Carbon(II) Oxide
Carbon(II) Oxide Uses, Dosage, Side Effects, Food Interaction and all others data.
Carbon(II) Oxide (CO) is a colorless, odorless, and tasteless gas that has a slightly lower density than air. It is toxic to hemoglobin utilizing animals (including humans), when encountered in concentrations above about 35 ppm, although it is also formed in normal animal metabolism in low quantities, and is thought to have some normal biological/homeostatic functions . Carbon(II) Oxide (CO), is a ubiquitous environmental product of organic combustion, which is also formed endogenously in the human body, as the byproduct of heme metabolism . Exhaled CO (eCO), similar to exhaled nitric oxide (eNO), has been evaluated as a candidate breath biomarker of pathophysiological states, including smoking status, and inflammatory diseases of the lung and other organs. Exhalation of corbon monoxide values have been studied as potential indicators of inflammation in asthma, stable COPD and exacerbations, cystic fibrosis, lung cancer, and during surgery or critical care .
A test of the diffusing capacity of the lungs for carbon monoxide (DLCO), is one of the most clinically valuable tests of lung function testing. The technique was first described 100 years ago, and applied to clinical practice many years after. The DLCO measures the ability of the lungs to transfer gas from inhaled air to the red blood cells in pulmonary capillaries. The DLCO test is both convenient and simple for the patient to undergo. The ten seconds of breath-holding required for the DLCO maneuver is easier for most patients to perform than the forced exhalation required for other respiratory tests .
Carbon(II) Oxide is presently used in small amounts in low oxygen modified atmosphere packaging systems (MAP) for fresh meat to stabilize and maintain natural meat color. This use of CO has been generally recognized as safe (GRAS) in several packaging applications for fresh meat products. Since 2002, FDA has favorably reviewed three GRAS notifications for carbon monoxide use in fresh meat packaging . The FDA classifies this drug as permitted as a food additive in the packaging and preparation of food products, while following the federal code of regulations .
| Trade Name | Carbon(II) Oxide |
| Generic | Carbon monoxide |
| Carbon monoxide Other Names | Carbon monoxide, carbon(II) oxide, Carboneum oxygenisatum |
| Type | |
| Formula | CO |
| Weight | Average: 28.01 Monoisotopic: 27.99491462 |
| Protein binding | Binds with very high affinity to hemoglobin in humans . |
| Groups | Approved, Investigational |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Carbon(II) Oxide is a gas used as a marker of respiratory status in spirometry tests.
Used as a marker of respiratory status in spirometry tests , .
Food additive for pigment fixation in meat .
How Carbon(II) Oxide works
In respiratory testing, the diffusing capacity for carbon monoxide (DLCO) is a measure of the ability of gas to transfer from the alveoli across the alveolar epithelium and the capillary endothelium to the red blood cells. The DLCO depends not only on the area and thickness of the blood-gas barrier but additionally on the volume of blood in the pulmonary capillaries. The distribution of alveolar volume and ventilation also has an impact on the measurement .
DLCO is measured by sampling end-expiratory gas for carbon monoxide (CO) after patients inspire a small and safe amount of exogenous CO, hold their breath, and exhale. Measured DLCO is adjusted for alveolar volume (which is estimated from dilution of helium) and the patient’s hematocrit level. DLCO is reported as mL/min/mm Hg and as a percentage of a predicted value .
Carbon(II) Oxide exerts effects on cell metabolism through both hypoxic and non-hypoxic modes of action. Both mechanisms of action are thought to be the result of the ability of carbon monoxide to bind strongly to heme and alter the function and/or metabolism of heme proteins. The binding affinity of carbon monoxide for hemoglobin is more than 200 times greater than that of oxygen for hemoglobin. The formation of carboxyhemoglobin (COHb) decreases the O2 carrying capacity of blood and disrupts the release of O2 from Hb for its use in tissues. Through similar mechanisms, carbon monoxide diminishes the O2 storage in muscle cells by binding to and displacing O2 from, myoglobin. Though all human tissues are vulnerable to carbon monoxide-induced hypoxic injury, those with the highest O2 demand are especially vulnerable, including the brain and heart .
