Hello divebostonforcharity:
The dive at such a shallow depth has only been performed in underwater habitats. This depth is considered safe from DCS. The listing of No Time Limit applies to both scuba and surface supplied diving. With scuba gear, a dive for hours would not be possible unless air battles were sent down. With surface supplied [hardhat or hooka] diving, a diver would come up after hours for reasons of fatigue and to get something to eat and drink. Another diver would replace him on that site.
The references below indicate that Doppler bubbles have been found in shallow/long situations. DCS is not a real concern.
Dr Deco :doctor:
References
Eckenhoff RG, Osborne SF, Parker JW, Bondi KR. Direct ascent from shallow air saturation exposures.Undersea Biomed Res. 1986 Sep;13(3):305-16.
Thirty-four healthy human subjects were exposed to shallow air saturation for 48 hours 25.5 fsw, n = 19, or 29.5 fsw, n = 15 and then decompressed to 1 ATA (0 fsw) in about 2 min. Symptoms included fatigue, limb and joint pain, headache, myalgias, and pruritus. No subject of 19 was diagnosed as having decompression sickness (DCS) after the shallower exposure, but 4 of 15 were diagnosed and treated for DCS subsequent to the deeper exposure. Almost all subjects in both groups had Doppler-detectable venous gas emboli (VGE) lasting up to 12 hours post decompression. Treated subjects had a recurrence of VGE several hours after the hyperbaric oxygen treatment. Only the duration of VGE, and not the VGE score, correlated with symptoms; and only the subjects body weight and age correlated with the VGE variables. This study indicates that hyperbaric air exposures of this magnitude are not as benign as previously thought.
Eckenhoff RG, Olstad CS, Carrod G.Human dose-response relationship for decompression and endogenous bubble formation. J Appl Physiol. 1990 Sep;69(3):914-8.
The dose-response relationship for decompression magnitude and venous gas emboli (VGE) formation in humans was examined. Pressure exposures of
12, 16, and 20.5 ft of seawater gauge pressure were conducted in an
underwater habitat for 48 h. The 111 human male volunteer subjects then ascended directly to the surface in less than 5 min and were monitored for VGE with a continuous-wave Doppler ultrasound device over the precordium or the subclavian veins at regular intervals for a 24-h period. No signs or symptoms consistent with decompression sickness occurred. However, a large incidence of VGE detection was noted. These data were combined with those from our previously reported experiments at higher pressures, and the data were fit to a Hill dose-response equation with nonlinear least-squares or maximum likelihood routines. Highly significant fits of precordial VGE incidences were obtained with the Hill equation (saturation depth pressure at which there is a 50% probability of
detectable VGE [D(VGE)50] = 150 +/- 1.2 kPa). Subclavian monitoring increased the sensitivity of VGE detection and resulted in a leftward shift [D(VGE)50 = 135 +/- 2 kPa] of the best-fit curve. We conclude that the reduction in pressure
necessary to produce bubbles in humans is much less than was previously thought; 50% of humans can be expected to generate endogenous bubbles after decompression from a steady-state pressure exposure of only 135 kPa (11 ft of seawater). This may have significant implications for decompression schedule formulation and for altitude exposures that are currently considered benign. These results also imply that endogenous bubbles arise from preexisting gas collections.
