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Persistent small-airways dysfunction after exposure to hyperoxia

E Thorsen1, B K Kambestad

  • 1Norwegian Underwater Technology Centre, Ytre Laksevåg, Norway.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 1, 1995
PubMed
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Hyperoxia exposure during saturation diving significantly impairs pulmonary function, specifically maximal expiratory flow rates. These reductions persist long-term, indicating hyperoxia contributes to airway obstruction in divers.

Area of Science:

  • Marine Biology
  • Physiology
  • Environmental Health

Background:

  • Saturation diving involves prolonged exposure to elevated environmental pressures.
  • Hyperoxia, elevated partial pressure of oxygen, is a potential risk factor during diving.
  • Pulmonary function impairment has been observed in divers, but the specific role of hyperoxia requires further investigation.

Purpose of the Study:

  • To evaluate the contribution of hyperoxia to reduced pulmonary function following saturation diving.
  • To assess long-term pulmonary function changes after controlled hyperoxic exposure during a simulated dive.

Main Methods:

  • A shallow saturation dive (0.25 MPa) simulated hyperoxic exposure from a deep dive (3.7 MPa).
  • Divers experienced controlled partial pressures of oxygen (PO2) over 28 days, including periods of 75 kPa and 50 kPa.

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  • Pulmonary function tests, including TLCO and lung volumes/flows, were conducted pre-dive and at multiple follow-up points up to 3 years post-dive.

    • Main Results:

    • Immediate post-dive showed reduced transfer factor for carbon monoxide (TLCO) and maximal expiratory flow rates.
    • Maximal expiratory flow rates remained significantly reduced at 1 and 3 years post-dive.
    • Forced midexpiratory flow rate showed persistent reductions of 8.7-9.3%, while forced expired volume in 1s and forced vital capacity recovered.

    Conclusions:

    • Hyperoxia exposure during saturation diving contributes to the development of airway obstruction in divers.
    • Persistent reductions in expiratory flow rates suggest long-term pulmonary damage.
    • Complete recovery of TLCO indicates specific mechanisms for different pulmonary function parameters.