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1.
Artigo em Inglês | MEDLINE | ID: mdl-33535701

RESUMO

Asthma is one of the most common chronic diseases worldwide affecting all age groups from children to the elderly. In addition to other factors such as smoking, air pollution and atopy, some environmental chemicals are shown or suspected to increase the risk of asthma, exacerbate asthma symptoms and cause other respiratory symptoms. In this scoping review, we report environmental chemicals, prioritized for investigation in the European Human Biomonitoring Initiative (HBM4EU), which are associated or possibly associated with asthma. The substance groups considered to cause asthma through specific sensitization include: diisocyanates, hexavalent chromium Cr(VI) and possibly p-phenylenediamine (p-PDA). In epidemiological studies, polyaromatic hydrocarbons (PAHs) and organophosphate insecticides are associated with asthma, and phthalates, per- and polyfluoroalkyl substances (PFASs), pyrethroid insecticides, mercury, cadmium, arsenic and lead are only potentially associated with asthma. As a conclusion, exposure to PAHs and some pesticides are associated with increased risk of asthma. Diisocyanates and Cr(VI) cause asthma with specific sensitization. For many environmental chemicals, current studies have provided contradicting results in relation to increased risk of asthma. Therefore, more research about exposure to environmental chemicals and risk of asthma is needed.


Assuntos
Arsênico , Asma , Poluentes Ambientais , Hidrocarbonetos Aromáticos , Praguicidas , Idoso , Asma/induzido quimicamente , Asma/epidemiologia , Monitoramento Biológico , Criança , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Monitoramento Ambiental , Poluentes Ambientais/análise , Poluentes Ambientais/toxicidade , Humanos
2.
Sci Total Environ ; 766: 142365, 2021 Apr 20.
Artigo em Inglês | MEDLINE | ID: mdl-33601665

RESUMO

Emerging evidence suggests associations between Perfluoroalkyl substances (PFASs) exposure and asthma, but the findings are inconsistent. The current study sought to investigate whether perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) could contribute to asthma exacerbation and to clarify the underlying biological mechanisms. The objectives are a) to determine whether PFOS or PFOA could aggravate the mouse asthma and pulmonary inflammation b) to investigate whether PFOS and PFOA regulate the balance of Th1/Th2 through the JAK-STAT signaling pathway and aggravated asthma. Ovalbumin (OVA) induced asthmatic mice were exposed to PFOS or PFOA by gavage. PFOS and PFOA serum level and toxicity in organs were assessed; and the impacts on respiratory symptoms, lung tissue pathology, T helper cell (Th2) response, and STAT6 pathway activity were also evaluated. In vitro Jurkat cells were used to study the mechanisms of PFOS and PFOA mediated Th1 and Th2 responses. Both PFOS and PFOA exacerbated lung tissue inflammation (greater number of eosinophils and mucus hyperproduction), upregulated Th2 cytokine production (IL-4 and IL-13), and promoted Th2 cells and STAT6 activation. Furthermore, PFOS and PFOA enhanced the Th2 response in Jurkat cells via STAT6 activation; and the effect of PFOS exposure on GATA-3, IL-4 and IFN-γ was blocked after the expression of STAT6 was suppressed in Jurkat cells, however, the effects of PFOA exposure were only partially blocked. PFOS and PFOA aggravated inflammation among OVA-induced asthmatic mice, by promoting the Th2 response in lymphocytes and disturbing the balance of Th1/Th2 through the JAK-STAT signaling pathway.


Assuntos
Asma , Fluorcarbonetos , Ácidos Alcanossulfônicos , Animais , Asma/induzido quimicamente , Caprilatos , Fluorcarbonetos/toxicidade , Inflamação/induzido quimicamente , Pulmão , Camundongos , Camundongos Endogâmicos BALB C
3.
Chemosphere ; 272: 129619, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33465612

