We have shown that tobacco smoke causes an increase in airways resistance and a drop in expiratory flow at 50% of the vital capacity (FEF50). To better define the nature and site of this bronchoconstrictive effect we measured maximal expiratory flow while breathing air and a low-density gas mixture (helium-oxygen), in 12 healthy volunteers, before and after smoking a cigarette. There was a significant drop in FEF50 while breathing air (FEF50Air) (5.52 ± 1.83–5.05 ± 1.86 liters/s; p < 0.001).No changes were observed in the helium-oxygen FEF50 (FEF50He) after smoking. The increase in FEF50 after breathing the low-density gas as a percentage of FEF50Air (ΔVmax50) increased from 47.1 ± 11.4% before smoking to 57.0 ± 13.3% after smoking (p < 0.05). There were no changes in forced vital capacity (FVC), flow at 75% FVC and volume of isoflow. We discuss these observations in light of the equal pressure point (EPP) analysis and wave speed theory of flow limitation. We conclude that after smoking flow becomes more density dependent because there is constriction of a flow-limiting segment downstream from the EPP, located in lobar and segmental bronchi. No acute effect of tobacco smoke on the small airways could be demons