Most of the non-hypoxic mechanisms of action of carbon monoxide have been thought to be due to binding of carbon monoxide to heme in proteins other than Hb. The most notable targets of carbon monoxide include components of many important physiological regulatory systems, including brain and muscle oxygen storage and use(myoglobin, neuroglobin); nitric oxide cell signaling (e.g., nitric oxide synthase, guanylyl cyclase); prostaglandin cell signaling (cyclooxygenase, prostaglandin H synthase); energy metabolism and mitochondrial respiration (cytochrome c oxidase, cytochrome c, NADPH oxidase); steroid and drug metabolism (cytochrome P450); cellular redox balance and reactive oxygen species (ROS; catalase, peroxidases); and numerous transcription factors (e.g., neuronal PAS domain protein, NPAS2, implicated in regulation of circadian rhythm) .
In meat processing, carbon monoxide reacts with myoglobin, to form carboxymyoglobin, imparting a red appearance to the meat .
Toxicity
LD50 is 1807 ppm in rats after 4 hours of exposure . In humans, exposure to 4000 ppm or more in less than 1 hour leads to death .
Carbon Monoxide Toxicity from Food Ingestion Treated with Carbon Monoxide
Very little information has been published in the literature on the consumer’s exposure to CO-packaged meat. The toxicological aspects of CO used in MAP of meat were reviewed by Sørheim et al. , and they concluded that, with up to about 0.5% of CO, no human toxicity is likely. It has been suggested that the consumption of CO-treated meat is not associated with any health risks, and meat from CO-MAP results only in negligible amounts of CO and COHb in humans , .
Mechanism of CO Toxicity
Once CO is inhaled, it binds with hemoglobin to form carboxyhemoglobin (COHb) with an affinity of 200 times greater than oxygen that leads to decreased oxygen-carrying capacity and the decreased release of oxygen to tissues, causing tissue hypoxia. Ischemia occurs with CO poisoning when there is a loss of consciousness combined with hypotension and ischemia in the arterial border areas of the brain. Besides binding to many heme-containing proteins, CO interrupts oxidative metabolism, leading to the formation of free radicals. Once hypotension and unconsciousness occur with CO poisoning, lipid peroxidation and apoptosis soon follow .
Failure to diagnose CO poisoning may result in morbidity and mortality and allow for continued exposure to a dangerous environment. The management of CO poisoning begins with inhalation of supplemental oxygen therapy and aggressive supportive measures. Hyperbaric oxygen therapy (HBOT) accelerates the dissociation of CO from hemoglobin .
The concentration, exposure time and physical activity of the individual will determine the percentage conversion of haemoglobin to carboxyhaemoglobin. The effects produced depend on the degree and duration of saturation of blood with carbon monoxide .
Levels of Intoxication with Carbon Monoxide
The first symptoms of carbon monoxide exposure when carboxyhemoglobin is 15-30% are generalized, and may include: headache, dizziness, nausea, fatigue, and impaired manual dexterity. Individuals with ischemic heart disease may suffer from chest pain and decreased exercise duration at COHb levels measured from 1% - 9% .
COHb levels between 30-70% lead to loss of consciousness and eventually death .
Long-term Effects
Following the resolution of the acute symptoms, there may be a lucid interval from 2-40 days before the development of delayed neurologic sequelae (DNS). Diffuse brain demyelination combined with lethargy, behavioral changes, memory loss, and parkinsonian features may occur. 75% of patients with DNS recover within 1 year. Neuropsychologic abnormalities with chronic CO exposure are found even when magnetic resonance imaging (MRI) and magnetic resonance spectroscopy findings are normal. White-matter damage in the centrum semiovale and periventricular area of the brain, and abnormalities in the globus pallidus, are most commonly observed on MRI following CO toxicity. Though less common, toxic or ischemic peripheral neuropathies are associated with high levels of CO exposure in humans. The basis for the management of CO poisoning is 100% hyperbaric oxygen therapy using a tight-fitting mask for at least 6 hours. The indications for treatment with hyperbaric oxygen to decrease the half-life of COHb remain controversial .
Food Interaction
No interactions found.Elimination Route
Although CO is not one of the respiratory gases, the similarity of physico-chemical properties of CO and oxygen (O2) permits an extension of the findings of studies on the kinetics of transport of O2 to those of CO. The rate of formation and elimination of COHb, its concentration in blood, and its catabolism is controlled by numerous physical factors and physiological mechanisms .
The absorption of carbon monoxide from the consumption treated food products is not significant. Risk of CO toxicity from the packaging process or from consumption of CO-treated meats is negligible .
Half Life
The half-life of carbon monoxide at room air temperature is 3-4 hours. 100% oxygen reduces the half-life to 30-90 minutes; hyperbaric oxygen at 2.5 atm (atmosphere units) with 100% oxygen reduces it to 15-23 minutes .
Innovators Monograph
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