RESUMO

RATIONALE: Although an association of fine particulate matter (PM2.5) with asthma incidence has been assumed, there is insufficient evidence regarding the effect of long-term exposure to PM2.5 on incident asthma among elderly adults. OBJECTIVES: This study aimed to investigate an association between long-term exposure to PM2.5 and incident asthma among elderly adults in South Korea. METHODS: Adults ≥65 years of age (n = 1,220,645) who did not visit hospitals for asthma during a washout period (between 2008 and 2010) were followed up until 2016 using data from the National Health Insurance System in South Korea. Incident asthma was defined as the number of patients with a primary diagnostic code of asthma who visited hospitals more than twice. We linked the health data with district-level PM2.5 concentrations and estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident asthma after adjusting for potential confounders in time-varying Cox proportional hazard models. MEASUREMENTS AND MAIN RESULTS: Over 5,942,256 person-years, 54,522 patients developed asthma, with an incidence of 9.2 cases/1000 person-years. A 10 µg/m3 increase in the 36-month mean PM2.5 concentration was significantly associated with a 9% increase in incident asthma (HR = 1.09, 95% CI: 1.04-1.14). This association was found to be robust for different definitions of incident asthma and washout periods. CONCLUSION: Long-term exposure to PM2.5 was associated with the incidence of asthma in elderly adults. This finding provides evidence of an association between PM2.5 and adult-onset asthma.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adulto , Idoso , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Asma/induzido quimicamente , Asma/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Incidência , Material Particulado/efeitos adversos , Material Particulado/análise , República da Coreia/epidemiologia
4.
Environ Pollut ; 270: 116297, 2021 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-33348144

RESUMO

BACKGROUND: Evidence proved that gestational ozone (O3) exposure can increase the risk of neonatal adverse respiratory outcomes, but offspring asthma is unclear. OBJECTIVE: This study aimed to investigate whether gestational O3 exposure could exacerbate offspring asthma, and to research the differences in effects of O3 exposure at different gestational periods on offspring asthma. METHODS: The pregnant ICR mice were randomly grouped and were administered O3 (air as control) at gestational day (GD) 1-6, 7-12, and 13-18, respectively. The pups aged 2-4 weeks were treated with ovalbumin (OVA) to establish a model of early life asthma. Asthma characteristics such as pulmonary inflammation, goblet cell proliferation, airway remodeling, OVA-specific immunoglobulin (Ig) E secretion and cytokines were examined. RESULTS: OVA sensitization and challenge successfully induced asthma in offspring. Compared with the air control, pulmonary inflammation infiltration, mucous secretion, the concentration of OVA-specific IgE, the level of tumor necrosis factor (TNF)-α, and T helper (Th) 2-skewed response were significantly exacerbated when O3 exposure at GD13-18 following inhaling OVA, while pulmonary inflammatory infiltration, mucus secretion, and Th2-skewed response were not significantly changed when O3 exposure at both GD1-6 and GD7-12. What's more, the above indicators in asthmatic offspring due to O3 exposure at GD13-18 were more severe than at GD1-6 and GD7-12. Interestingly, the signs of asthma only appeared in the offspring after OVA inhalation. When offspring were not treated with OVA, the prenatal O3 exposure alone did not lead to asthmatic reactions in offspring. In addition, O3 exposure at GD13-18 markedly increased the number of neutrophils and macrophages in Bronchoalveolar Lavage Fluid (BALF) of asthmatic offspring, and significantly exacerbated Th2 immune imbalance in asthmatic offspring, but had no effect on Th17 immune imbalance. CONCLUSION: Exposure to O3 during pregnancy aggravated asthma in offspring, in which the third trimester is the most sensitive window.


Assuntos
Asma , Animais , Asma/induzido quimicamente , Líquido da Lavagem Broncoalveolar , Modelos Animais de Doenças , Feminino , Pulmão , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos ICR , Ovalbumina , Gravidez
5.
Methods Mol Biol ; 2223: 101-114, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33226590

RESUMO

Mouse models of allergic asthma have been utilized to establish the role of T helper type 2 (Th2) cells in driving lung inflammation, airway hyperresponsiveness, and obstruction. Here, we present the allergic asthma models, in which mice are hypersensitized to ovalbumin (OVA) and house dust mite (HDM). These models mimic the major characteristics of human asthma including the eosinophilic inflammation and hyperactivity of the airway, overproduction of Th2 cytokines in the lung, and elevated total and allergen-specific immunoglobulin E (IgE) in serum.


Assuntos
Asma/imunologia , Células Dendríticas/efeitos dos fármacos , Modelos Animais de Doenças , Ovalbumina/administração & dosagem , Pyroglyphidae/imunologia , Hipersensibilidade Respiratória/imunologia , Células Th2/efeitos dos fármacos , Adjuvantes Imunológicos/administração & dosagem , Alérgenos/administração & dosagem , Hidróxido de Alumínio/administração & dosagem , Animais , Asma/induzido quimicamente , Asma/genética , Asma/patologia , Biomarcadores/metabolismo , Células Dendríticas/imunologia , Células Dendríticas/patologia , Eosinófilos/efeitos dos fármacos , Eosinófilos/imunologia , Eosinófilos/patologia , Citometria de Fluxo/métodos , Fatores de Transcrição Forkhead/genética , Fatores de Transcrição Forkhead/imunologia , Expressão Gênica , Imunoglobulina E/genética , Imunoglobulina E/imunologia , Interferon gama/genética , Interferon gama/imunologia , Interleucinas/genética , Interleucinas/imunologia , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Pulmão/patologia , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Macrófagos/patologia , Camundongos , Camundongos Endogâmicos C57BL , Pyroglyphidae/química , Testes de Função Respiratória , Hipersensibilidade Respiratória/induzido quimicamente , Hipersensibilidade Respiratória/genética , Hipersensibilidade Respiratória/patologia , Células Th2/imunologia , Células Th2/patologia
6.
Methods Mol Biol ; 2223: 217-236, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33226598

