Previous findings have revealed impairment of several host defense mechanisms in animals and humans resulting from ozone exposure. In this study we have examined the effect of in vitro ozone exposure on human peripheral blood natural killer (NK) cell activity measured against K562 tumor target cells. The data show that NK activity is inhibited in a time-dependent manner with marked suppression observed after 6 h of ozone exposure. Significant inhibition occurred at three different levels of ozone exposure (1.0, 0.5, and 0.78 ppm) and effector cell:target cell (E:T) ratios (50:1; 259 and 72.5:1) compared to air controls (p <.05). The capacity of ozone exposed NK cells to kill tumor cells decreased in a linear fashion as the level of ozone increased from 0.78 to 7.0 ppm (p -006 at 50:l;.004 at 25:1). The ozone effect was not merely due to a nonspecific toxicity; as NK activity recovered within 78 h following exposure either spontaneously or by stimulation with IL 2. Moreover, unexposed cells treated with supernatant from ozone exposed cells showed no decrease in NK activity. Exposure of enriched NK cells to ozone resulted in a decrease similar to that seen when non-adherent mononuclear cells were exposed, suggesting that NK cells are directly affected by ozone exposure. Since conjugate formation of the ozone exposed NK cells with K562 target cells was unchanged, we assume that the inhibitory effect of ozone was at a postbinding step in the lytic pathway.
ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis