from layer house and the underlying mechanism also unclear. In this study, human adenocarcinoma alveolar basal epithelial cells (A549 cell) was subjected to the PM2.5 from layer house to evaluate the inflammation reaction caused by PM2.5 and explore the role of Nrf2 and autophagy in regulating the inflammation. Results showed that the viability of A549 cell decreased in a time - and concentration - dependent manner after PM2.5 treatment. TNFα, IL6, and IL8 increased significantly treated with PM2.5 at 12 h. RNA sequencing indicated differentially expressed genes were enriched in immune system process, oxidative stress (OS), endoplasmic reticulum stress (ERS), and autophagy. Further studies showed TLR4 - NFκB p65 signal pathway involved in the inflammation reaction caused by PM2.5. The overexpression of Nrf2 decreased the level of TNFα, IL6, IL8 markedly as well as the level of NFκB p65 and NFκB pp65. OS and ERS were also limited under overactivation of Nrf2 in PM2.5 treated cells. Autophagy induced by PM2.5 promoted the inflammation through increasing the level of NFκB p65 and NFκB pp65. Autophagy deficient strengthened the expression of Nrf2. Collectively, our study revealed Nrf2 prevents inflammation caused by layer house PM2.5 stimulation, however, autophagy exerts a promotive role in TLR4 - NFκB p65 mediating inflammation in A549 cell.


Assuntos
Autofagia/fisiologia , Inflamação/etiologia , Fator 2 Relacionado a NF-E2/fisiologia , Material Particulado/efeitos adversos , Receptor 4 Toll-Like/metabolismo , Fator de Transcrição RelA/metabolismo , Células A549 , Animais , Autofagia/efeitos dos fármacos , Estresse do Retículo Endoplasmático/genética , Humanos , Inflamação/induzido quimicamente , Inflamação/prevenção & controle , Fator 2 Relacionado a NF-E2/farmacologia , Estresse Oxidativo/genética , Transdução de Sinais
2.
Life Sci ; 233: 116714, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31376370

RESUMO

Increased levels of particulate matter (PM) air pollutants in East Asia have resulted in detrimental health impacts increasing morbidity and mortality. Epidemiological studies suggest a possible relation between the cutaneous exposure of PM and increased oxidative stress and inflammation which lead to skin lesions. The present study utilizes an integrated cell culture model of keratinocytes and fibroblasts to mimic viable skin layers and investigate the possible effects of PM exposure after penetration through corneocytes. The skin perfection is upheld by homeostatic functionality of epidermal cells and the integrity of connective tissues. Exposure to xenobiotics could alter the skin cell homeostasis aggravating premature skin aging. Stimulation of HaCaT keratinocytes by PM collected from Beijing, China (CPM) increased the intracellular ROS levels triggering a cascade of events aggravating inflammatory responses and connective tissue degradation. In HDF fibroblasts, treatment with preconditioned keratinocyte culture media augmented inflammatory responses, cellular differentiation, and connective tissue degradation. Above events were marked by the increased intracellular ROS, inflammatory mediators, pro-inflammatory cytokines, matrix metalloproteinases (MMP)-1 and -2 levels, collagenase, and elastase activity. Fucosterol treatment of keratinocytes dose-dependently attenuated the detrimental effects both in keratinocytes and fibroblasts restoring the conditions near to physiological levels. Further evaluations could be advanced on developing fucosterol, in forms such as rejuvenating cosmeceuticals which could attenuate detrimental responses of CPM exposure.


Assuntos
Fibroblastos/efeitos dos fármacos , Inflamação/tratamento farmacológico , Queratinócitos/efeitos dos fármacos , Material Particulado/efeitos adversos , Dermatopatias/tratamento farmacológico , Pele/efeitos dos fármacos , Estigmasterol/análogos & derivados , Poluentes Atmosféricos/efeitos adversos , Células Cultivadas , Técnicas de Cocultura , Citocinas/metabolismo , Fibroblastos/metabolismo , Fibroblastos/patologia , Humanos , Inflamação/etiologia , Inflamação/metabolismo , Inflamação/patologia , Queratinócitos/metabolismo , Queratinócitos/patologia , NF-kappa B/metabolismo , Estresse Oxidativo , Espécies Reativas de Oxigênio/metabolismo , Pele/patologia , Dermatopatias/etiologia , Dermatopatias/metabolismo , Dermatopatias/patologia , Estigmasterol/farmacologia
3.
Environ Res ; 177: 108638, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31421449

RESUMO

Air pollution is a modifiable and preventable factor, and it is a possible risk factor for dementia. However, evidence from epidemiological studies is still limited. We conducted a systematic review and meta-analysis to summarize the epidemiological evidence for long-term effects of particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) on dementia/Alzheimer's disease (AD). Our inclusion criteria for eligible studies were: longitudinal cohort study design, no overlap in study population, age of study subject ≥50 years, detailed description of exposure assessment for PM2.5, outdoor assessment of exposure to PM2.5, usage of a clear definition of dementia/AD, and accessibility of sufficient information for meta-analysis. Six databases were searched for eligible studies. The random-effect model was used to synthesize the associations between PM2.5 and dementia. After exclusion of all irrelevant studies, we analyzed the results of four cohort studies conducted in Canada, Taiwan, the UK, and the US during 2015-2018 among more than 12 million elderly subjects aged ≥50 years (N = 12,119,853). Our meta-analysis reveals that exposure to a 10 µg/m3 increase in PM2.5 was significantly and positively associated with dementia (pooled HR = 3.26, 95% CI: 1.20, 5.31). In subgroup analyses, exposure to a 10 µg/m3 increase in PM2.5 was found to be positively associated with AD (pooled HR = 4.82, 95% CI: 2.28, 7.36). Analysis of current epidemiological research on PM2.5 and dementia confirmed that exposure to PM2.5 was positively associated with a higher risk for dementia. However, it is to be noted that the included studies mainly relied on claim-based diagnosis and showed large differences in methods of exposure assessment, hence further epidemiological studies with well validated outcomes and with standardized exposure assessment models are required to ascertain the relationship between PM2.5 and dementia/AD.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Doença de Alzheimer/epidemiologia , Material Particulado/efeitos adversos , Canadá , Humanos , Taiwan , Reino Unido , Estados Unidos
4.
Environ Res ; 177: 108660, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31445438