RESUMO

Cellular inflammation, with elevated levels of Th1/Th2 cytokines, airway mucus hypersecretion, and thickening of the airway smooth muscle, are characteristic features of the allergic lung. Assessment of pathophysiological changes in allergic lungs serves as an important tool to determine disease progression and understand the underlying mechanisms of pathogenesis. This can be achieved by evaluating the lung tissue for inflammation and airway structural changes along with the measurement of important pro-inflammatory mediators such as Th1/Th2 cytokines and eotaxins. This chapter describes procedures to histologically evaluate inflammatory and pathological changes observed during allergic airway inflammation using lung tissue from mice.


Assuntos
Alérgenos/administração & dosagem , Asma/imunologia , Pulmão/imunologia , Hipersensibilidade Respiratória/imunologia , Coloração e Rotulagem/métodos , Equilíbrio Th1-Th2 , Animais , Asma/induzido quimicamente , Asma/metabolismo , Asma/patologia , Líquido da Lavagem Broncoalveolar/citologia , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/biossíntese , Citocinas/imunologia , Progressão da Doença , Pulmão/metabolismo , Pulmão/patologia , Camundongos , Microtomia/métodos , Muco/imunologia , Miócitos de Músculo Liso/imunologia , Miócitos de Músculo Liso/patologia , Inclusão em Parafina/métodos , Hipersensibilidade Respiratória/induzido quimicamente , Hipersensibilidade Respiratória/metabolismo , Hipersensibilidade Respiratória/patologia , Células Th1/imunologia , Células Th1/patologia , Células Th2/imunologia , Células Th2/patologia
7.
Methods Mol Biol ; 2223: 237-266, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33226599

RESUMO

Eosinophils are rare white blood cells that are recruited from circulation to accumulate in the lung in mouse models of allergic respiratory inflammation. In hematoxylin-eosin (HE) stained lungs, eosinophils may be difficult to detect despite their bright eosin staining in the secondary granules. For this reason, antibody-mediated detection of eosinophils is preferable for specific and clearer identification of these cells. Moreover, eosinophils may degranulate, releasing their granule proteins into surrounding tissue, and remnants of cytolysed cells cannot be detected by HE staining. The methods here demonstrate the use of eosinophil-specific anti-mouse antibodies to detect eosinophil granule proteins in formalin-fixed cells both in situ in paraffin-embedded lungs, as well as in cytospin preparations from the lung. These antibody staining techniques enable either colorimetric or fluorescence imaging of eosinophils or their granule proteins with the potential for additional antibodies to be added for detection of multiple molecules.


Assuntos
Asma/imunologia , Eosinófilos/imunologia , Imuno-Histoquímica/métodos , Pulmão/imunologia , Hipersensibilidade Respiratória/imunologia , Coloração e Rotulagem/métodos , Alérgenos/administração & dosagem , Animais , Asma/induzido quimicamente , Asma/metabolismo , Asma/patologia , Biomarcadores/metabolismo , Proteína Básica Maior de Eosinófilos/imunologia , Proteína Básica Maior de Eosinófilos/metabolismo , Peroxidase de Eosinófilo/imunologia , Peroxidase de Eosinófilo/metabolismo , Eosinófilos/patologia , Formaldeído/química , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Microtomia/métodos , Inclusão em Parafina/métodos , Hipersensibilidade Respiratória/induzido quimicamente , Hipersensibilidade Respiratória/metabolismo , Hipersensibilidade Respiratória/patologia , Fixação de Tecidos/métodos
8.
Methods Mol Biol ; 2223: 281-293, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33226601

RESUMO

Allergic disease is on the rise and yet the underlying cause and risk factors are not fully understood. While lifesaving in many circumstances, the use of antibiotics and the subsequent disruption of the microbiome are positively correlated with the development of allergies. Here, we describe the use of the antibiotic vancomycin in combination with the papain-induced mouse model of allergic disease that allows for the assessment of microbiome perturbations and the impact on allergy development.


