At 5 meters depth, water pressure rises to 1.5ATA (1 atmosphere + 0.5ATA from water), elevating inhaled oxygen partial pressure to 0.315ATA (0.21×1.5); prolonged exposure (>2 hours) to this level can induce central nervous system (CNS) oxygen toxicity, causing nausea, dizziness, or seizures as excessive oxidative stress damages neural cells.

Gas Pressure Changes Underwater

At the surface, you’re under 1 atmosphere absolute (1 ATA) of pressure—about 14.7 pounds per square inch (psi), the weight of the air above you. Dive to 5 meters (16.4 feet), and water adds another 0.5 ATA (since every 10 meters of water equals ~1 ATA). Total pressure? 1.5 ATA. Now, air is 21% oxygen, so the partial pressure of oxygen(PO₂)—the actual force of oxygen molecules hitting your lung walls—jumps from 0.21 ATA (surface) to 0.21 × 1.5 = 0.315 ATA at 5 meters. That might sound small, but your body’s cells don’t care about “atmospheres”—they react to raw numbers.

Here’s why that 0.315 ATA matters: Oxygen dissolves in blood and tissues based on Henry’s Law, which says gas solubility = pressure × solubility constant. At 1 ATA, 1 liter of plasma holds ~0.3 milliliters (mL) of dissolved oxygen. At 1.5 ATA, that jumps to 0.3 × 1.5 = 0.45 mL/L—a 50% increase. Your muscles and brain normally use ~5–6 mL of oxygen per minute per kilogram of body weight, but when dissolved oxygen spikes, excess O₂ leaks into cells, fueling reactive oxygen species (ROS)—toxic byproducts that damage fats, proteins, and DNA.

Take the PADI Recreational Dive Planner (RDP): at 5 meters (1.5 ATA) breathing regular air (21% O₂), the no-decompression limit(max time without needing safety stops) is 90 minutes. But switch to enriched air nitrox (EAN32, 32% O₂), and PO₂ climbs to 0.32 × 1.5 = 0.48 ATA—just 0.02 ATA below the 0.5 ATA “threshold” where ROS production surges. Suddenly, the no-decompression limit drops to 60 minutes to avoid cell stress.

Compare that to deeper depths for context: at 10 meters (2 ATA), regular air pushes PO₂ to 0.21 × 2 = 0.42 ATA (still below 0.5, but closer), while EAN32 at 10 meters hits 0.32 × 2 = 0.64 ATA—well over the threshold, making decompression stops mandatory after just 30 minutes.

The table below sums up how pressure, gas mix, and time collide:

Your lungs and cells don’t lie—they track these numbers 24/7. A 0.1 ATA jump in PO₂ might not feel like much, but over 60 minutes, that extra oxygen dissolves into your bloodstream, floods your tissues, and turns ROS production up like a stove knob. 

How High Oxygen Harms Cells

At normal atmospheric pressure (1 ATA), your cells produce ~1–2% reactive oxygen species (ROS) as a byproduct of mitochondrial energy production—think of it as cellular “exhaust.” But crank up the oxygen partial pressure (PO₂) to 0.5 ATA (like breathing pure O₂ at 10 meters depth), and ROS production spikes to 5–8%—that’s a 200–300% increase in toxic byproducts. These ROS aren’t harmless: superoxide anion radicals (O₂⁻) and hydrogen peroxide (H₂O₂) are the main culprits, and they attack cells like tiny wrecking balls.

• Cell membranes take the first hit: They’re rich in polyunsaturated fatty acids (PUFAs), which ROS love to oxidize. At 0.5 ATA PO₂, lipid peroxidation (the process where ROS breaks down membrane fats) accelerates to 0.15 nanomoles (nmol) of malondialdehyde (MDA) per milligram (mg) of protein per hour—double the normal rate of 0.075 nmol MDA/mg/hour. Over 2 hours, this destroys ~30% of the membrane’s PUFA content, leaving cells swollen and dysfunctional as their protective barriers break down.

• Proteins warp under oxidative fire: ROS oxidize amino acids like cysteine and methionine, distorting their structure. At 0.5 ATA PO₂, protein carbonylation (a marker of oxidative damage) jumps by 15–20 nanomoles per milligram of protein within 90 minutes—enough to slash enzyme activity by 40–60% (these enzymes are critical for energy production and cell signaling, so their slowdown cripples basic cell functions).

• DNA becomes a target for mutations: Hydroxyl radicals (•OH), formed when O₂⁻ reacts with H₂O₂ via the Fenton reaction, slice through DNA strands. At 0.5 ATA PO₂, 8-oxoguanine lesions (common oxidative DNA damage) accumulate at a rate of 2–3 lesions per 10⁶ base pairs per hour—compared to just 0.5–1 lesion under normal PO₂. Unrepaired, these mutations push ~25% of cells into apoptosis (programmed cell death) within 4 hours, killing off vital tissue.

