Dataset Information

Development of a novel aerosol generation system for conducting inhalation exposures to ambient particulate matter (PM).

ABSTRACT: In this study, we developed a novel method for generating aerosols that are representative of real-world ambient particulate matter (PM) in terms of both physical and chemical characteristics, with the ultimate objective of using them for inhalation exposure studies. The protocol included collection of ambient PM on filters using a high-volume sampler, which were then extracted with ultrapure Milli-Q water using vortexing and sonication. As an alternative approach for collection, ambient particles were directly captured into aqueous slurry samples using the versatile aerosol concentration enrichment system (VACES)/aerosol-into-liquid collector tandem technology. The aqueous samples from both collection protocols were then re-aerosolized using commercially available nebulizers. The physical characteristics (i.e., particle size distribution) of the generated aerosols were examined by the means of a scanning mobility particle sizer (SMPS) connected to a condensation particle counter (CPC) at different compressed air pressures of the nebulizer, and dilution air flow rates. In addition, the collected PM samples (both ambient and re-aerosolized) were chemically analyzed for water-soluble organic carbon (WSOC), elemental and organic carbon (EC/OC), inorganic ions, polycyclic aromatic hydrocarbons (PAHs), and metals and trace elements. Using the aqueous filter extracts, we were able to effectively recover the water-soluble components of ambient PM (e.g., water-soluble organic matter, and water-soluble inorganic ions); however, this method was deficient in recovering some of the important insoluble components such as EC, PAHs, and many of the redox-active trace elements and metals. In contrast, using the VACES/aerosol-into-liquid collector tandem technology for collecting ambient PM directly into water slurry, we were able to preserve the water-soluble and water-insoluble components very effectively. These results illustrate the superiority of the VACES/aerosol-into liquid collector tandem technology to be used in conjunction with the re-aerosolization setup to create aerosols that fully represent ambient PM, making it an attractive choice for application in inhalation exposure studies.

SUBMITTER: Taghvaee S

PROVIDER: S-EPMC6430148 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Development of a novel aerosol generation system for conducting inhalation exposures to ambient particulate matter (PM).

Taghvaee Sina S Mousavi Amirhosein A Sowlat Mohammad H MH Sioutas Constantinos C

The Science of the total environment 20190214

In this study, we developed a novel method for generating aerosols that are representative of real-world ambient particulate matter (PM) in terms of both physical and chemical characteristics, with the ultimate objective of using them for inhalation exposure studies. The protocol included collection of ambient PM on filters using a high-volume sampler, which were then extracted with ultrapure Milli-Q water using vortexing and sonication. As an alternative approach for collection, ambient particl ...[more]

PMID: 30893735

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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:BackgroundEpidemiological studies report fairly consistent associations between various air pollution metrics and autism spectrum disorder (ASD), with some elevated risks reported for different prenatal and postnatal periods.ObjectivesTo examine associations between ASD and ambient fine particulate matter (PM2.5) and ozone concentrations during the prenatal period through the second year of life in a case-control study.MethodsASD cases (n = 428) diagnosed at Cincinnati Children's Hospital Medical Center were frequency matched (15:1) to 6420 controls from Ohio birth records. We assigned daily PM2.5 and ozone estimates for 2005-2012 from US EPA's Fused Air Quality Surface Using Downscaling model to each participant for each day based on the mother's census tract of residence at birth. We calculated adjusted odds ratios (aORs) using logistic regression across continuous and categorical exposure window averages (trimesters, first and second postnatal years, and cumulative measure), adjusting for maternal- and birth-related confounders, both air pollutants, and multiple temporal exposure windows.ResultsWe detected elevated aORs for PM2.5 during the 2nd trimester, 1st year of life, and a cumulative period from pregnancy through the 2nd year (aOR ranges across categories: 1.41-1.44, 1.54-1.84, and 1.41-1.52 respectively), and for ozone in the 2nd year of life (aOR range across categories: 1.29-1.42). Per each change in IQR, we observed elevated aORs for ozone in the 3rd trimester, 1st and 2nd years of life, and the cumulative period (aOR range: 1.19-1.27) and for PM2.5 in the 2nd trimester, 1st year of life, and the cumulative period (aOR range: 1.11-1.17).DiscussionWe saw limited evidence of linear exposure-response relationships for ASD with increasing air pollution, but the elevated aORs detected for PM2.5 in upper exposure categories and per IQR unit increases were similar in magnitude to those reported in previous studies, especially for postnatal exposures.

