Ok, did a quick search. Here is one article with one good (I think) NCBI reference. Second and third reference didn't seem relevant to me, or didn't catch my interest.
The article has the usual vague "may be" and "too much", when I looked at the first reference I didn't find anything to worry about considering the chambers we use and how long we use them in general.
Oxygen, the gas vital to sustain life, can also destroy it. It may become toxic at an elevated partial pressure, which may be the result of a rise in inspired oxygen concentration, an increase in environmental pressure or a combination of both. The toxicity ...
www.ncbi.nlm.nih.gov
I thought this was the most interesting...
Central Nervous System Toxicity
CNS toxicity, as described originally by Bert, occurred at oxygen pressures of > 3 ATA. However, lower pressures may result in similar effects if exposure is prolonged, as shown in
Fig 1. Early symptoms and signs are quite variable but twitching of perioral and small muscles of the hand is a fairly constant feature. Facial pallor and ‘cogwheel’ breathing are also often noticed, thought to be the result of intense peripheral vasoconstriction due to hyperoxia and diaphragmatic twitching respectively [
5,
6]. If exposure is continued, vertigo and nausea, followed by altered behaviour, clumsiness, and finally convulsions result. The convulsions begin with a loss of conciousness and develop in three phases; a tonic phase with a generalized hypertonus lasting for about 1 min, a clonic phase with convulsion for about 2–3 mins and a post critical phase of about 10 mins. The patient has no memory of the crisis. A neurogenic pulmonary edema concomitant with the convulsions has also been reported [
1]. CNS toxicity is hastened by factors such as raised PCO2, stress, fatigue and cold [
2].
[IMG alt="An external file that holds a picture, illustration, etc.
Object name is gr1.jpg"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4925834/bin/gr1.jpg[/IMG]
Fig. 1
Predicted human pulmonary and central nervous system tolerance to high pressure oxygen
Pulmonary Toxicity
Pulmonary toxic effect of oxygen can arise after prolonged exposure to oxygen > 0.5 ATA. Symptoms appear after a latent period whose duration decreases with increase in PO2. In normal humans the first signs of toxicity appear after about 10 hours of oxygen at 1ATA. Clinical features can be divided into three phases (a) Tracheobronchitis (b) ARDS (c) Pulmonary interstitial fibrosis. Absorption atelectasis due to washout of N2 can lead to collapse of parts of the lung in the event of air trapping.
100% oxygen can be tolerated at sea level for about 24–48 hours without any serious tissue damage. Longer exposures produce definite tissue injury. Oxygen at 2 ATA produces characteristic pulmonary signs and symptoms beginning with mild carinal irritation on deep inspiration 3–6 hours into the exposure, intense carinal irritation an uncontrolled cough after about 10 hours and finally chest pain and dyspnoea. Symptoms subside 4 hours after cessation of exposure in majority of patients [
7].