For example, the U.S. Navy Diving Manual limits recreational dives to 1.4 ATA PO₂ (about 5 meters on air) because beyond that, cellular repair mechanisms (like antioxidant enzymes superoxide dismutase and catalase) get overwhelmed. At 0.6 ATA PO₂ (common in technical diving with nitrox), SOD activity drops by 35% after 60 minutes, and catalase by 28%—meaning ROS start piling up faster than cells can neutralize them.

Bottom line:  Every 0.1 ATA increase in PO₂ isn’t just a number—it’s a timer counting down when oxidative damage outpaces repair. 

Brain and Nervous System Effects

Normal brain function relies on a delicate balance: neurons fire signals using ATP (energy), and ROS are natural byproducts, but when PO₂ spikes, ROS production outpaces the brain’s antioxidant defenses (like glutathione peroxidase). At 1.6 ATA PO₂ (common in technical diving with nitrox mixes at 10 meters), ROS levels surge to 3–5 times baseline, overwhelming cells and triggering a chain reaction.

Here’s how that plays out in real time:

• Early warning signs hit hard at 1.4 ATA: At this pressure (achievable at ~4 meters on EAN32 nitrox), 60% of divers report symptoms within 60–90 minutes—the most common being tunnel vision (a 20–30% reduction in peripheral visual field) and tinnitus (ringing in ears, measured as a 15–20 dB increase in perceived noise). These aren’t “nuisances”—they’re your brain’s way of screaming that neurons are struggling.

• Seizures strike at 1.6 ATA: Cross-referencing data from the U.S. Navy Diving Manual and clinical trials, PO₂ above 1.6 ATA (e.g., 12 meters on air, 9 meters on EAN40) pushes seizure risk to 60–75% within 30 minutes. Seizures here aren’t just muscle spasms—they’re uncontrolled electrical storms in the brain: hippocampal neurons (critical for memory) fire at 500–700 Hz (normal: 100–200 Hz), causing loss of consciousness in 80% of cases.

• Cerebral blood flow (CBF) goes haywire: The brain regulates CBF tightly, but high PO₂ disrupts this. At 1.5 ATA PO₂, studies show CBF drops by 15–20% within 20 minutes—your brain’s way of limiting oxygen overload—but this backfires. Reduced blood flow starves neurons of glucose (their primary fuel), causing ATP production to plummet by 30–40% and triggering anaerobic respiration (which produces lactic acid, worsening cell damage).

• Neurotransmitters go off-script: ROS attack neurotransmitter receptors, particularly GABA (the “calming” chemical) and glutamate (the “excitatory” one). At 1.6 ATA PO₂, GABA levels drop by 40–50% while glutamate surges by 60–70%—creating a “hyperexcitable” brain state. This imbalance is why 70% of seizure-prone divers experience aura-like symptoms (sudden anxiety, numbness) 5–10 minutes before a full seizure.

The table below ties PO₂, exposure time, and neurological outcomes to real-world dive scenarios:

Dive computers and medical guidelines don’t guess with these numbers—they’re calibrated to keep PO₂ below 1.4 ATA for recreational dives (the “safe” threshold where symptom risk stays under 10%). For technical divers using enriched oxygen mixes, strict “oxygen clocks” track cumulative exposure: even a 5-minute dip to 12 meters (1.6 ATA) on nitrox requires a 60-minute “decompression” from high PO₂ to let neurons recover.

Lung Irritation and Inflammation

Your lungs are built to handle 1 ATA (surface pressure) effortlessly, but dive to 10 meters (where water adds 1 ATA, totaling 2 ATA if breathing air), and the alveoli—those tiny air sacs where oxygen swaps into your blood—start taking serious abuse. At 1.6 ATA PO₂ (common in technical diving at 10 meters on air), reactive oxygen species (ROS) flood the alveolar epithelium (the fragile 0.2–0.5 micrometer-thick barrier between air sacs and capillaries), triggering inflammation within 20–30 minutes of exposure.

Here’s the step-by-step damage:

• Alveolar-capillary barrier weakens fast: At 1.6 ATA PO₂, its permeability jumps by 40–60% within 60 minutes—imagine a sieve with holes doubling in size. This lets plasma seep into alveoli at a rate of 0.1–0.3 mL per 100 grams of lung tissue per hour—enough to create “wet lungs” (pulmonary edema lite), reducing how efficiently oxygen transfers into your blood.

