The dynamicity of acute ozone-induced systemic leukocyte trafficking and adrenal-derived stress hormones.

Ozone exposure induces neuroendocrine stress response, which causes lymphopenia. It was hypothesized that ozone-induced increases in stress hormones will temporally follow changes in circulating granulocytes, monocytes- and lymphocyte subpopulations. The goal of this study was to chronicle the changes in circulating stress hormones, cytokines, and leukocyte trafficking during 4 h exposure to ozone.

Exacerbation of ozone-induced pulmonary and systemic effects by β-adrenergic and/or glucocorticoid receptor agonist/s.

Agonists of β adrenergic receptors (βAR) and glucocorticoid receptors (GR) are prescribed to treat pulmonary diseases. Since ozone effects are mediated through the activation of AR and GR, we hypothesized that the treatment of rats with relevant therapeutic doses of long acting βAR agonist (LABA; clenbuterol; CLEN) and/or GR agonist (dexamethasone; DEX) would exacerbate ozone-induced pulmonary and systemic changes. In the first study, male 12-week-old Wistar-Kyoto rats were injected intraperitoneally with vehicle (saline), CLEN (0.

Smoldering and flaming biomass wood smoke inhibit respiratory responses in mice.

Acute and chronic exposures to biomass wildfire smoke pose significant health risks to firefighters and impacted communities. Susceptible populations such as asthmatics may be particularly sensitive to wildfire effects. We examined pulmonary responses to biomass smoke generated from combustion of peat, oak, or eucalyptus in control and house dust mite (HDM)-allergic mice.

The role of fuel type and combustion phase on the toxicity of biomass smoke following inhalation exposure in mice.

The characteristics of wildland fire smoke exposures which initiate or exacerbate cardiopulmonary conditions are unclear. We previously reported that, on a mass basis, lung toxicity associated with particulate matter (PM) from flaming smoke aspirated into mouse lungs is greater than smoldering PM. In this study, we developed a computer-controlled inhalation system which can precisely control complex biomass smoke emissions from different combustion conditions.

Source-apportioned coarse particulate matter exacerbates allergic airway responses in mice.

Exposure to coarse particulate matter (PM) is associated with lung inflammation and exacerbation of respiratory symptoms in sensitive populations, but the degree to which specific emission sources contribute to these effects is unclear. We examined whether coarse PM samples enriched with diverse sources differentially exacerbate allergic airway responses. Coarse PM was collected weekly (7/2009-6/2010) from urban (G.

Beta-2 Adrenergic and Glucocorticoid Receptor Agonists Modulate Ozone-Induced Pulmonary Protein Leakage and Inflammation in Healthy and Adrenalectomized Rats.

We have shown that acute ozone inhalation activates sympathetic-adrenal-medullary and hypothalamus-pituitary-adrenal stress axes, and adrenalectomy (AD) inhibits ozone-induced lung injury and inflammation. Therefore, we hypothesized that stress hormone receptor agonists (β2 adrenergic-β2AR and glucocorticoid-GR) will restore the ozone injury phenotype in AD, while exacerbating effects in sham-surgery (SH) rats. Male Wistar Kyoto rats that underwent SH or AD were treated with vehicles (saline + corn oil) or β2AR agonist clenbuterol (CLEN, 0.

Inhalation of Simulated Smog Atmospheres Affects Cardiac Function in Mice.

The health effects of individual criteria air pollutants have been well investigated. However, little is known about the health effects of air pollutant mixtures that more realistically represent environmental exposures. The present study was designed to evaluate the cardiac effects of inhaled simulated smog atmospheres (SA) generated from the photochemistry of either gasoline and isoprene (SA-G) or isoprene (SA-Is) in mice.