Effect of sulfur dioxide inhalation on cytokine levels in lungs and serum of mice.

In order to elucidate the immunotoxic mechanism exerted by sulfur dioxide (SO(2)), we investigated the effect of SO(2), a major air pollutant, on the cytokine levels in lungs and serum of male mice. Levels of interlukin-6(IL-6), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta1 (TGF-beta1) in lungs and serum from male mice exposed to SO(2) at various concentrations were measured by the enzyme-linked immunosorbent assay. Sixty Kunming albino male mice were divided randomly into six equal groups: three groups exposed to SO(2) (14.00 +/- 1.25, 28.00 +/- 1.98, and 56.00 +/- 3.11 mg/m(3), which are 5 +/- 0.45, 10 +/- 0.71, and 20 +/- 1.11 ppm) and their respective control groups. The results were as follows: (1) For lung tissues of male mice, exposure to SO(2) at 14 mg/m(3) (5 ppm) caused statistically significant increase of levels of IL-6 and TNF-alpha (p < .05) compared with the control group; exposure at 28 mg/m(3) (10 ppm) caused a statistically highly significant increase of level of IL-6 (p < .01) and a significant increase of TNF-alpha (p < .05); and exposure at 56 mg/m(3) (20 ppm) caused no any significant increase of levels of IL-6 and TNF-alpha. SO(2) at all concentrations tested could not cause significant change of level of TGF-beta1 in lungs. (2) For serum from male mice, after exposure to SO(2) at 14 mg/m(3) (5 ppm), the level of TNF-a was significantly increased (p < .05) compared with the control group, but the changes of levels of IL-6 and TGF-beta1 were not significant. After exposure to SO(2) at 28 mg/m(3) (10 ppm) and 56 mg/m(3) (20 ppm), levels of IL-6 and TNF-alpha were increased nonsignificantly, but the level of TGF-beta1 was decreased nonsignificantly. These results imply that inflammation reaction could be induced in lung tissue by SO(2) inhalation and the inflammation reaction might relate to these cytokines. And determination of cytokines in lung may be more valuable than in serum when lung injury caused by SO(2).