RESUMO

BACKGROUND: Previous studies have estimated the association between meteorological factors and mumps outbreaks without assessing the influence of air pollution. In this research, we explored the effects of short-term exposure to air pollution on the incidence of mumps. METHODS: Our time-series analysis was conducted using data collected in Wuhan, China from 2015 to 2017. Daily number of mumps cases was obtained from Disease Reporting System in Hubei Provincial Center for Disease Control and Prevention. Data on air pollution was obtained from 10 national air quality monitoring stations, including nitrogen dioxide (NO2), sulfur dioxide (SO2), ground-level ozone (O3), particulate matter less than or equal to 10 µm in aerodynamic diameter (PM10), and particulate matter less than or equal to 2.5 µm in aerodynamic diameter (PM2.5). Daily meteorological data including temperature and relative humidity were obtained from Hubei Meteorological Bureau. We performed a Poisson regression in generalized additive models (GAM) to explore the association between the incidence of mumps and exposure to air pollution. RESULTS: We observed that the effects of air pollutants were statistically significant mainly in two periods, lag 0 to lag 5 and lag 20 to lag 25, with the strongest effects appearing at lag 2 and lag 23. The cumulative effects were stronger than single-day lag effects. The stratified analysis showed the effect of pollutants during the hot season was stronger than that during the cold season, especially for NO2 and SO2. CONCLUSIONS: We found that exposure to NO2 and SO2 was significantly associated with higher risk of developing mumps. Our findings could help deepen the understanding of how air pollution exposure affects the incidence of mumps.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Caxumba/epidemiologia , China/epidemiologia , Humanos , Incidência , Dióxido de Nitrogênio/efeitos adversos , Ozônio/efeitos adversos , Material Particulado/efeitos adversos , Estações do Ano , Dióxido de Enxofre/efeitos adversos
5.
JAMA ; 322(6): 546-556, 2019 08 13.
Artigo em Inglês | MEDLINE | ID: mdl-31408135

RESUMO

Importance: While air pollutants at historical levels have been associated with cardiovascular and respiratory diseases, it is not known whether exposure to contemporary air pollutant concentrations is associated with progression of emphysema. Objective: To assess the longitudinal association of ambient ozone (O3), fine particulate matter (PM2.5), oxides of nitrogen (NOx), and black carbon exposure with change in percent emphysema assessed via computed tomographic (CT) imaging and lung function. Design, Setting, and Participants: This cohort study included participants from the Multi-Ethnic Study of Atherosclerosis (MESA) Air and Lung Studies conducted in 6 metropolitan regions of the United States, which included 6814 adults aged 45 to 84 years recruited between July 2000 and August 2002, and an additional 257 participants recruited from February 2005 to May 2007, with follow-up through November 2018. Exposures: Residence-specific air pollutant concentrations (O3, PM2.5, NOx, and black carbon) were estimated by validated spatiotemporal models incorporating cohort-specific monitoring, determined from 1999 through the end of follow-up. Main Outcomes and Measures: Percent emphysema, defined as the percent of lung pixels less than -950 Hounsfield units, was assessed up to 5 times per participant via cardiac CT scan (2000-2007) and equivalent regions on lung CT scans (2010-2018). Spirometry was performed up to 3 times per participant (2004-2018). Results: Among 7071 study participants (mean [range] age at recruitment, 60 [45-84] years; 3330 [47.1%] were men), 5780 were assigned outdoor residential air pollution concentrations in the year of their baseline examination and during the follow-up period and had at least 1 follow-up CT scan, and 2772 had at least 1 follow-up spirometric assessment, over a median of 10 years. Median percent emphysema was 3% at baseline and increased a mean of 0.58 percentage points per 10 years. Mean ambient concentrations of PM2.5 and NOx, but not O3, decreased substantially during follow-up. Ambient concentrations of O3, PM2.5, NOx, and black carbon at study baseline were significantly associated with greater increases in percent emphysema per 10 years (O3: 0.13 per 3 parts per billion [95% CI, 0.03-0.24]; PM2.5: 0.11 per 2 µg/m3 [95% CI, 0.03-0.19]; NOx: 0.06 per 10 parts per billion [95% CI, 0.01-0.12]; black carbon: 0.10 per 0.2 µg/m3 [95% CI, 0.01-0.18]). Ambient O3 and NOx concentrations, but not PM2.5 concentrations, during follow-up were also significantly associated with greater increases in percent emphysema. Ambient O3 concentrations, but not other pollutants, at baseline and during follow-up were significantly associated with a greater decline in forced expiratory volume in 1 second per 10 years (baseline: 13.41 mL per 3 parts per billion [95% CI, 0.7-26.1]; follow-up: 18.15 mL per 3 parts per billion [95% CI, 1.59-34.71]). Conclusions and Relevance: In this cohort study conducted between 2000 and 2018 in 6 US metropolitan regions, long-term exposure to ambient air pollutants was significantly associated with increasing emphysema assessed quantitatively using CT imaging and lung function.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Pulmão/fisiologia , Enfisema Pulmonar , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Carbono/efeitos adversos , Carbono/análise , Estudos de Coortes , Progressão da Doença , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Pulmão/diagnóstico por imagem , Masculino , Pessoa de Meia-Idade , Óxidos de Nitrogênio/efeitos adversos , Óxidos de Nitrogênio/análise , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Enfisema Pulmonar/epidemiologia , Enfisema Pulmonar/fisiopatologia , Testes de Função Respiratória , Tomografia Computadorizada por Raios X , Estados Unidos/epidemiologia
6.
Zhonghua Yu Fang Yi Xue Za Zhi ; 53(8): 817-823, 2019 08 06.
Artigo em Chinês | MEDLINE | ID: mdl-31378042

RESUMO

Objective: To explore the association between the exposure to major air pollutants in pre-pregnancy and early pregnancy (peri-conceptional period) and gestational diabetes mellitus (GDM). Methods: From March 2015 to April 2018, 4 817 pregnancies were recruited at three prenatal check-ups hospital in Hefei (Hefei First People's Hospital, Hefei. Maternal and Child Care Hospital and the First Affiliated Hospital of Anhui Medical University), China. Questionnaire was used to collect the demographic data, the health status and lifestyle of pregnant women. GDM was diagnosed according to the Chinese Guidelines for the Prevention and Treatment of Type 2 Diabetes (2017 Edition). Logistic regression was used to investigate the association of exposure to major air pollutants (PM(2.5), PM(10), SO(2), CO and NO(2)) during different periods of pre-pregnancy (12 weeks before pregnancy) and first trimester (12 weeks after last menstruation) and duration of exposure to high levels of pollutants with GDM. Results: The mean±SD of the age of subjects was (29.14±4.19) years old and the prevalence of GDM was 21.4% (n=1 030). The results of multivariate logistic regression analysis showed that after adjusting for confounding factors, the risk of GDM increased gradually with the prolonged exposure time of high-concentration pollutants compared with pregnant women who were not exposed to high pollution during the pre-pregnancy (χ(2)=61.28, P(trend)<0.001) with the OR (95%CI) values for exposure time of 1, 2, and 3 months about 1.42 (1.10-1.84), 1.73 (1.29-2.33), and 2.51 (1.75-3.59), respectively. In the pre-pregnancy period, in every 10 µg/m(3) increase of PM(2.5) and PM(10), the OR (95%CI) values of GDM were 1.14 (1.08-1.20) and 1.13 (1.08-1.19), respectively; for each increase of 1 µg/m(3) and 0.10 mg/m(3) of SO(2) and CO, the OR (95% CI) values of GDM were 1.03 (1.01-1.05) and 1.07 (1.01-1.13), respectively. For every 1 µg/m(3) increase in the average concentration of SO(2) in the first trimester, the OR (95%CI) value of GDM was 1.02 (1.01-1.05). Conclusion: PM(2.5), PM(10), SO(2) and CO exposure during the pre-pregnancy and SO(2) exposure in first trimester were positively correlated with the risk of GDM.


Assuntos
Poluição do Ar/efeitos adversos , Diabetes Gestacional/epidemiologia , Adulto , China/epidemiologia , Feminino , Humanos , Material Particulado/efeitos adversos , Gravidez , Estudos Prospectivos
7.
N Engl J Med ; 381(8): 705-715, 2019 08 22.
Artigo em Inglês | MEDLINE | ID: mdl-31433918

RESUMO

BACKGROUND: The systematic evaluation of the results of time-series studies of air pollution is challenged by differences in model specification and publication bias. METHODS: We evaluated the associations of inhalable particulate matter (PM) with an aerodynamic diameter of 10 µm or less (PM10) and fine PM with an aerodynamic diameter of 2.5 µm or less (PM2.5) with daily all-cause, cardiovascular, and respiratory mortality across multiple countries or regions. Daily data on mortality and air pollution were collected from 652 cities in 24 countries or regions. We used overdispersed generalized additive models with random-effects meta-analysis to investigate the associations. Two-pollutant models were fitted to test the robustness of the associations. Concentration-response curves from each city were pooled to allow global estimates to be derived. RESULTS: On average, an increase of 10 µg per cubic meter in the 2-day moving average of PM10 concentration, which represents the average over the current and previous day, was associated with increases of 0.44% (95% confidence interval [CI], 0.39 to 0.50) in daily all-cause mortality, 0.36% (95% CI, 0.30 to 0.43) in daily cardiovascular mortality, and 0.47% (95% CI, 0.35 to 0.58) in daily respiratory mortality. The corresponding increases in daily mortality for the same change in PM2.5 concentration were 0.68% (95% CI, 0.59 to 0.77), 0.55% (95% CI, 0.45 to 0.66), and 0.74% (95% CI, 0.53 to 0.95). These associations remained significant after adjustment for gaseous pollutants. Associations were stronger in locations with lower annual mean PM concentrations and higher annual mean temperatures. The pooled concentration-response curves showed a consistent increase in daily mortality with increasing PM concentration, with steeper slopes at lower PM concentrations. CONCLUSIONS: Our data show independent associations between short-term exposure to PM10 and PM2.5 and daily all-cause, cardiovascular, and respiratory mortality in more than 600 cities across the globe. These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies. (Funded by the National Natural Science Foundation of China and others.).