Assuntos
Antibacterianos/farmacologia , Asma/imunologia , Macrófagos Alveolares/efeitos dos fármacos , Microbiota/efeitos dos fármacos , Coloração e Rotulagem/métodos , Vancomicina/farmacologia , Animais , Animais Recém-Nascidos , Asma/induzido quimicamente , Asma/genética , Asma/microbiologia , Linfócitos B/efeitos dos fármacos , Linfócitos B/imunologia , Linfócitos B/patologia , Líquido da Lavagem Broncoalveolar/química , Líquido da Lavagem Broncoalveolar/imunologia , Líquido da Lavagem Broncoalveolar/microbiologia , Células Dendríticas/efeitos dos fármacos , Células Dendríticas/imunologia , Células Dendríticas/patologia , Modelos Animais de Doenças , Amarelo de Eosina-(YS)/química , Feminino , Hematoxilina/química , Humanos , Imunoglobulina E/genética , Imunoglobulina E/imunologia , Interleucina-13/genética , Interleucina-13/imunologia , Interleucina-4/genética , Interleucina-4/imunologia , Interleucina-5/genética , Interleucina-5/imunologia , Pulmão/patologia , Macrófagos Alveolares/imunologia , Macrófagos Alveolares/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Papaína/administração & dosagem , Linfócitos T/efeitos dos fármacos , Linfócitos T/imunologia , Linfócitos T/patologia
9.
Sci Total Environ ; 754: 142089, 2021 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-33254941

RESUMO

Nitrogen dioxide (NO2) is responsible for aggravating respiratory diseases, particularly asthma. The aim of this study is to investigate the association between NO2 exposure and asthma emergency department (ED) visits during the cold season (November-February) in five populated locations (Sacramento, San Francisco, Fresno, Los Angeles, and San Diego) of California from 2005 to 2015 (1320 Days). Conditional logistic regression models were used to obtain the odds ratio (OR) and 95% confidence interval (CI) associated with a 5 ppb increase in NO2 concentration for the 19,735 ED visits identified. An increase in NO2 exposure increased the odds of having asthma ED visits for the studied population. The potential effect modification by sex (female and male), race (White, Black, Hispanic, and Asian), and age (2-5, 6-18, 19-40, 41-64, and ≥65) was explored. A 5 ppb increase in the concentration of NO2 during lag 0-30 was associated with a 56% increase in the odds of having an asthma ED visit (OR = 1.560, CI: 1.428-1.703). Sex was not found to be a modifier. Asthma ED visits among all the races/ethnicities (except Asians) were associated with NO2 exposure. Whites had the highest OR 75% (OR = 1.750, CI: 1.417-2.160) at lag 0-30 in response to NO2 exposure. The association between NO2 exposure and asthma ED visits was positive among all age groups except for 19 to 40 years old; the OR was higher among 2 to 18 year old (at lag 0-30: age group 2-5 (OR = 1.699, CI: 1.399-2.062), and age group 6-18 (OR = 1.568, CI 1.348-1.825)). For stratification by location, San Diego and Fresno were found to have the highest OR, compared to the other studied locations.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adolescente , Adulto , Poluentes Atmosféricos/efeitos adversos , Asma/induzido quimicamente , Asma/epidemiologia , Criança , Pré-Escolar , Serviço Hospitalar de Emergência , Feminino , Humanos , Los Angeles , Masculino , Dióxido de Nitrogênio , São Francisco , Estações do Ano , Adulto Jovem
10.
Mol Immunol ; 131: 60-67, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33358566

RESUMO

BACKGROUND: Growing evidence shows that enhancer of zeste homolog 2 (EZH2) plays a role in various physiological functions and cancer pathogenesis. However, its contribution to allergic diseases remains controversial. We sought to investigate the role of EZH2 in the pathogenesis of allergic airway inflammation. METHODS: 3-Deazaneplanocin A (DZNep), an indirect inhibitor of EZH2, was administered via intraperitoneal injection in an ovalbumin (OVA)-induced murine model of allergic airway inflammation. The expression of EZH2 in the allergic airway tissues was examined by immunohistochemistry (IHC) and western blot. The inflammatory cell infiltration and the goblet cell hyperplasia in the murine nose and lung were detected by hematoxylin and eosin (H&E) staining and periodic acid-Schiff (PAS) staining. Levels of cytokines, including IL-4, IFN-γ, IL-6, and IL-10, were evaluated in the bronchoalveolar lavage fluid (BALF) using Enzyme-linked immune sorbent assay (ELISA). RESULTS: EZH2 expression was inhibited by DZNep treatment (P < 0.05). The administration of DZNep significantly inhibited the inflammatory cell infiltration (P < 0.0001) and goblet cell hyperplasia (P < 0.001). Moreover, it suppressed the secretion of IL-4 (P < 0.0001) and IL-6 (P < 0.01) in the BALF. CONCLUSIONS: Our findings demonstrate that DZNep attenuates allergic airway inflammation and could be a new therapeutic option for allergic rhinitis and asthma.


