Aim: Ozone is a main component of secondary pollutants of vehicle exhausts, and ozone exposure to children in urban areas may be associated with the development of asthma. However, little is known about the mechanism(s) by which ozone affects human airway epithelium and subsequent airway inflammation.
Methods: Human bronchial epithelial cells were exposed to ozone at 0.16 mg/m(3) for varying periods. The concentrations of IL-1 and IL-6 secreted by the cells were measured by enzyme-linked immunosorbent assay (ELISA) and the contents of intracellular malondialdehyde (MDA) were determined. Furthermore, the conditional medium from the ozone-exposed cells was examined for stimulating human peripheral T lymphocytes from asthmatic patients and healthy subjects, and the production of cytokines was characterized by ELISA and quantitative real-time polymerase chain reaction (RT-PCR).
Results: Ozone stimulated the IL-1 and IL-6 production by BEAS-2B cells and its stimulatory effects were time dependent. Furthermore, ozone exposure significantly increased the levels of MDA in BEAS-2B cells, as compared with that of the cells without ozone exposure, in a time-dependent manner. In addition, the conditional medium from the cells exposed to ozone, but not control condition medium, significantly increased the relative levels of IL-1 mRNA transcripts in human peripheral T lymphocytes from asthmatic patients, but not healthy subjects. However, the conditional medium did not induce significantly increased levels of IL-2 production by peripheral T cells.
Conclusions: Our data indicated that exposure to low levels of ozone for a short period induced increases in the pro-inflammatory markers and oxidative stress in epithelial cells, which might contribute to airway inflammation particularly in asthmatic children.