Project description:BackgroundAmbient fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5)] is a major health risk for children, particularly in South Asia, which currently experiences the highest PM2.5 levels globally. Nevertheless, there is comparatively little epidemiological evidence from this region to quantify the effects of PM2.5 on child survival.ObjectivesWe estimated the association between PM2.5 exposure and child survival in India.MethodsWe constructed a large, retrospective, and nationally representative cohort of children <5 years of age, born between 2009-2016, from the publicly available, cross-sectional 2015-2016 Demographic Health Surveys in India. In utero and post-delivery lifetime average ambient PM2.5 exposures were estimated with data from satellite remote sensing, meteorology, and land use information (model R2= 0.82). We used Cox proportional hazards regression to estimate the association between both average in utero and post-delivery lifetime PM2.5 and all-cause child mortality, controlling for individual- and household-level covariates, seasonality, location, and meteorology.ResultsOver 7,447,724 child-months of follow-up, there were 11,559 deaths at <5 years of age reported by the children's mothers. The mean concentrations of 9-month in utero and post-delivery lifetime average ambient PM2.5 exposure were 71.1 μg/m3 (range: 20.9-153.5 μg/m3) and 73.7 μg/m3 (range: 14.0-247.3 μg/m3), respectively. Estimated child mortality adjusted hazard ratios were 1.023 [95% confidence interval (CI): 1.008, 1.038] and 1.013 (95% CI: 1.001, 1.026) per 10-μg/m3 increase of in utero and post-delivery lifetime PM2.5, with both exposures in the model.DiscussionThis study adds to the growing body of evidence about the adverse health effects of PM2.5 by demonstrating the association between exposure, both in utero and post-delivery, on child survival at the national level in India. Strategies to reduce ambient air pollution levels, including steps to minimize in utero and early life exposures, are urgently needed in India and other countries where exposures are above recommended guideline values. https://doi.org/10.1289/EHP8910.

Project description:Short-and long-term exposure to particulate matter (PM) has been associated with cardiovascular disease (CVD). It is well recognized that oxidative stress is a potential major mechanism in PM-induced vascular injuries, in which the nuclear factor E2-related factor 2 (Nrf2) signaling pathway plays a critical role. 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 vascular injury and the potential role of Nrf2 in the angiotensin II (Ang II)-associated vascular injury. After 6-or 11-week exposure to PM, the histopathology assay revealed that PM exposure resulted in the thickening of the walls of vascular. After 6 weeks exposure to PM, the ELISA assay revealed that PM exposure resulted in the elevated plasma concentration of Ang II. The expression levels of genes of interest were then further investigated with quantitative real-time PCR. Notably, the results showed that Angiotensinogen (AGT), Angiotensin converting enzyme (ACE) and Angiotensin type I receptor (AT1R) were involved in PM-induced pathological changes. Western blotting for ACE showed similar results. Moreover, the extent of vascular thickening and the Ang II elevation was most prominent in the Nrf2 gene knockout PM exposure group (KOE). Furthermore, the expression of Nrf2 downstream relevant genes (HO1, Nqo1, Gclc, Gsta4) were significantly enhanced in the wildtype PM exposure group (WTE), while those were remarkably suppressed in the Nrf2 gene knockout groups. The ELISA result of monocyte chemoattractant protein-1 (MCP-1) serum levels in the KOE group was significantly higher in relation to that in the Nrf2 knockout control group (KOC). In summary, PM exposure is associated with thickening of vascular wall, while Nrf2 knockout may further enhance this effect. A potential mechanistic contributor of such effects is the activation of ACE/ANGII/AT1R axis, in which Nrf2 played a regulatory role.

Dataset Information

Development of a novel aerosol generation system for conducting inhalation exposures to ambient particulate matter (PM).

Publications

Development of a novel aerosol generation system for conducting inhalation exposures to ambient particulate matter (PM).

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