Respiratory toxicology, lung histopathology and pathophysiology, optical and electron microscopic techniques.
Mechanisms of toxicity of particulate matter (PM) using transgenic mouse strains.
Inhaled PM is hypothesized to cause the release of inflammatory mediators from cells in the lung that become bloodborne and target the cardiovascular system, particularly the heart. In compromised individuals (age, diet, disease status), the cascade of mediators released from the lung may act on the cardiovascular system and cause acute morbidity and mortality. We use transgenic mouse strains with specific cardiovascular genetic alterations to study mechanisms of toxicity. Biological measurements include physiological monitoring of cardiovascular function, molecular biological assays to determine mRNA and peptide levels of inflammatory mediators, and histopathology. See Particular Matter Center
In vitro and in vivo toxicity of airborne pollutants and chemicals.
The effects of gaseous air pollutants (ozone, nitrogen dioxide, and sulfur dioxide) are studied in cultured human nasal epithelial cells and primate bronchial epithelial cells. The cell culture chamber also allows quantitative exposures of cell cultures to aerosols and complex airborne mixtures. Assays measure changes in levels of cytokines, interleukins and extracellular matrix molecules in response to air pollutant exposures.
Micro-circulation in the lung.
The histology and dynamics of blood flow in normal and compromised lungs are studied using morphometric analyses of fluorescent microsphere flow and computer-aided three-dimensional reconstruction. See Fluorescent Microsphere Resource Center: http://fmrc.pulmcc.washington.edu/