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ambiental/análise , Mortalidade , Material Particulado/efeitos adversos , Poluição do Ar/análise , Doenças Cardiovasculares/mortalidade , Causas de Morte , Exposição Ambiental/efeitos adversos , Exposição Ambiental/legislação & jurisprudência , Saúde Global , Humanos , Tamanho da Partícula , Material Particulado/análise , Doenças Respiratórias/mortalidade , Risco
8.
Environ Pollut ; 253: 667-679, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31330358

RESUMO

Many cities fail to meet air quality standards, which results in increased risk for pulmonary disorders, including asthma. Human and experimental studies have shown that diesel exhaust (DE) particles are associated with worsening of allergic asthma. Biodiesel (BD), a cleaner fuel from renewable sources, was introduced in the eighties. Because of the reduction in particulate matter (PM) emissions, BD was expected to cause fewer adverse pulmonary effects. However, only limited data on the effect of BD emissions in asthma are available. OBJECTIVE: Determine whether BD exhaust exposure in allergic sensitized mice leads to different effects on inflammatory and functional responses compared to DE exposure. METHODS: Balb/C mice were orotracheally sensitized with House Dust Mite (HDM) or a saline solution with 3 weekly instillations. From day 9 until day 17 after sensitization, they were exposed daily to filtered air (FA), DE and BD exhaust (concentration: 600 µg/m3 PM2.5). Lung function, bronchoalveolar lavage fluid (BALF) cell counts, cytokine levels (IL-2, IL-4, IL-5, IL-17, TNF-α, TSLP) in the BALF, peribronchiolar eosinophils and parenchymal macrophages were measured. RESULTS: HDM-sensitized animals presented increased lung elastance (p = 0.046), IgG1 serum levels (p = 0.029), peribronchiolar eosinophils (p = 0.028), BALF levels of total cells (p = 0.020), eosinophils (p = 0.028), IL-5 levels (p = 0.002) and TSLP levels (p = 0.046) in BALF. DE exposure alone increased lung elastance (p = 0.000) and BALF IL-4 levels (p = 0.045), whereas BD exposure alone increased BALF TSLP levels (p = 0.004). BD exposure did not influence any parameters after HDM challenge, while DE exposed animals presented increased BALF levels of total cells (p = 0.019), lymphocytes (p = 0.000), neutrophils (p = 0.040), macrophages (p = 0.034), BALF IL-4 levels (p = 0.028), and macrophagic inflammation in the lung tissue (p = 0.037), as well as decreased IgG1 (p = 0.046) and IgG2 (p = 0.043) levels when compared to the HDM group. CONCLUSION: The results indicate more adverse pulmonary effects of DE compared to BD exposure in allergic sensitized animals.


Assuntos
Biocombustíveis/toxicidade , Emissões de Veículos/toxicidade , Alérgenos , Animais , Asma/induzido quimicamente , Biocombustíveis/análise , Líquido da Lavagem Broncoalveolar , Citocinas , Modelos Animais de Doenças , Humanos , Inflamação/induzido quimicamente , Interleucina-17 , Pulmão/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Neutrófilos , Material Particulado/efeitos adversos , Testes de Toxicidade , Emissões de Veículos/análise
9.
Environ Sci Pollut Res Int ; 26(25): 25491-25499, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31264151

RESUMO

Numerous studies have investigated the impacts of ambient fine particulate matter (PM2.5) on human health. In this study, we examined the association of daily PM2.5 concentrations with the number of deaths for the cerebrovascular disease on the same day, using the generalized additive model (GAM) controlling for temporal trend and meteorological variables. We used the data between 2012 and 2014 from Shanghai, China, where the adverse health effects of PM2.5 have been of particular concern. Three different approaches (principal component analysis, shrinkage smoothers, and the least absolute shrinkage and selection operator regularization) were used in GAM to handle multicollinear meteorological variables. Our results indicate that the average daily concentration of PM2.5 in Shanghai was high, 55 µg/m3, with an average daily death for cerebrovascular disease (CVD) of 62. There was 1.7% raised cerebrovascular disease deaths per 10 µg/m3 increase in PM2.5 concentration in the unadjusted model. However, PM2.5 concentration was no longer associated with CVD deaths after controlling for meteorological variables. The results were consistent in the three modelling techniques that we used. As a large number of people are exposed to air pollution, further investigation with longer time period including individual-level information is needed to examine the association.


Assuntos
Poluição do Ar/análise , Transtornos Cerebrovasculares/mortalidade , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/complicações , Material Particulado/análise , China , Morte , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/fisiopatologia , Humanos , Meteorologia , Material Particulado/efeitos adversos , Material Particulado/química , Análise de Componente Principal , Projetos de Pesquisa
10.
BMC Public Health ; 19(1): 877, 2019 Jul 04.
Artigo em Inglês | MEDLINE | ID: mdl-31272504

RESUMO

BACKGROUND: This study uses bibliometric analysis to describe the state of research about the association of NO2, PM2.5 and noise exposures - three traffic-related pollutants - with cardiometabolic disorders. METHODS: We retrieved references published 1994-2017 from Scopus and classified references with respect to exposure, health outcome and study design using index keywords. Temporal trend, top cited references, used index keywords and the number of hypothesis testing and non-hypothesis testing study design for each group were identified. RESULTS: Results show PM2.5 is the most frequently studied exposure (47%), followed by both NO2 and PM2.5 exposure (29%). Only 3% of references considered multiple exposures between NO2 and/or PM2.5 and noise, and these were published after 2008. While we observed a growing trend in studies with NO2 and/or PM2.5 and noise and diabetes in the last decade, there is a diminishing trend in studies with noise and diabetes. Different patterns of study designs were found through H/NH ratio, the number of references classified as having a hypothesis (H)-testing design relative to the number of references classified as having a non-hypothesis (NH)-testing design. Studies with NO2 and/or PM2.5 exposure are more likely to have a H-testing design, while those with noise exposure are more likely to have a NH-testing design, such as cross-sectional study design. CONCLUSIONS: We conclude with three themes about research trends. First, the study of simultaneous exposures to multiple pollutants is a current trend, and likely to continue. Second, the association between traffic-related pollutants and diabetes and metabolic symptoms is an area for growth in research. Third, the transition to the use of H-testing study designs to explore associations between noise and cardiometabolic outcomes may be supported by improved understanding of the mechanism of action, and/or improvements to the accuracy and precision of air pollution and noise exposure assessments for environmental health research.


