Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness when hyperbaric oxygen is breathed in diving and hyperbaric medical therapy. Lin and Jamieson (J Appl Physiol 75: 1980-1983, 1993) reported that humidity in the inspired gas enhances CNS oxygen toxicity. Because alveolar gas is fully saturated with water vapor, we could not see a cause and effect and surmised that other factors, such as metabolic rate, might be involved. Rats were exposed to 507- and 608-kPa O₂ in dry (31 or 14%) or humid (99%) atmosphere until the appearance of the first electrical discharge preceding the clinical convulsions. Each rat served as its own control. A thermoneutral temperature (28 ± 0.4°C) yielded resting CO₂ production of 0.81 ± 0.06 ml · g¹ · h¹. Latency to the first electrical discharge was not affected by humidity. At 507-kPa O₂, latency was 23 ± 0.4 and 22 ± 0.7 min in dry and humid conditions, respectively, and, at 608-kPa O₂, latency was 15 ± 4 and 14 ± 3 min in dry and humid conditions, respectively. When no effects of CO₂ and metabolic rate are present, humidity does not affect CNS oxygen toxicity. Relevance of the findings to diving and hyperbaric therapy is discussed.