Dataset Information

Ambient Particulate Matter Size Distributions Drive Regional and Global Variability in Particle Deposition in the Respiratory Tract.

ABSTRACT: Human exposure to airborne particulate matter (PM) increases the risk of negative health outcomes; however, substantial uncertainty remains in quantifying these exposure-response relationships. In particular, relating increased risk of mortality to exposure to PM with diameters smaller than 2.5 ?m (PM2.5) neglects variability in the underlying size distribution of PM2.5 exposure and size-resolved deposition in human airways. In this study, we combine a size-resolved respiratory particle-deposition model with a global size-resolved aerosol model to estimate the variability in particle deposition along the respiratory tract due to variability in ambient PM size distributions. We find that the ratio of deposited PM mass in the tracheobronchial and alveolar regions per unit ambient PM2.5 exposure (deposition ratio and DRTB + AV) varies by 20-30% between populated regions due to variability in ambient PM size distributions. Furthermore, DRTB + AV can vary by as high as a factor of 4 between the fossil-fuel-dominated region of the Eastern United States and the desert-dust-dominated region of North Africa. When considering individual PM species, such as sulfate or organic matter, we still find variability in the DRTB + AV on the order of 30% due to regional variability in the size distribution. Finally, the spatial distribution of DRTB + AV based on number or surface area is substantially different than the DRTB + AV based on mass. These results suggest that regional variability in ambient aerosol size distributions drive variability in PM deposition in the body, which may lead to variability in the health response from exposure to PM2.5.

SUBMITTER: Kodros JK

PROVIDER: S-EPMC7007101 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Ambient Particulate Matter Size Distributions Drive Regional and Global Variability in Particle Deposition in the Respiratory Tract.

Kodros J K JK Volckens J J Jathar S H SH Pierce J R JR

GeoHealth 20181017 10

Human exposure to airborne particulate matter (PM) increases the risk of negative health outcomes; however, substantial uncertainty remains in quantifying these exposure-response relationships. In particular, relating increased risk of mortality to exposure to PM with diameters smaller than 2.5 μm (PM<sub>2.5</sub>) neglects variability in the underlying size distribution of PM<sub>2.5</sub> exposure and size-resolved deposition in human airways. In this study, we combine a size-resolved respira ...[more]

PMID: 32159003

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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: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 Âµm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) âinduced 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 naÃ¯ve 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. Experiment Overall Design: animals were treated by PBS, Oval albumin, PM, or both OVA/PM

Dataset Information

Ambient Particulate Matter Size Distributions Drive Regional and Global Variability in Particle Deposition in the Respiratory Tract.

Publications

Ambient Particulate Matter Size Distributions Drive Regional and Global Variability in Particle Deposition in the Respiratory Tract.

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