Assuntos
Doenças Cardiovasculares/epidemiologia , Doenças Metabólicas/epidemiologia , Emissões de Veículos/toxicidade , Bibliometria , Diabetes Mellitus/epidemiologia , Humanos , Dióxido de Nitrogênio/efeitos adversos , Ruído/efeitos adversos , Material Particulado/efeitos adversos
11.
Pneumologie ; 73(7): 407-429, 2019 Jul.
Artigo em Alemão | MEDLINE | ID: mdl-31291669

RESUMO

The third part of the DGP statement introduces the current body of knowledge on less studied health outcomes associated with exposure to ambient air pollution: the negative impact on metabolism leading to impaired glucose tolerance and diabetes as well as contribution to the development of neurodegenerative disorders and delayed cognitive function in children. Furthermore, prenatal exposure and adverse effects on mother and child are addressed. Finally, the currently discussed biological mechanisms underlying various health effects associated with exposure to air pollution are described.Differing, but often complementary biological mechanisms create the basis for the diverse health outcomes caused by air pollution. Oxidative stress and a subclinical inflammatory response in the lungs and on a systemic level ("low-grade systemic inflammation") are considered to be key mechanisms. They promote secondary alterations in the body, such as vascular or metabolic processes, and may also result in the currently studied epigenetic phenomena or neuroinflammation. In this context, the health significance of soluble particulate matter and the role of ultrafine particles translocated across biological membranes into blood vessel and transported via the circulation to secondary target organs, such as liver, brain or the fetus, are intensively discussed.Diabetes is one of the leading chronic diseases worldwide, with a prevalence of almost 14 % in Germany. Although lifestyle factors are the main causes, current evidence suggests that long-term exposure to air pollution may additionally increase the risk for type 2 diabetes. Supporting evidence for a causal role of air pollution is provided by studies addressing the regulation of the blood glucose levels in metabolically healthy participants, insulin sensitivity, or pregnancy-related diabetes. Experimental studies provide further support for plausible biological mechanisms. However, prospective studies are needed to gain more evidence, taking multiple lifestyle and environmental factors, such as green space and noise, and an improved individual exposure assessment into account.The aging population has an increased risk of neurodegenerative diseases. First studies point towards a contribution of chronic exposure to air pollution, specifically by particulate matter. Several studies report its association with decreased neurocognitive capacity or an increased prevalence of dementia or Alzheimer's disease in adults. However, the studies are inhomogeneous regarding design, exposure and outcome, leading to inconsistent results. With respect to the influence on neurocognitive development of children, first studies suggest an association between the level of air pollution, e. g. at school, and delayed cognitive development.Even though the evidence for the different biological endpoints during pregnancy is still heterogeneous, the studies generally point towards an adverse impact of air pollution on the maternal and fetal organisms. The strongest evidence exists for low birth weight, with small effect sizes of only some grams, and for a higher incidence of reduced birth weight (< 2500 g). An increased risk for gestational hypertension and preeclampsia underscores the possible impact of exposure to air pollution on the maternal organism. However, the current body of evidence does not yet allow a final conclusion on the influence of intrauterine exposure to air pollution regarding early childhood lung function and development of allergies, particularly in light of the fact that it is hard to distinguish in epidemiological studies between the effects of pre- and postnatal exposure.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Diabetes Mellitus Tipo 2/epidemiologia , Exposição Ambiental , Material Particulado/efeitos adversos , Resultado da Gravidez/epidemiologia , Adulto , Idoso , Criança , Pré-Escolar , Feminino , Alemanha/epidemiologia , Humanos , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Estudos Prospectivos
12.
Artigo em Chinês | MEDLINE | ID: mdl-31315358

RESUMO

Objective: To explore the role of autophagy in PM2.5-induced inflammation in human nasal epithelial cells and related mechanism. Methods: Human nasal epithelial cells were exposed to different concentration of PM2.5 for different times, and the expression levels of microtubule-associated protein-1 light chain-3 Ⅱ (LC3 Ⅱ) and Beclin1 proteins were measured by Western blot. The typical autophagosome and autolysosome were observed by using transmission electron microscopy (TEM). To observe autophagic flux, mRFP-GFP-LC3 plasmid was transfected to nasal epithelial cells and the punctate staining of mRFP-GFP-LC3 were determined by confocal laser scanning microscope. The expression of inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) in cell culture supernatant were assessed by enzyme-linked immunosorbent assay (ELISA). To assess the role of autophagy in PM2.5-mediated inflammation, autophagy related gene Atg5 and Beclin-1 were silenced by siRNA knockdown, and inflammatory cytokines were analyzed.GraphPad Prism 6.0 was used for statistical analysis. Results: PM2.5 exposure increased the expression of LC3 Ⅱ and Beclin-1 proteins in a dose- (in PM2.5 group with concentration of 0, 15, 30, 60, 120 µg/ml, the expression of LC3 Ⅱ was 0.021±0.001(x±s), 0.037±0.002, 0.058±0.005, 0.075±0.006, 0.085±0.004, respectively, F=126.8, P<0.05; the expression of Beclin-1 was 0.002±0.000, 0.003±0.000, 0.005±0.000, 0.007±0.001, 0.008±0.001, respectively, F=137.3, P<0.05) and time-dependent manner (in PM2.5 group with exposure time of 0, 3, 6, 12, 24 h, the expression of LC3Ⅱ was 0.160±0.007, 0.222±0.003, 0.251±0.015, 0.483±0.029, 0.585±0.035, respectively, F=215.3, P<0.05; the expression of Beclin-1 was 0.059±0.002, 0.080±0.002, 0.087±0.002, 0.183±0.007, 0.228±0.005, respectively, F=137.3, P<0.05) in human nasal epithelial cells. TEM analysis showed typical autophagosome and autolysosome in cells after PM2.5 exposure for 24 h. PM2.5 significantly increased the number of yellow and red dots representing autophagosomes and autolysosomes respectively, indicating autophagic flux was elevated. Moreover, PM2.5 enhanced the secretion of inflammatory cytokines such as IL-6 and TNF-α, which was dramatically prevented by Atg5-siRNA and Beclin-1-siRNA. Conclusion: Autophagy plays an important role in PM2.5-caused inflammation response in nasal epithelial cells, which can induce release of inflammatory factors such as IL-6 and TNF-α and advance the inflammatory reaction.