Assuntos
Adenosina/análogos & derivados , Anti-Inflamatórios/farmacologia , Hipersensibilidade/tratamento farmacológico , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Pulmão/efeitos dos fármacos , Ovalbumina/farmacologia , Adenosina/farmacologia , Animais , Asma/induzido quimicamente , Asma/tratamento farmacológico , Asma/metabolismo , Líquido da Lavagem Broncoalveolar , Citocinas/metabolismo , Modelos Animais de Doenças , Feminino , Hipersensibilidade/metabolismo , Inflamação/metabolismo , Pulmão/metabolismo , Camundongos , Camundongos Endogâmicos BALB C
11.
Life Sci ; 266: 118884, 2021 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-33310038

RESUMO

AIMS: Growing evidence indicates insufficient autophagy is crucial to airway remodeling in asthma. However, it is uncertain whether p62, an autophagy major regulator, mediates the airway remodeling process. This study aimed to evaluate the role and underlying mechanism of p62 in airway remodeling in asthma. MATERIALS AND METHODS: Airway remodeling was confirmed via histopathology. Western blotting and RT-PCR were used to detect the expression of autophagic and glycolytic proteins, as well as glycolytic genes. Glycolysis was measured by glucose consumption and lactate production. Cell proliferation was analyzed by CCK8 assays while and the scratch test and transwell method were used for cell migration. KEY FINDINGS: We found that insufficient autophagic flux and increased p62 expression existed in chronic asthma mice. Additionally, knockdown of p62 inhibited asthmatic human bronchial smooth muscle cells (BSMCs) proliferation and migration in vitro. To elucidate the underlying mechanism of p62-mediated autophagy flux in directing BSMCs function, we demonstrated that knockdown of p62 decreased the glucose consumption and lactate production in BSMCs, whereas p62 overexpression had the opposite effect. Furthermore, we showed that p62 regulated glycolysis in BSMCs by the mTOR/c-Myc/hexokinase 2 (HK2) pathway. SIGNIFICANCE: Our findings suggest that p62 is involved in BSMCs proliferation and migration via the mTOR/c-Myc/HK2-mediated glycolysis, thereby providing a new target for airway remodeling treatment.


Assuntos
Remodelação das Vias Aéreas , Asma/patologia , Autofagia , Reprogramação Celular , Modelos Animais de Doenças , Miócitos de Músculo Liso/patologia , Proteína Sequestossoma-1/metabolismo , Animais , Asma/induzido quimicamente , Asma/metabolismo , Movimento Celular , Proliferação de Células , Feminino , Glicólise , Hexoquinase/genética , Hexoquinase/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Miócitos de Músculo Liso/metabolismo , Ovalbumina/toxicidade , Proteínas Proto-Oncogênicas c-myc/genética , Proteínas Proto-Oncogênicas c-myc/metabolismo , Proteína Sequestossoma-1/genética , Serina-Treonina Quinases TOR/genética , Serina-Treonina Quinases TOR/metabolismo
12.
Parasitol Res ; 119(11): 3719-3728, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32955617

RESUMO

This study aimed to evaluate the effects of early-life exposure to different extracts of Angiostrongylus cantonensis (A. cantonensis) on airway inflammation in an allergic asthma model. The total soluble extract (TE) and the soluble extracts of the digestive (AcD), reproductive (AcR), and cuticle (AcC) systems of A. cantonensis were used for immunisation before ovalbumin (OVA)-sensitisation/challenge in an OVA-induced allergic asthma model. The initial hypothesis of the study was that some soluble extract of the systems (AcD, AcR, or AcC) could be more potent to the modulation of inflammation than the TE. Our data, however, shows that immunisation with the TE is more promising because it decreased the high influx of inflammatory cells on airways and promoted an increase of interferon-γ (IFN-ɣ) and interleukin-10 (IL-10) levels. Besides this, the immunisation with the TE also led to a reduction of goblet cells and mucus overproduction in the lung tissue of asthmatic mice. We believe that the extracts have a distinct capacity to modulate the immune system, due to the TE possessing a greater variability of molecules, which together leads to control of airway inflammation. In conclusion, this is the first study to reveal that the TE of A. cantonensis adult worms has a greater potential for developing a novel therapeutic for allergic asthma.


