Tobacco Smoke Modulates Ozone-Induced Toxicity In Rat Lungs And Central Nervous System

Adult Sprague-Dawley (SD) male rats were exposed for a single 3 h period to air, ozone (O-3) or O-3 followed by tobacco smoke (O-3/nTS). For pulmonary effects, bronchoalveolar lavage (BAL) cells and fluid were analyzed. Data revealed a significant increase in polymorphonuclear leukocytes (PMN), total protein and albumin concentrations in the O-3 group, reflecting inflammatory and toxic responses. A subsequent exposure to TS attenuated PMN infiltration into the airspaces and their recovery in the BAL. A similar reduction was observed for BAL protein and albumin in the O-3/nTS group, but it was not statistically significant. We also observed a significant increase in BAL total antioxidant capacity following O-3 exposure, suggesting development of protective mechanisms for oxidative stress damage from O-3. Exposure to TS attenuated the levels of total antioxidant capacity. Lung tissue protein analysis showed a significant reduction of extracellular superoxide dismutase (EC-SOD) in the O-3 or O-3/nTS group and catalase in the O-3/nTS group. TS further altered O-3-induced EC-SOD and catalase protein expression, but the reductions were not significant. For effects in the central nervous system (CNS), we measured striatal dopamine levels by HPLC with electrochemical detection. O-3 exposure produced a nonsignificant decrease in the striatal dopamine content. The effect was partially reversed in the O-3/nTS group. Overall, the results show that the toxicity of O-3 in the lung is modulated by TS exposure, and the attenuating trend, though nonsignificant in many cases, is contrary to the synergistic toxicity predicted for TS and O-3, suggesting limited cross-tolerance following such exposures.