Assuntos
Autofagia/imunologia , Células Epiteliais/imunologia , Inflamação/imunologia , Mucosa Nasal/imunologia , Material Particulado/imunologia , Proteína Beclina-1/biossíntese , Humanos , Interleucina-6/biossíntese , Proteínas Associadas aos Microtúbulos/biossíntese , Material Particulado/efeitos adversos , Fator de Necrose Tumoral alfa/biossíntese
13.
Mol Immunol ; 112: 163-174, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31153046

RESUMO

Exposure to airborne particulate matter (PM) not only causes lung inflammation and chronic respiratory diseases, but also increases the incidence and mortality of cardiopulmonary diseases. The nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome activation has been shown to play a critical role in the formation of many chronic disorders. On the other hand, carbon monoxide (CO) has been shown to possess anti-inflammatory and antioxidant effects in many tissues and organs. Here, we investigated the effects and mechanisms of carbon monoxide releasing molecule-2 (CORM-2) on PM-induced inflammatory responses in human pulmonary alveolar epithelial cells (HPAEpiCs). We found that PM induced C-reactive protein (CRP) expression, NLRP3 inflammasome activation, IL-1ß secretion, and caspase-1 activation, which were inhibited by pretreatment with CORM-2. In addition, transfection with siRNA of Toll-like receptor 2 (TLR2) or TLR4 and pretreatment with an antioxidant (N-acetyl-cysteine, NAC), the inhibitor of NADPH oxidase (diphenyleneiodonium, DPI), or a mitochondria-specific superoxide scavenger (MitoTEMPO) reduced PM-induced inflammatory responses. CORM-2 also inhibited PM-induced NADPH oxidase activity and NADPH oxidase- and mitochondria-derived ROS generation. However, pretreatment with inactivate CORM-2 (iCORM-2) had no effects on PM-induced inflammatory responses. Finally, we showed that CORM-2 inhibited PM-induced CRP, NLRP3 inflammasome, and ASC protein expression in the lung tissues of mice and IL-1ß levels in the serum of mice. PM-enhanced leukocyte count in bronchoalveolar lavage fluid in mice was reduced by CORM-2. The results of this study suggested a protective role of CORM-2 in PM-induced lung inflammation by inhibiting the TLR2 and TLR4/ROS-NLRP3 inflammasome-CRP axial.


Assuntos
Inflamassomos/efeitos dos fármacos , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Compostos Organometálicos/farmacologia , Pneumonia/tratamento farmacológico , Espécies Reativas de Oxigênio/metabolismo , Receptor 2 Toll-Like/metabolismo , Receptor 4 Toll-Like/imunologia , Animais , Líquido da Lavagem Broncoalveolar , Monóxido de Carbono/efeitos adversos , Caspase 1/metabolismo , Humanos , Inflamassomos/metabolismo , Interleucina-1beta/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Material Particulado/efeitos adversos , Pneumonia/induzido quimicamente , Pneumonia/metabolismo , Substâncias Protetoras/farmacologia , Transdução de Sinais/efeitos dos fármacos
14.
Environ Monit Assess ; 191(Suppl 2): 272, 2019 Jun 28.
Artigo em Inglês | MEDLINE | ID: mdl-31254074

RESUMO

PM2.5 air pollution is a significant issue for human health all over the world, especially in East Asia. A large number of ground-based measurement sites have been established over the last decade to monitor real-time PM2.5 concentration. However, even this enhanced observational network leaves many gaps in characterizing the PM2.5 spatial distribution. Machine learning provides a variety of algorithms to help deal with these large spatial gaps-combining both remotely sensed and in situ observation data to estimate the global PM2.5 concentration. This study used a PM2.5 data product of six regions from the results of an unsupervised self-organizing map (SOM) with optimized ensemble learning approaches to highlight the most important meteorological and surface variables associated with PM2.5 concentration. These variables were then examined via multiple linear regression models to provide physical mechanistic insights into the morphology of the PM2.5 annual cycles.