Assuntos
Angiostrongylus cantonensis/metabolismo , Asma/imunologia , Imunomodulação , Angiostrongylus cantonensis/anatomia & histologia , Animais , Asma/induzido quimicamente , Asma/prevenção & controle , Citocinas/metabolismo , Modelos Animais de Doenças , Feminino , Imunização , Inflamação , Pulmão/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Ovalbumina/efeitos adversos , Mucosa Respiratória/metabolismo
13.
Artigo em Inglês | MEDLINE | ID: mdl-32784540

RESUMO

Background: Associations of early antibiotics exposures with childhood asthma, allergies, and airway illnesses are debated. Objectives: We aimed to investigate associations of first-year antibiotics exposure with childhood asthma, allergies, and airway illnesses. Methods: A cross-sectional study was conducted among preschoolers in Shanghai, China during 2011-2012. A questionnaire regarding household environment and lifestyles and childhood health outcomes was reported by the child's parents. Results: In total, 13,335 questionnaires (response rate: 85.3%) were analyzed and 3049 (24.1%) children had first-year antibiotics exposure. In the multivariate logistic regression analyses, first-year antibiotics exposure had significant associations with the higher odds of lifetime-ever pneumonia (adjusted OR, 95% CI: 2.15, 1.95-2.37), croup (1.46, 1.24-1.73), wheeze (1.44, 1.30-1.60), asthma (1.38, 1.19-1.61), food allergy (1.29, 1.13-1.46), and allergic rhinitis (1.23, 1.07-1.41), and as well as current (one year before the survey) common cold (≥3 times) (1.38, 1.25-1.52), dry cough (1.27, 1.13-1.42), atopic dermatitis (1.25, 1.09-1.43), wheeze (1.23, 1.10-1.38), and rhinitis symptoms (1.15, 1.04-1.26). These associations were different in children with different individual characteristics (age, sex, family history of atopy, and district) and other early exposures (breastfeeding, home decoration, pet-keeping, and environmental tobacco smoke). Conclusions: Our results indicate that first-year antibiotics exposure could be a strong risk factor for childhood pneumonia, asthma, allergies, and their related symptoms. The individual characteristics and other early exposures may modify effects of early antibiotic exposure on childhood allergies and airway illnesses.


Assuntos
Antibacterianos/efeitos adversos , Asma/epidemiologia , Dermatite Atópica/epidemiologia , Antibacterianos/uso terapêutico , Asma/induzido quimicamente , Pré-Escolar , China/epidemiologia , Estudos Transversais , Eczema , Feminino , Hipersensibilidade Alimentar/epidemiologia , Humanos , Lactente , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Inquéritos e Questionários
14.
Environ Health ; 19(1): 92, 2020 08 27.
Artigo em Inglês | MEDLINE | ID: mdl-32854703

RESUMO

BACKGROUND: Health risks due to particulate matter (PM) from wildfires may differ from risk due to PM from other sources. In places frequently subjected to wildfire smoke, such as Reno, Nevada, it is critical to determine whether wildfire PM poses unique risks. Our goal was to quantify the difference in the association of adverse asthma events with PM on days when wildfire smoke was present versus days when wildfire smoke was not present. METHODS: We obtained counts of visits for asthma at emergency departments and urgent care centers from a large regional healthcare system in Reno for the years 2013-2018. We also obtained dates when wildfire smoke was present from the Washoe County Health District Air Quality Management Division. We then examined whether the presence of wildfire smoke modified the association of PM2.5, PM10-2.5, and PM10 with asthma visits using generalized additive models. We improved on previous studies by excluding wildfire-smoke days where the PM concentration exceeded the maximum PM concentration on other days, thus accounting for possible nonlinearity in the association between PM concentration and asthma visits. RESULTS: Air quality was affected by wildfire smoke on 188 days between 2013 and 2018. We found that the presence of wildfire smoke increased the association of a 5 µg/m3 increase in daily and three-day averages of PM2.5 with asthma visits by 6.1% (95% confidence interval (CI): 2.1-10.3%) and 6.8% (CI: 1.2-12.7%), respectively. Similarly, the presence of wildfire smoke increased the association of a 5 µg/m3 increase in daily and three-day averages of PM10 with asthma visits by 5.5% (CI: 2.5-8.6%) and 7.2% (CI: 2.6-12.0%), respectively. We did not observe any significant increases in association for PM10-2.5 or for seven-day averages of PM2.5 and PM10. CONCLUSIONS: Since we found significantly stronger associations of PM2.5 and PM10 with asthma visits when wildfire smoke was present, our results suggest that wildfire PM is more hazardous than non-wildfire PM for patients with asthma.