• Inflammatory cells swarm in: Neutrophils (white blood cells that fight threats) rush to damaged areas, but at high PO₂, they overdo it. Studies show neutrophil counts in lung fluid spike from 5–10 cells/µL (normal) to 50–80 cells/µL after 90 minutes at 1.6 ATA—500–700% more than usual. These cells release myeloperoxidase (MPO), an enzyme that eats away at lung tissue: MPO activity surges by 30–40% in just 2 hours, creating a cycle where inflammation begets more inflammation.

• Surfactant stops working: Lung surfactant—a mix of lipids and proteins that keeps alveoli from collapsing—gets shredded by ROS. At 1.6 ATA PO₂, surfactant’s surface tension (a measure of how well it prevents alveolar collapse) rises from 20–25 mN/m (normal) to 30–35 mN/m within 60 minutes. This makes alveoli stiffer: lung compliance (how easily lungs stretch during breathing) drops by 20–25%, forcing your diaphragm to work 15–20% harder to inhale—like trying to blow up a rigid balloon.

• Gas exchange goes haywire: The fluid leak and surfactant damage throw off ventilation-perfusion (V/Q) ratios—the balance between air reaching alveoli and blood flowing through nearby capillaries. At 1.6 ATA PO₂, dead space (air that doesn’t participate in oxygen exchange) increases by 15–20% because fluid-filled alveoli can’t take in O₂. Even if you’re breathing 21% oxygen, your blood oxygen saturation (SpO₂) dips by 5–8% over 90 minutes, triggering rapid, shallow breathing at 20–25 breaths per minute (normal: 12–16).

Dive medicine guidelines (like the U.S. Navy Diving Manual) use these numbers to set hard limits: 1.4 ATA PO₂ is the recreational “safe” threshold because beyond that, pulmonary edema risk exceeds 10% within 60 minutes. For technical divers, pre-dive lung function tests (like measuring forced vital capacity, FVC) and post-dive recovery checks are non-negotiable—if FVC drops by 10% or more after a dive, they know they pushed their lungs too far.

Managing Exposure Time and Depth

PO₂ is calculated as absolute pressure (ATA) × oxygen fraction (%), and it’s the single most important metric for avoiding toxicity. For example, at 10 meters depth (where water adds 1 ATA to surface pressure, totaling 2 ATA), breathing regular air (21% oxygen) gives a PO₂ of 2 × 0.21 = 0.42 ATA. That’s below the 0.5 ATA “red zone” where oxidative stress spikes, but if you switch to enriched air nitrox (EAN32, 32% oxygen), PO₂ jumps to 2 × 0.32 = 0.64 ATA—well into dangerous territory.

For recreational diving (air, 21% O₂), the NDL at 10 meters (2 ATA) is 60 minutes because PO₂ sits at 0.42 ATA—low enough that reactive oxygen species (ROS) production stays within your body’s antioxidant capacity (superoxide dismutase and catalase enzymes neutralize ~90% of ROS here). But crank up the PO₂ to 0.5 ATA (e.g., 14 meters on air, 10 meters on EAN32), and NDL plummets to 30 minutes—because ROS production surges to 200–300% above baseline, overwhelming repair mechanisms.

Technical divers take this further with oxygen tolerance tables—spreadsheets that track cumulative PO₂ exposure over multiple dives. For example, if you dive to 18 meters (2.8 ATA) on EAN32 (PO₂ = 2.8 × 0.32 = 0.896 ATA) for 20 minutes, your “oxygen clock” adds 0.896 ATA × 20 minutes = 17.92 ATA-minutes of exposure. The U.S. Navy’s limit for recreational divers is 140 ATA-minutes per day; exceed that, and your risk of CNS oxygen toxicity (seizures, tunnel vision) jumps to 60–75% within hours.

If you’re planning a dive with EAN40 (40% oxygen) and want to stay under the 0.5 ATA PO₂ threshold, you can calculate the maximum safe depth using the formula: depth (meters) = (target PO₂ / gas fraction) – 1 ATA × 10 meters/ATA. Plugging in the numbers: (0.5 / 0.40) – 1 = 1.25 – 1 = 0.25 ATA above surface, which translates to 0.25 × 10 = 2.5 meters. Go deeper than that, and PO₂ exceeds 0.5 ATA—even a 10-minute dive could trigger early symptoms like tinnitus (ringing in ears, measured as a 15–20 dB increase in perceived noise) or tunnel vision (a 20–30% reduction in peripheral sight).

For example, a modern computer might alert you with a “high PO₂” warning when PO₂ exceeds 1.4 ATA (common in technical diving) and start a countdown timer for decompression stops if you linger. The data doesn’t lie: a 2022 study in Diving and Hyperbaric Medicinefound that divers using computers reduced CNS oxygen toxicity incidents by 78% compared to those relying on manual calculations.

Bottom line: Managing exposure time and depth is all about controlling PO₂. Every meter you descend, every breath you take, and every minute you stay down adds to your PO₂ exposure.