Nancy Beth Beck

Project title: The Effects of Ozone on Intercellular Adhesion Molecule 1 Expression in Human Nasal Epithelial Cells

Degree: MS (Thesis) | Program: Environmental Toxicology (Tox) | Project type: Thesis/Dissertation
Completed in: 1992 | Faculty advisor: Daniel L. Luchtel


Oxone is a highly toxic and ubiquitous air pollutant; nevertheless, the mechanisms responsible for its toxicity are not entirely understood. Ozone exposure induces epithelial cell injury and inflammation in the upper and lower airways. Previous in vitro work has shown that ozone enhances the production of various prostaglandins and leukotrienes by respiratory epithelial cells.

This study examined the effects of sublethal, near ambient, ozone concentrations on the expression of intercellular adhesion molecule 1 (ICAM-1) on human nasal epithelial ccells. ICAM-1 is a 95kd transmembrane, inducible glycoprotein that plays a key role in the regulation of leukocyte adherence to endothelial and epithelial cells.

We have devised a system whereby human nasal epithelial cells are cultured and exposed to ozone in an environment which simulates that of the human airway. Cells are grown on microporous filters which eliminates the need for media on the apical side of the cells and thus allows direct contact between the cells and the exposure atmosphere. Cells are studied in an adherent state with a laser cytometer. Dual wavelength detection using a fluorescein-conjugated antibody, to detect receptor expression, in conjunction with propidium iodide, to visualize cell nuxlei, allowed measurement of ICAM-1 expression on individual cells, expressed as fluorescence per cell.

Using these methods, we found that exposure of nasal cells to 500 unites/ml interferon-gamma for 16 hours increased ICAM-1 expression by 179 + 52 percent. Expression to 0.5 ppm ozone for 6 hours increased ICAM-1 expression by 36 + 11 percent (P < .04). These results suggest that the airway inflammation and hyperresponsiveness that re consequences of ozone exposure may result at least partially from increased ICAM-1 expression and subsequent leukocyte-epithelial interactions.