Assuntos
Poluentes Atmosféricos/análise , Poluição do Ar/análise , Monitoramento Ambiental , Aprendizado de Máquina , Material Particulado/análise , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Algoritmos , Extremo Oriente , Humanos , Modelos Lineares , Material Particulado/efeitos adversos
15.
Sci Total Environ ; 684: 458-465, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31154218

RESUMO

Fine particulate matter (PM2.5) exposure has been associated with lung function decline, but impact of PM2.5 constituents especially for polycyclic aromatic hydrocarbons (PAHs) on lung function is unclear among community population. We enrolled 224 Chinese participants who participated in two study periods (2014-2015 and 2017-2018) of the Wuhan-Zhuhai cohort as a panel, and quantified the associations of personal PM2.5 and sixteen PM2.5-bound PAHs with lung function levels as well as lung function change in three years by linear mixed models. Diagnostic ratios were calculated to identify potential sources of PM2.5-bound PAHs in Wuhan and Zhuhai separately. In single-constituent models, we found that each one interquartile-range increase of naphthalene, acenaphthene, fluoranthene and pyrene were associated with 26.82, 60.99, 45.25 and 23.37 mL decline in FVC respectively; while fluoranthene and pyrene were associated with 27.43 and 15.49 mL decline in FEV1 respectively. Similar results were observed in consitituent-PM2.5 joint models and single-constituent residual models. Persistently long-term high levels of three HMW-PAHs (benzo[a]anthracene, dibenzo[a,h]anthracene, and benzo[ghi]perylene) were associated with 214.65, 226.13, and 265.00 mL decline in FVC decline in three years, compared with persistently low exposure level groups. The associations were different between Wuhan and Zhuhai. The results of diagnostic ratios suggested the differences in PAH emissions between two cities. Our findings provide evidence that both short- and long-term PM2.5-bound PAH exposures might affect lung function.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Exposição por Inalação/efeitos adversos , Pulmão/efeitos dos fármacos , Material Particulado/efeitos adversos , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Adulto , Estudos Transversais , Relação Dose-Resposta a Droga , Feminino , Humanos , Estudos Longitudinais , Pulmão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Testes de Função Respiratória
16.
Sci Total Environ ; 684: 548-566, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31154227

RESUMO

Due to their hydrophobicity and relatively large surface area, microplastics (MPs) can act as carriers of hydrophobic pollutants in the ocean and may facilitate their transfer to organisms. This study examined effects of dietary exposure to polystyrene MPs of 0.5 and 4.5 µm alone and with sorbed benzo[a]pyrene (BaP) on mussels Mytilus galloprovincialis in order to elucidate the effects of MP size and the presence of sorbed BaP on the organism. MPs were provided daily, mixed with algae, during 26 days at equivalent mass (0.058 mg/L), corresponding to 1000 particles/mL for 4.5 µm MPs and to 7.44 × 105 particles/mL for 0.5 µm MPs. Effects were determined on early cellular biomarkers in hemocytes, structure and cell type composition of digestive tubules (DTs), histopathology and whole organism responses (condition index (CI), clearance rate (CR), food absorption efficiency (AE), respiration rate (RR) and scope for growth (SFG)). BaP concentrations in mussels increased with time, in particular when sorbed to smaller MPs. Large MPs were abundant in the lumen of stomach and DTs, but were also occasionally found within epithelial cells. Effects in all treatments increased with exposure time. MPs with sorbed BaP were more toxic than MPs alone according to hemocyte viability and catalase activity and to the quantitative structure of DT epithelium. Higher toxicity of small MPs compared to larger ones was recorded for DNA damage and cell composition of DTs. At tissue level a slight increase in prevalence of inflammatory responses occurred in all exposed groups. At whole organism level a compensatory effect was observed on absorption efficiency across MP treatments at day 26, resulting in increased SFG in mussels exposed to small MPs with sorbed BaP. This could be related to an increased energy need to deal with stress observed in biomarkers. Further work is required to understand the Trojan horse effect of a variety of plastic type, size, shape combinations together with a wide variety of pollutants.


Assuntos
Benzo(a)pireno/efeitos adversos , Mytilus/efeitos dos fármacos , Material Particulado/efeitos adversos , Poliestirenos/efeitos adversos , Absorção Fisiológica , Animais , Biomarcadores/análise , Dieta , Mytilus/fisiologia , Tamanho da Partícula
17.
Sci Total Environ ; 684: 610-620, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31158624

RESUMO

Air pollution is a growing problem in developing countries, and there exists a wide range of evidence documenting the large health and productivity losses associated with high concentrations of pollutants. South Africa is a developing country with high levels of air pollution in some regions, and the costs of air pollution on human health and economic growth in South Africa are still uncertain. The environmental Benefits Mapping and Analysis Program (BenMAP) model was applied to South Africa using local data on population, mortality rates, and concentrations of fine particulate matter (PM2.5), as well as mortality risk coefficients from the epidemiological literature. BenMAP estimates the number of premature deaths that would likely have been avoided if South African air quality levels met the existing annual National Ambient Air Quality Standard (NAAQS) of 20 µg m-3, and the more stringent World Health Organization (WHO) guideline for annual average PM2.5 of 10 µg m-3. We estimate 14,000 avoided premature mortalities in 2012 if all of South Africa met the existing NAAQS annual average standard for PM2.5. These avoided cases of mortality have an estimated monetary value of $14.0 billion (US2011$), which is equivalent to 2.2% of South Africa's 2012 GDP (PPP, US2011$). We estimate 28,000 avoided premature mortalities if the more stringent WHO guideline for annual average PM2.5 is met across South Africa, which when expressed as a national burden is equivalent to 6% of all deaths in South Africa being attributable to PM2.5 exposure. These avoided cases of mortality have an estimated monetary value of $29.1 billion, which is equivalent to 4.5% of South Africa's 2012 GDP. These results show that there are significant public health benefits to lowering PM2.5 concentrations across South Africa, with correspondingly high economic benefits.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Exposição Ambiental/efeitos adversos , Mortalidade Prematura , Material Particulado/efeitos adversos , Saúde Pública , Humanos , Modelos Teóricos , África do Sul
18.
Chemosphere ; 233: 309-318, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31176132

