Carbon Monoxide Toxicity

Toxic exposure most typically occurs in fire-related circumstances, accounting for over two-thirds of fire-related deaths.¹ Other common causes of toxicity include inhalation of vehicle exhaust, fire smoke, and improperly managed heating systems. It is estimated that 20,000 to 50,000 cases of carbon monoxide poisoning occur every year, resulting in grave illness and fatalities, as well as an overall cost of $1.3 billion annually upon the U.S. healthcare system.²

Carbon monoxide poisoning occurs when the toxin replaces oxygen molecules that the body needs. Mitochondria contained within our cells depend on oxygen to produce energy that drives all cellular processes. But upon exposure, the oxygen molecules are replaced and the body is saturated with carbon monoxide.

Because carbon monoxide is odorless, colorless, and tasteless, toxicity is difficult to diagnose prior to the onset of symptoms. Although exposure higher than 35 ppm is considered toxic to humans, other studies indicate that exposure as low as 10 ppm can result in traceable quantities of carboxyhemoglobin (COHb), the molecule that forms within the blood marking the degradation of one’s ability to consider and utilize oxygen.³ The clinical diagnosis of carbon monoxide toxicity is based on a three-pronged approach:⁴

1. Symptoms
2. Recent exposure
3. Increased blood levels

In non-smokers, the COHb concentration is less than 2% but can be as high as 15% in smokers. Symptoms typically present once the concentration exceeds 10%.⁵ Once they reach 30% to 50%, symptoms include increases in respiratory rates, tachycardia, motor paralysis, confusion, and possible loss of consciousness. A concentration above 50% is considered life-threatening.⁶

Acute Symptoms

Shortly after exposure, a person may feel dizziness, headaches, fatigue, vomiting, nausea, altered mentation, chest pain, shortness of breath, and loss of consciousness. A person may also present with symptoms of cardiac toxicity such as angina, myocardial ischemia, cardiac arrythmia, or cute chronic heart failure exasperation. Specific symptoms are experienced as the carbon monoxide concentrations increase:¹

• 10-20% - headache, fatigue, ear ringing
• 20-30% - headache, weakness, nausea, vomiting
• 30-40% - severe headache, dizziness, nausea, vomiting
• 40-50% - syncope, confusion, increased respiration and heart rate
• 50-60% - coma, convulsions, depressed respiration
• 60-70% - coma, convulsions, cardiopulmonary depression, risk of fatality
• 70% > - respiratory failure, death

Chronic Symptoms

Chronic symptoms are more difficult to diagnose but may include:¹

• Chronic fatigue
• Vertigo
• Paraesthesias
• Polycythemia
• Abdominal pain
• Diarrhea
• Recurrent infections

Symptoms can persist for years after initial exposure. Although patients may improve over the course of months or up to a year, at the six-year mark of CO poisoning, some usually suffer from long-term neurocognitive sequelae related to brain injury.³ One study found that 48.7% of patients exhibited neurologic symptoms 33 years after CO poisoning.

Long-term symptoms are categorized in two general groups –

• Persistent neurological sequelae (PNS) – occurs immediately and persists over time
• Delayed neurological sequelae (DNS) – begins to develop at around 40 day after exposure and tends to be more severe than PNS
  • DNS can develop in up to 45% of patients after acute exposure.⁷

Long-term symptoms can be tracked using brain imaging, which can spot where the brain injuries occur, most commonly, in the region known as the globus pallidus. Imaging can also spot lesions of those exposed to CO in low levels over time, such as smokers.

Mood and Behavior Changes

Several studies have indicated changes in mood and behavior after CO inhalation, including impaired memory, cognitive dysfunction, depression, anxiety, and vestibular and motor deficits.³ These changes are typically evident by six weeks after exposure.

Another study indicated significantly lower cognitive performance than controls on processing speed, mental flexibility, inhibition, and working and verbal episodic memories.¹²

• High-flow oxygen via a non-rebreather mask
  • This is the immediate and necessary treatment for acute exposure and should be administered even in the absence of confirmed toxicity
• Intubation (if the patient is comatose or neurologically impaired) and given 100% oxygen
• Monitoring for potential cardiac arrhythmia and other concomitant conditions
• Determining whether the exposure was intentional or unintentional and addressing any suicidal ideations if present
• Hyperbaric oxygen therapy (if the patient is experiencing loss of consciousness, neurological deficits, or mental status changes or if the COHb is greater than 25%)
  • This treatment is the most effective if administered within six hours after exposure
  • Patients have fewer behavioral changes when receiving this therapy³

• Fezza v. Legal Sea Foods, LLC – alleged CO poisoning in the workplace resulting in depression and neurocognitive changes
• Suresh v. Ford Motor Company – putative class action alleging defects related to 2016 and 2017 Ford Explorers where exhaust fumes infiltrated the passenger cabin