The direct decompression limits for a group of divers over a range of pressure-time air exposures was determined using ultrasonic detection of venous gas emboli (VGE). In addition to dry chamber exposures, ranging from 233 ft for 7 min to 25 ft for 720 min, we exposed six divers to open ocean dives at 165 ft for 10 min. Findings demonstrated a strong individual propensity to form VGE, correlating with susceptibility to bends. No bends developed without the prior detection of precordial VGE. The present concept of no problems after any period of time at 30 fsw was not confirmed. Isopleths of equal percentage occurrence of VGE were computed between 10 and 60%. Open ocean exposures increased the percentage of VGE and bends, when compared to dry chamber exposures. Limiting tissue half times computed from the 20% VGE isopleth suggested that saturation exposures are controlled by a greater sensitivity of the short-half-time tissues than previously appreciated, rather than by additionally extended half times.