Inhalation Exposure

Publication Title: 
Environmental Research

OBJECTIVES: Particulate matter (PM) air pollution is associated with alterations in cardiac conductance and sudden cardiac death in epidemiological studies. Traffic-related air pollutants, including diesel exhaust (DE) may be at least partly responsible for these effects. In this experimental study we assessed whether short-term exposure to DE would result in alterations in heart rate variability (HRV), a non-invasive measure of autonomic control of the heart.

Author(s): 
Peretz, Alon
Kaufman, Joel D.
Trenga, Carol A.
Allen, Jason
Carlsten, Chris
Aulet, Mary R.
Adar, Sara D.
Sullivan, Jeffrey H.
Publication Title: 
American Journal of Physiology. Lung Cellular and Molecular Physiology

Viral infection is associated with approximately one-half of acute exacerbations of chronic obstructive pulmonary disease (COPD), which in turn, accelerate disease progression. In this study, we infected mice exposed to a combination of elastase and LPS, a constituent of cigarette smoke and a risk factor for development of COPD, with rhinovirus serotype 1B, and examined animals for viral persistence, airway resistance, lung volume, and cytokine responses.

Author(s): 
Sajjan, Umadevi
Ganesan, Shyamala
Comstock, Adam T.
Shim, Jee
Wang, Qiong
Nagarkar, Deepti R.
Zhao, Ying
Goldsmith, Adam M.
Sonstein, Joanne
Linn, Marisa J.
Curtis, Jeffrey L.
Hershenson, Marc B.
Publication Title: 
Inhalation Toxicology

BACKGROUND: Traffic-related air pollution is associated with cardiovascular morbidity and mortality. Although the biological mechanisms are not well understood, oxidative stress may be a primary pathway. Subpopulations, such as individuals with metabolic syndrome (MeS), may be at increased risk of adverse effects associated with air pollution. Our aim was to assess the relationship between exposure to diesel exhaust (DE) and indicators of systemic antioxidant and oxidative responses in adults with MeS.

Author(s): 
Allen, Jason
Trenga, Carol A.
Peretz, Alon
Sullivan, Jeffrey H.
Carlsten, Christopher C.
Kaufman, Joel D.
Publication Title: 
Occupational and Environmental Medicine

OBJECTIVE: To determine if the GSTM1 null genotype is a risk factor for increased inflammatory response to inhaled endotoxin. METHODS: 35 volunteers who had undergone inhalation challenge with a 20 000 endotoxin unit dose of Clinical Center Reference Endotoxin (CCRE) were genotyped for the GSTM1 null polymorphism. Parameters of airway and systemic inflammation observed before and after challenge were compared in GSTM1 null (n=17) and GSTM1 (n=18) sufficient volunteers.

Author(s): 
Dillon, Madeline A.
Harris, Bradford
Hernandez, Michelle L.
Zou, Baiming
Reed, William
Bromberg, Philip A.
Devlin, Robert B.
Diaz-Sanchez, David
Kleeberger, Steven
Zhou, Haibo
Lay, John C.
Alexis, Neil E.
Peden, David B.
Publication Title: 
Inhalation Toxicology

CONTEXT: Ozone exposure triggers airway inflammatory responses that may be influenced by biologically active purine metabolites. OBJECTIVE: To examine the relationships between airway purine metabolites and established inflammatory markers of ozone exposure, and to determine if these relationships are altered in individuals with atopy or asthma.

Author(s): 
Esther, Charles R.
Peden, David B.
Alexis, Neil E.
Hernandez, Michelle L.
Publication Title: 
Inhalation Toxicology

BACKGROUND: The evaluation of sputum leukocytes by flow cytometry (FCM) is an opportunity to assess characteristics of cells residing in the central airways, yet it is hampered by certain inherent properties of sputum including mucus and large amounts of contaminating cells and debris. OBJECTIVE: To develop a gating strategy based on specific antibody panels in combination with light scatter properties for flow cytometric evaluation of sputum cells. METHODS: Healthy and mild asthmatic volunteers underwent sputum induction.

Author(s): 
Lay, John C.
Peden, David B.
Alexis, Neil E.
Publication Title: 
Respiratory Research

BACKGROUND: Exposure to ozone activates innate immune function and causes neutrophilic (PMN) airway inflammation that in some individuals is robustly elevated. The interplay between immuno-inflammatory function and genomic signaling in those with heightened inflammatory responsiveness to ozone is not well understood. OBJECTIVES: Determine baseline predictors and post exposure discriminators for the immuno-inflammatory response to ozone in inflammatory responsive adult volunteers.

Author(s): 
Fry, Rebecca C.
Rager, Julia E.
Zhou, Haibo
Zou, Baiming
Brickey, June W.
Ting, Jenny
Lay, John C.
Peden, David B.
Alexis, Neil E.
Publication Title: 
Respiratory Research

BACKGROUND: Cigarette smoke (CS) is the major etiologic factor of chronic obstructive pulmonary disease (COPD). CS-exposed mice develop emphysema and mild pulmonary inflammation but no airway obstruction, which is also a prominent feature of COPD. Therefore, CS may interact with other factors, particularly respiratory infections, in the pathogenesis of airway remodeling in COPD. METHODS: C57BL/6 mice were exposed to CS for 2 h a day, 5 days a week for 8 weeks. Mice were also exposed to heat-killed non-typeable H. influenzae (HK-NTHi) on days 7 and 21.

Author(s): 
Ganesan, Shyamala
Comstock, Adam T.
Kinker, Brenton
Mancuso, Peter
Beck, James M.
Sajjan, Uma S.
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