Hi Adam,
CNS ox-tox is a random occurrence whose time-to-event becomes briefer as ppO2 elevates. There is solid evidence to support your contention of inter-individual (as well as intra-individual) variability in response to a given ppO2 across time & situation. This obviously complicates matters immensely.
The exact threshold for CNS ox-tox is no doubt multifactorial and very likely includes temperature, activity level & stress exposure, but we simply have not as yet quantified all possible contributors in the individual case, and perhaps never will. For >2 decades, the Naval Safety/Special Warfare Center conducted a test of individual sensitivity to HBO2 for combat swimmer ops, but dropped it in '97 because it really wasn't doing a good job of predicting individual candidate thresholds.
I am not aware of any published research that pointedly & specifically addresses your inquiry, but there are plenty of research findings that offer general support for the quite conservative proposed ppO2s of 1.4 for rec & 1.6 for tech, and for the extremely tiny likelihood of sustaining CNS ox-tox during recreational diving where ppO2 is kept at or below 1.4.
E.g.:
- Undersea Hyperb Med. 2004 Summer; 31(2):199-202.
Incidence of oxygen toxicity during the treatment of dysbarism.
Smerz RW.
SourceHyperbaric Treatment Center, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii, USA.
Abstract
Oxygen (O2) toxicity may result from exposure to partial pressures of O2 above 0.6ATA. Potential toxic exposure for divers occurs during the treatment of dysbarism. In the recompression chamber, PO2 may range from 0.9ATA to 3.3ATA depending upon the treatment table employed. This retrospective study examines the nature and incidence of O2 toxicity in 998 patients who underwent recompression treatment at our facility from 1983 through 2001. Only patients evaluated for diving related injury were considered for this study. Of 1189 charts reviewed, 998 patients received recompression and were entered into this study. The total number of treatment exposures was determined as was the total number of O2 toxicity events characterized as either pulmonary or CNS, and patients were divided into male/female analysis. Overall incidence as well as the incidence for both toxicity types was determined, and their occurrence in both male and female patients was ascertained. 2166 recompressions were undertaken, 449 female and 1717 male. The peak PO2 for these treatments ranged from 2.6ATA to 2.9ATA. 155 O2 toxicity events occurred in 152 patients, 49 females and 103 males. Three patients, 2 females and 1 male, had mixed events. Incidence of an O2 toxic event = 7.0 per 100 recompressions. Incidence of pulmonary toxicity overall = 5.0 per 100 recompressions, while CNS events = 2.0 per 100 recompressions with overall seizure rate = 0.6 per 100 recompressions. In females, pulmonary toxicity rate = 6.9 per 100 recompressions, CNS toxicity rate = 4.4 per 100 recompressions with seizures occurring at 1.3 per 100 recompressions. In males, pulmonary toxicity rate = 4.6 per 100 recompressions, CNS toxicity rate = 1.4 per 100 recompressions, and seizures at 0.4 per 100 recompressions.
- Seizure incidence in 80,000 patient treatments with hyperbaric oxygen.
Yildiz S, Aktas S, Cimsit M, Ay H, Toğrol E.
Source: Gülhane Military Medical Academy, Haydarpaşa Training Hospital, Department of Underwater and Hyperbaric Medicine, 81100 Kadiköy-Istanbul, Turkey.
syildiz@gata.edu.tr
Abstract
INTRODUCTION: Hyperbaric oxygen treatment (HBOT) involves some risk of central nervous system (CNS) oxygen toxicity, which may be revealed by various signs and symptoms including seizures in patients breathing O2 at pressures of 2 ATA or higher. The aim of this study was to determine the incidence of such seizures in the Underwater and Hyperbaric Medicine Departments of two university hospitals.
METHODS: We retrospectively evaluated 80,679 patient-treatments for 9 clinical indications to determine the incidence of seizures attributable to CNS O2 toxicity. Because different protocols were used for HBOT, the treatments were studied in four groups according to the chamber type used and the medical facility at which it was located.
RESULTS: Only 2 seizures were documented, yielding an incidence of 2.4 per 100,000 patient-treatments. Both cases occurred in a multiplace chamber pressurized to 2.4 ATA with O2 delivered by mask for three x 30 min with 5-min air breaks.
DISCUSSION: The seizure incidence reported here is lower than other studies published in the literature. The delivery of O2 by mask rather than hood may be a factor. Nevertheless, it appears that the risk of seizures due to CNS O2 toxicity during HBOT is very low as long as appropriate exclusion criteria and treatment profiles are used.
I, personally, have not heard of a case from out in the field (or should I say water?) of CNS ox-tox occurring at a ppO2 of <2.
Hope this proves useful.
Regards,
DocVikingo