Assuntos
Asma/epidemiologia , Serviço Hospitalar de Emergência/estatística & dados numéricos , Exposição Ambiental/efeitos adversos , Hospitalização/estatística & dados numéricos , Material Particulado/efeitos adversos , Fumaça/efeitos adversos , Incêndios Florestais , Asma/induzido quimicamente , Cidades , Nevada/epidemiologia , Material Particulado/análise
16.
Adv Clin Exp Med ; 29(7): 825-832, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32725971

RESUMO

BACKGROUND: Epidemiological studies and mice models have demonstrated that air pollution containing particulate matter smaller than 2.5 µm (PM2.5) exacerbates acute episodes of asthma in both children and adults. OBJECTIVES: To investigate the effect of continuous PM2.5 treatment on asthma regulation mechanism behind this effect. MATERIAL AND METHODS: In this study, the effects of continuous exposure to PM2.5 on asthma and eosinophil recruitment was compared to the effect of a single pre-ovalbumin (OVA)-sensitization exposure to PM2.5. Wild-type mice were either challenged once with PM2.5 + OVA before sensitization and asthma induction over a 27-day period, or with 5 times of PM2.5 + OVA treatment and sensitization/asthma induction over the same period. RESULTS: Continuous exposure to PM2.5 significantly increased total plasma immunoglobulin E (IgE), bronchial alveolar lavage fluid (BALF) cell numbers, eosinophils, and macrophages, leading to increased lung injury. This effect was regulated through increased production of chemokines and cytokines, such as interleukin (IL)-1ß, monocyte chemoattractant protein 1 (MCP-1), IL-12, IL-5, IL-13, and prostaglandin D2 (PGD2). Eosinophil recruitment during continuous PM2.5 treatment was regulated through phosphorylation of the JAK/STAT6 pathway. As this study shows, continuous PM2.5 treatment significantly worsens asthma as compared to single exposure to PM2.5 or OVA exposure alone. CONCLUSIONS: Our findings reveal that continuous exposure of PM2.5 exacerbates OVA-induced asthma in mouse lung through JAK-STAT6 signaling pathway.


Assuntos
Asma , Animais , Asma/induzido quimicamente , Líquido da Lavagem Broncoalveolar , Modelos Animais de Doenças , Janus Quinases , Pulmão , Camundongos , Camundongos Endogâmicos BALB C , Ovalbumina , Material Particulado/toxicidade , Fator de Transcrição STAT6 , Transdução de Sinais
17.
Environ Sci Pollut Res Int ; 27(34): 43117-43124, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32729038

RESUMO

Epidemiological studies have suggested the effects of ambient fine particles (PM2.5) on asthma, but the effects of specific components of PM2.5 on asthma remain to be explored. Here, we studied the effect of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) on asthma acute exacerbation. The data on daily counts of emergency room visits (ERVs) were obtained from Wan Fang Medical Center, Taipei, Taiwan, from 2012 to 2015. The daily concentrations of PM2.5 and pollutant gases were obtained from a local air quality monitoring station. The levels of PM2.5-bound PAH were estimated by an established grid-scale model. Relative risks for ERVs as the increase in the level of ambient pollutants were calculated by using a generalized additive model of Poisson regression. In the present study, we observed statistically significant positive associations between PM2.5 and asthma ERVs for all age groups. PM2.5-bound PAH was also associated with asthma ERVs for all age groups. In the adult subgroup analysis, there was a significant association between PM2.5-bound PAH and asthma ERVs at lags 1 and 2 (RR 1.289, 95% CI 1.050-1.582 and RR 1.242, 95% CI 1.039-1.485). The impacts of air pollution on the risk of pediatric asthma ERV were found to be significant for PM2.5 at lag day 0 (RR 1.310, 95% CI 1.069-1.606). Moreover, pediatric asthma ERVs were significantly associated with the levels of PM2.5-bound PAH at lag 1 and 2 days (RR 1.576, 95% CI 1.371-1.810 and RR 1.426, 95% CI 1.265-1.607). The study provides evidence that PM2.5-bound PAHs were associated with an increased risk of asthma attacks. Our data further suggested that traffic exhaust is a primary source of PM2.5-bound PAHs.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Hidrocarbonetos Policíclicos Aromáticos , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Asma/induzido quimicamente , Asma/epidemiologia , Criança , Serviço Hospitalar de Emergência , Humanos , Material Particulado/análise , Estações do Ano , Taiwan/epidemiologia
18.
Ecotoxicol Environ Saf ; 199: 110740, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32446102