RESUMO

Nasal epithelium provides a physical barrier to potentially harmful stimuli. Cilia, which is on the apical side of the human nasal epithelial cells (HNEpCs), plays a critical role in removing inhaled harmful matter. Ciliary beat frequency (CBF) and ciliary beat pattern (CBP) are the two important indicators for ciliary beat function. However, impacts of the fine particulate matter (PM2.5) on CBF and CBP are still unknown. We aimed to evaluate the impact of PM2.5 on the ciliary beat function of the HNEpCs and its potential mechanisms. After exposed to PM2.5 for 12 h, cilia of HNEpCs were in disordered arrangement. The ciliary coverage rate was decreased after PM2.5 exposure of a series of concentration, while the proportion of basal cells was continuously increased and could be observed on the apical side of the HNEpCs which is hardly be observed without PM2.5 exposure. PM2.5 increased the CBF after 12 h exposure, while 24 h exposure increased the CBF at the relative lower dosage groups and then made a decrease at relative higher dosage groups. CBF were classified into two different types, which had different changes following PM2.5 exposure. CBP showed significant changes characterized as the increased dyskinesia index. Total levels of cellular ATP and the mitochondrial membrane potential were decreased following 12 h exposure of PM2.5, while no change was found in O2 consumption. In conclusion, PM2.5 impact the ciliary beat function of HNEpCs, and the mitochondrial dysfunction might play an important role in it.


Assuntos
Mucosa Nasal/citologia , Mucosa Nasal/efeitos dos fármacos , Material Particulado/efeitos adversos , Trifosfato de Adenosina/metabolismo , Células Cultivadas , Cílios/efeitos dos fármacos , Exposição Ambiental/efeitos adversos , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Material Particulado/administração & dosagem , Material Particulado/análise , Material Particulado/química
19.
Environ Pollut ; 252(Pt B): 1318-1324, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31252129

RESUMO

The increase in ambient fine dust particles (FDP) due to urbanization and industrialization has been identified as a major contributor to air pollution. It has become a serious issue that threatens human health because it causes respiratory diseases and skin aging. In the present study, the protective effect of the green tea catechin, (-)-epigallocatechin gallate (EGCG), against FDP (ERM-CZ100)-stimulated skin aging in human dermal fibroblasts (HDFs) was investigated. The results demonstrate that EGCG significantly and dose-dependently scavenged intracellular reactive oxygen species (ROS) in and increased the viability of FDP-stimulated HDFs. In addition, EGCG dose-dependently recovered collagen synthesis and inhibited intracellular elastase and collagenase activities. Moreover, EGCG decreased the expression of human matrix metalloproteinases (MMPs) via regulation of nuclear factor kappa B (NF-κB), activator protein 1 (AP-1), and mitogen-activated protein kinases (MAPKs) signaling pathways in FDP-stimulated HDFs. This study suggests that EGCG is a potential anti-aging candidate that can be used for FDP-induced skin aging as a therapeutic agent itself or as an ingredient in pharmaceutical and cosmeceutical products.


Assuntos
Catequina/análogos & derivados , Sistema de Sinalização das MAP Quinases/fisiologia , NF-kappa B/metabolismo , Material Particulado/efeitos adversos , Envelhecimento da Pele/efeitos dos fármacos , Fator de Transcrição AP-1/metabolismo , Catequina/farmacologia , Linhagem Celular , Colagenases , Poeira/análise , Fibroblastos/efeitos dos fármacos , Humanos , Inibidores de Metaloproteinases de Matriz/farmacologia , Elastase Pancreática/antagonistas & inibidores , Espécies Reativas de Oxigênio/metabolismo , Pele/fisiopatologia , Envelhecimento da Pele/fisiologia , Chá/química
20.
Environ Sci Pollut Res Int ; 26(23): 24112-24120, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31228058

RESUMO

To determine the association between daily air pollution and the hospital admissions for respiratory diseases in children aged from 0 to 17 years in Jinan, China. Generalized linear models were used to explore the acute effects of ambient fine particulate matter (PM2.5) on the children's hospital admissions for respiratory diseases. We evaluated the lag associations (including lag 0 to lag 3, lag 01, and lag 03) between daily PM2.5 and the number of children's hospital admissions for respiratory diseases, and stratified by gender, age group (baby group: age 0-1 years; child group: age 1-5 years; student group: age 6-17 years), and cause-specific disease (including upper infection, pneumonia, and acute bronchitis) during 2011-2015. PM2.5 had significant positive impacts on the number of children's hospital admissions for respiratory disease. The results showed that per 10 µg/m3 increase of PM2.5 at lag 1 was associated with an increase in total and male hospital admissions of 0.23% (95% CI, 0.02%-0.45%) and 0.32% (95% CI, 0.04%-0.06%). The corresponding risk of the student group (age 6-17 years) hospital admissions was increased 0.90% (95% CI, 0.39%-1.42%) at lag 1 day. The corresponding risk of the upper infection was increased 0.96% (95% CI, 0.37-1.55%) at lag 1 day. Males and student groups (age 6-17 years) were more vulnerable to PM2.5 exposure. Upper infection admission was identified as the sensitive disease for children. It is a better way to reduce children's outdoor activities to avoid health effects when the air pollution increases.


Assuntos
Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Hospitalização/estatística & dados numéricos , Doenças Respiratórias/epidemiologia , Adolescente , Bronquite/epidemiologia , Criança , Pré-Escolar , China/epidemiologia , Feminino , Humanos , Lactente , Recém-Nascido , Modelos Lineares , Masculino , Material Particulado/efeitos adversos , Material Particulado/análise , Pneumonia/epidemiologia
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