Dataset Information

Airway microbiome is associated with respiratory functions and responses to ambient particulate matter exposure.

ABSTRACT: BACKGROUND:Ambient particulate matter (PM) exposure has been associated with respiratory function decline in epidemiological studies. We hypothesize that a possible underlying mechanism is the perturbation of airway microbiome by PM exposure. METHODS:During October 2016-October 2017, on two human cohorts (n?=?115 in total) in Shanghai China, we systematically collected three categories of data: (1) respiratory functions, (2) airway microbiome from sputum, and (3) PM2.5 (PM of ? 2.5?µm in diameter) level in ambient air. We investigated the impact of PM2.5 on airway microbiome as well as the link between airway microbiome and respiratory functions using linear mixed regression models. RESULTS:The respiratory function of our primary interest includes forced vital capacity (FVC) and forced expiratory volume in 1st second (FEV1). FEV1/FVC, an important respiratory function trait and key diagnosis criterion of COPD, was significantly associated with airway bacteria load (p?=?0.0038); and FEV1 was associated with airway microbiome profile (p?=?0.013). Further, airway microbiome was significantly influenced by PM2.5 exposure (p?=?4.48E-11). CONCLUSIONS:To our knowledge, for the first time, we demonstrated the impact of PM2.5 on airway microbiome, and reported the link between airway microbiome and respiratory functions. The results expand our understanding on the scope of PM2.5 exposure's influence on human respiratory system, and point to novel etiological mechanism of PM2.5 exposure induced diseases.

SUBMITTER: Wang L

PROVIDER: S-EPMC6257984 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Airway microbiome is associated with respiratory functions and responses to ambient particulate matter exposure.

Wang Liping L Cheng Haoxiang H Wang Dongbin D Zhao Bo B Zhang Jushan J Cheng Long L Yao Pengfei P Di Narzo Antonio A Shen Yuan Y Yu Jing J Li Yuanyuan Y Xu Shunqing S Chen Jia J Fan Lihong L Lu Jianwei J Jiang Jingkun J Zhou Yang Y Wang Changhui C Zhang Zhongyang Z Hao Ke K

Ecotoxicology and environmental safety 20181018

<h4>Background</h4>Ambient particulate matter (PM) exposure has been associated with respiratory function decline in epidemiological studies. We hypothesize that a possible underlying mechanism is the perturbation of airway microbiome by PM exposure.<h4>Methods</h4>During October 2016-October 2017, on two human cohorts (n = 115 in total) in Shanghai China, we systematically collected three categories of data: (1) respiratory functions, (2) airway microbiome from sputum, and (3) PM<sub>2.5</sub> ...[more]

PMID: 30342360

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Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression

Project description:It is generally accepted that exposure to particulate matter (PM) increases the risk of cardiovascular-related morbidity and mortality, though the exact mechanism behind this has yet to be elucidated. Oxidative stress plays a potentially important role in the mechanism of toxicity, with Nrf2 serving as a major antioxidant gene. In the current study, a Nrf2 knockout mouse model was used in combination with an individual ventilated cage (IVC)-based real-ambient PM exposure system to assess the potential cardiotoxicity induced by real-ambient PM exposure and the potential role of Nrf2 and related signaling in this endpoint. After 6- or 11-weeks exposure to PM, ICP-mass spectrometry was used to assess the metal depositions in the heart tissue following PM exposure. Functional and morphological changes in the hearts were investigated with echocardiography and histopathology, and oxidative stress levels were assessed with a serum malondialdehyde content assay. In the further mechanistic study, an RNA-seq technique was utilized to assess the gene transcription status in the hearts of C57/B6 mice exposed to PM with or without Nrf2 knockout. The expression levels of genes of interest were then further investigated with quantitative real-time PCR and western blotting. The results indicated that PM exposure resulted in significant elevation of sodium, potassium, selenium, and ferrum levels in mouse heart tissue. Meanwhile, significantly altered heart function and morphology were observed. Interestingly, Nrf2 knockout led to abolishment of PM-induced effects in several functional parameters but not the morphological changes. Meanwhile, elevated malondialdehyde content was observed in Nrf2 knockout animals. RNA-seq results revealed thousands of genes altered by PM exposure and/or Nrf2 knockout, and this affected several pathways, such as MAPK, phagosome, calcium signaling, and JAK-STAT. In subsequent molecular studies, enhanced nuclear translocation of Nrf2 was also observed following PM exposure, while the MAPK signaling pathway along with related JAK-STAT and TGF-?1 pathway genes, such as p38MAPK, AKT, TAK1, JAK1, STAT3, GRB2, TGFb1, and SMAD2, were confirmed to be affected by PM exposure and/or Nrf2 knockout. The data suggested that PM may induce cardiotoxicity in C57/B6 mice in which Nrf2 plays both protective and detrimental roles involving cardiac-related pathways, such as MAPK, JAK-STAT, and TGF-?1.

