The magnificent Brooklyn Bridge, the 5,989-ft long suspension bridge linking Brooklyn and Manhattan, opened for business on May 24, 1883, after 13 years of construction. To lay the foundation, the workers must work in caissons under the East River, with compressed air pumped in from the surface. A lot of workers suffered from decompression diseases, i.e., the "bends" which also afflict deep-sea divers if the decompression rate was too fast. Air bubbles are trapped especially in the joints causing severe pains and injuries. However, no one seemed to have complained of blurred vision during that time. Perhaps in a harsh working environment, vision was not a first priority issue. In fact, the complaint of blurred vision should probably have been noted and registered.
A 2002 report in Japan indeed shows myopia in some workers after completing 11 weeks (4 days/week) of work in pneumatic caissons. When they were examined 6 months later, a recovery towards hyperopia was found. The speculation was that this transient myopia was caused by excessive oxygen which somehow altered the structure(s) of the eye. In fact, the same myopia shift has been found in patients undergoing hyperbaric oxygen therapy.
(The inside of a hyperbaric chamber - from hyperchamber.com)
Hyperbaric oxygen therapy has a long history. It started as a treatment for the bends and logically for carbon monoxide poisoning. Now it is used to promote wound-healing and inhibit recalcitrant anaerobic bacterial infection (for example, in gangrenes). In another 2002 publication in Acta Ophthalmologica Scandinavica, with a regimen of 95-min sessions at > 95% oxygen at 2.5 atmospheres given daily Monday to Friday for a total of 30 sessions, the patients exhibited a 0.58D of myopia shift. There was no change in the axial length; although a "minimal" yet significant change in keratometric readings was noted. The investigators suspected alterations in lenticular refractive index and/or curvatures.
And in a 2006 case report from Norway: A 58-year-old man showed a hypermetropic shift, which followed the myopic shift after each of two series of treatments. The maximal refractive amplitude was 3.00 D (range -1.37 D to +1.62 D) in the right eye and 2.75 D (range -1.25 D to + 1.50 D) in the left eye. And refraction stabilized after 1.5 years to pretreatment values.
So what's going on? Given the paucity of experimental data, a reasonable speculation is a change principally in the refractive index of the lens nucleus.The best approach is probably photo-documentation with a Scheimpflug camera supplemented with ultrasound A-scan, corneal topography, and cycloplegic refraction. Scheimpflug images allow lens density as well as anterior lens thickness determination:
Some investigators have proposed that the high oxygen might have caused protein aggregation in the lens nucleus, as part of the oxidative damage, hence the increase in the refractive index. However, by and large, changes in lens protein structure are irreversible. This does not agree with the transient nature of the myopia. Alternatively, it may just be a simple increase in lens thickness owing to an increasing intake of sodium and/or loss of potassium, i.e., an ionic pump malfunction from oxygen toxicity.
All guesses. Someone out there should pick up this project.