Carbon monoxide toxicity mechanism: Why does prolonged exposure to high concentrations of CO (greater than 5000 ppm) commonly lead to death in humans?

Introduction / Context:
Carbon monoxide is a colorless, odourless gas produced by incomplete combustion. Understanding its toxicology is crucial for indoor air safety, vehicular exhaust management, and emergency response.

Given Data / Assumptions:

• Exposure levels are very high (> 5000 ppm), well above ambient standards.
• Victim has no supplemental oxygen therapy during exposure.
• Mechanism sought is physiological, not mechanical obstruction.

Concept / Approach:
CO binds haemoglobin approximately 200–250 times more strongly than oxygen, forming carboxyhemoglobin (COHb). This both reduces available haemoglobin for oxygen transport and shifts the oxyhemoglobin dissociation curve leftward, impairing oxygen release to tissues. The net effect is cellular hypoxia despite normal or high PaO2 in blood plasma.

Step-by-Step Solution:
Identify binding affinity: CO + Hb → COHb (very high affinity).Consequence: reduced oxygen carriage and delivery to tissues (hypoxic injury).Outcome at high exposure: loss of consciousness, arrhythmias, death.

Verification / Alternative check:
Treatment protocols (100% oxygen or hyperbaric oxygen) accelerate CO elimination from Hb, directly targeting the mechanism described.

Why Other Options Are Wrong:
Clotting/lysis: not the mechanism of CO toxicity.Respiratory tract jamming: CO is a gas; no physical blockage occurs.Reaction to form CO2: CO does not simply combine with blood oxygen to make CO2 in vivo to cause hypoxia.

Common Pitfalls:
Assuming low oxygen readings alone diagnose CO poisoning; pulse oximeters can misread COHb as oxyhemoglobin, masking hypoxia.

Final Answer:
It forms carboxyhemoglobin with haemoglobin, preventing oxygen transport