Project description:BackgroundExposure to fine particulate matter (PM2.5), an ambient air pollutant with mass-based standards promulgated under the Clean Air Act, and black carbon (BC), a common component of PM2.5, are both associated with cardiovascular health effects.ObjectivesTo elucidate whether BC is associated with distinct, or stronger, cardiovascular responses compared to PM2.5, we conducted a systematic review. We evaluated the associations of short- and long-term BC, or the related component elemental carbon (EC), with cardiovascular endpoints including heart rate variability, heart rhythm, blood pressure and vascular function, ST segment depression, repolarization abnormalities, atherosclerosis and heart function, in the context of what is already known about PM2.5.Data sourcesWe conducted a stepwise systematic literature search of the PubMed, Web of Science and TOXLINE databases and applied Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines for reporting our results.Study eligibility criteriaStudies reporting effect estimates for the association of quantitative measurements of ambient BC (or EC) and PM2.5, with relevant cardiovascular endpoints (i.e. meeting inclusion criteria) were included in the review. Included studies were evaluated for risk of bias in study design and results.Study appraisal and synthesis methodsRisk of bias evaluations assessed aspects of internal validity of study findings based on study design, conduct, and reporting to identify potential issues related to confounding or other biases. Study results are presented to facilitate comparison of the consistency of associations with PM2.5 and BC within and across studies.ResultsOur results demonstrate similar associations for BC (or EC) and PM2.5 with the cardiovascular endpoints examined. Across studies, associations for BC and PM2.5 varied in their magnitude and precision, and confidence intervals were generally overlapping within studies. Where differences in the magnitude of the association between BC or EC and PM2.5 within a study could be discerned, no consistent pattern across the studies examined was apparent.LimitationsWe were unable to assess the independence of the effect of BC, relative the effect of PM2.5, on the cardiovascular system, nor was information available to understand the impact of differential exposure misclassification.ConclusionsOverall, the evidence indicates that both BC (or EC) and PM2.5 are associated with cardiovascular effects but the available evidence is not sufficient to distinguish the effect of BC (or EC) from that of PM2.5 mass.

Project description:BACKGROUND: Studies have shown a relationship between air pollution and increased risk of cardiovascular morbidity and mortality. Due to the complexity of ambient air pollution composition, recent studies have examined the effects of co-exposure, particularly particulate matter (PM) and gas, to determine whether pollutant interactions alter (e.g. synergistically, antagonistically) the health response. This study examines the independent effects of fine (FCAPs) and ultrafine (UFCAPs) concentrated ambient particles on cardiac function, and determine the impact of ozone (O?) co-exposure on the response. We hypothesized that UFCAPs would cause greater decrement in mechanical function and electrical dysfunction than FCAPs, and that O? co-exposure would enhance the effects of both particle-types. METHODS: Conscious/unrestrained radiotelemetered mice were exposed once whole-body to either 190 ?g/m³ FCAPs or 140 ?g/m³ UFCAPs with/without 0.3 ppm O?; separate groups were exposed to either filtered air (FA) or O? alone. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure, and cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 hrs post-exposure. RESULTS: FCAPs alone caused a significant decrease in baseline left ventricular developed pressure (LVDP) and contractility, whereas UFCAPs did not; neither FCAPs nor UFCAPs alone caused any ECG changes. O? co-exposure with FCAPs caused a significant decrease in heart rate variability when compared to FA but also blocked the decrement in cardiac function. On the other hand, O? co-exposure with UFCAPs significantly increased QRS-interval, QTc and non-conducted P-wave arrhythmias, and decreased LVDP, rate of contractility and relaxation when compared to controls. CONCLUSIONS: These data suggest that particle size and gaseous interactions may play a role in cardiac function decrements one day after exposure. Although FCAPs?+?O? only altered autonomic balance, UFCAPs?+?O? appeared to be more serious by increasing cardiac arrhythmias and causing mechanical decrements. As such, O? appears to interact differently with FCAPs and UFCAPs, resulting in varied cardiac changes, which suggests that the cardiovascular effects of particle-gas co-exposures are not simply additive or even generalizable. Additionally, the mode of toxicity underlying this effect may be subtle given none of the exposures described here impaired post-ischemia recovery.

Project description:BackgroundFetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.MethodsA total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).ResultsThe full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, - 1.91), 5.57 (- 6.66, - 4.47), and 5.47 (- 6.39, - 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, - 13.49) grams by Hadlock's third formula and 13.56 (- 14.71, - 12.50) grams by Shepard's formula with each 10 μg/m3 increase in PM2.5 exposure.ConclusionsA negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Dataset Information

Airway microbiome is associated with respiratory functions and responses to ambient particulate matter exposure.

Publications

Airway microbiome is associated with respiratory functions and responses to ambient particulate matter exposure.

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