RESUMO

Dibutyl phthalate (DBP) is one of the most ubiquitous phthalate esters found in everyday products, and is receiving increased attention as an immunologic adjuvant. However, information regarding DBP-aggravated allergic asthma is still limited. This study used a mouse model sensitized with ovalbumin (OVA) to determine any adverse effects of DBP on allergic asthma. Our results reveal that allergic asthmatic mice exposed to DBP for an extended period had a significant increase in inflammatory cell infiltration; a significant increase in levels of serum immunoglobulin and T helper 2 cell (Th2) and T helper 17 cell (Th17) cytokines in lung tissue; and significant changes in lung histology and AHR, all of which are typical asthmatic symptoms. The levels of oxidative stress and levels of the neuropeptide, calcitonin gene related peptide (CGRP), were also elevated after DBP exposure. Interestingly, blocking oxidative stress by administering melatonin (MT) not only reduced oxidative stress and CGRP levels, but also ameliorated the asthmatic symptoms. Collectively, these results show that DBP exacerbates asthma-like pathologies by increasing the expression of CGRP mediated by oxidative stress.


Assuntos
Asma/induzido quimicamente , Peptídeo Relacionado com Gene de Calcitonina/metabolismo , Dibutilftalato/toxicidade , Poluentes Ambientais/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Animais , Asma/imunologia , Asma/metabolismo , Citocinas/metabolismo , Modelos Animais de Doenças , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Melatonina/farmacologia , Camundongos , Camundongos Endogâmicos BALB C , Ovalbumina/imunologia , Células Th17/efeitos dos fármacos , Células Th17/imunologia , Células Th2/efeitos dos fármacos , Células Th2/imunologia
19.
Rev Med Suisse ; 16(689): 694-697, 2020 Apr 08.
Artigo em Francês | MEDLINE | ID: mdl-32270937

RESUMO

NSAID-Exacerbated respiratory disease (also known as Samter's or Widal's triad, aspirin-exacerbated respiratory disease) is characte- rized by asthma, nasal polyposis and hypersensitivity to NSAIDs. The pathogenesis of this chronic inflammation arises from an imbalance in arachidonic acid metabolism, leading to an increase in pro- inflammatory cysteinyl-leukotrienes. The treatment is based on drug management of asthma and polyps and, in advanced situations, surgical management of polyposis. Monoclonal antibodies have shown promising results in the further medical treatment of this entity.


Assuntos
Anti-Inflamatórios não Esteroides/efeitos adversos , Asma , Hipersensibilidade a Drogas , Pólipos Nasais , Sinusite , Anti-Inflamatórios não Esteroides/imunologia , Aspirina/efeitos adversos , Aspirina/imunologia , Asma/induzido quimicamente , Humanos , Pólipos Nasais/induzido quimicamente , Sinusite/induzido quimicamente
20.
Environ Res ; 185: 109180, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32278153

RESUMO

BACKGROUND: Despite evidence that ambient air pollution may play a role in the development of asthma, little is known about the potential contribution of industrial emissions. OBJECTIVE: We used a population-based birth cohort to investigate the association between asthma onset in childhood and residential exposure to industrial emissions, estimated from atmospheric dispersion modeling. METHODS: The study population comprised all children born in the province of Quebec, Canada, 2002-2011. Asthma onset were ascertained from health administrative databases with validated algorithms. We used atmospheric dispersion modeling to develop time-varying annual mean concentration of ambient PM2.5, NO2 and SO2 at participants' residence from industries. For each pollutant, we assessed the association between industrial emissions exposure and childhood asthma onset using Cox proportional hazard model, adjusted for sex, material and social deprivation and calendar year. Sensitivity analysis included adjusting for long-term regional and traffic-related ambient PM2.5 and NO2, and assessing potential confounding by unmeasured secondhand smoke. RESULTS: The cohort included 722,667 children and 66,559 incident cases of asthma. For all pollutants, we found a non-linear association between childhood asthma onset and residential ambient air pollutant concentration from industries, with stronger effects at lower concentrations. A change from 25th to the 75th percentile in the mean annual ambient concentration of PM2.5 (0.13 µg/m3), NO2 (1.0 µg/m3) and SO2 (1.6 µg/m3) from industrial emissions was associated with a 19% (95% CI: 17-20%), 21% (95% CI: 19-23%) and 23% (95% CI: 21-24%) increase in the risk of asthma onset in children, respectively. For PM2.5 and NO2, associations were persisting after adjustments for long-term regional PM2.5 and traffic-related NO2 ambient concentration. CONCLUSION: Residential exposure to industrial emissions estimated from dispersion modeling was associated with asthma onset in childhood. Importantly, associations were stronger at lower concentrations and independent from those of other sources, thus adding up to the burden of regional and traffic-related air pollution.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Asma/induzido quimicamente , Asma/epidemiologia , Canadá , Criança , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Material Particulado/análise , Material Particulado/toxicidade , Quebeque/epidemiologia
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