Epithelial and inflammatory responses in the airways of laboratory rats coexposed to ozone and biogenic substances: enhancement of toxicant-induced airway injury.

People are often concurrently exposed to more than one air pollutant whether they are in outdoor or indoor environments. Therefore, inhalation studies that are designed to examine the toxicity of coexposures to two or more airborne toxicants may be more relevant for assessing human health risks than those studies that investigate the toxic effects of only one airborne toxicant at a time. Furthermore, airborne biogenic substances such as pollens, bacteria, fungi, and microbial toxins often coexist with common air pollutants in the ambient air, and when inhaled may also cause specific adverse effects on the respiratory tract. One such biogenic substance, bacterial endotoxin, is a potent stimulus of airway inflammation and is commonly found in domestic, agricultural, and industrial settings. Little is known about the interaction of exposures to biogenic substances and common air pollutants, such as ozone or airborne particulate matter. In the last few years, we have performed a series of in vivo studies using laboratory rodents that examined how airway surface epithelial cells are altered by coexposure to ozone and a biogenic substance, either bacterial endotoxin or a commonly used experimental aeroallergen (ovalbumin). Results from these studies indicate that the ozone-induced epithelial and inflammatory responses in laboratory rodents may be markedly enhanced by coexposure to an inhaled biogenic substance. Conversely, the adverse airway alterations caused by exposure to biogenic substances may be enhanced by coexposure to ozone. The results from these initial studies have also suggested some of the cellular and molecular mechanisms underlying the phenotypic epithelial alterations induced by these coexposures. Many more studies are needed to fully elucidate the potential risk to human health from coexposure to air pollutants and airborne biogenic substances.